Hyperfermentemia what is it. A method for diagnosing hyperenzymemia in violation of the exocrine function of the pancreas. Choice of term and method of delivery
Viral hepatitis is a group of human diseases caused by various hepatotropic viruses with multiple mechanisms of transmission and manifested by predominant damage to the liver with impaired functions, intoxication, dyspeptic syndromes, and often hepatomegaly and jaundice.
The group of the most common and studied viral hepatitis hepatitis A, hepatitis B, hepatitis C, hepatitis D, hepatitis E. New candidates for the role of pathogens of hepatitis are discussed. These are viruses G, F, TTV, SEN V, etc. serious problem presently represent mixed hepatitis.
VIRAL HEPATITIS WITH FECA-ORAL TRANSMISSION
Hepatitis A
Hepatitis A - acute cyclic viral infection with fecal-oral transmission of the pathogen, characterized by impaired liver function.
Epidemiology
Hepatitis A - intestinal infection, severe anthroponosis.
The source of infection is patients with inapparent and manifest forms of hepatitis A. Persons with subclinical, obliterated and anicteric forms of the disease have the greatest epidemiological significance, the number of which can many times exceed the number of patients with icteric forms of hepatitis A. Infection of contact persons is possible already from the end of the incubation period, most intensively continues during the prodromal (preicteric) period and persists in the first days of the height of the disease (jaundice). The total duration of virus isolation with faeces usually does not exceed 2-3 weeks. In recent years, it has been shown that viremia in hepatitis A can be longer (78-300 days or more). The fecal-oral mechanism of transmission of the pathogen is realized by the water, food and contact-household route with the absolute predominance of the water route, which provides outbreaks and epidemics of hepatitis A. The possibility of the blood-contact (parenteral) route of transmission of the hepatitis A virus (about 5%) from patients with manifest and inapparent forms of infection (post-transfusion infection with hepatitis A in patients with hemophilia, infection of intravenous drug users).
The sexual route of transmission of the pathogen, which is facilitated by promiscuity, the presence of other sexually transmitted infections, non-traditional sexual intercourse (primarily oral-anal contacts), is not excluded. It occurs predominantly in children and young adults; In recent years, cases of hepatitis A in people older than 30 years and even 40 years have become noticeably more frequent. The disease is characterized by seasonality (mainly summer-autumn period). The frequency of ups and downs of the disease ranges from 5 to 20 years. Susceptibility to hepatitis A is high. Classification
Allocate inapparent (subclinical) and manifest forms of hepatitis A. The latter includes erased, anicteric and icteric forms. According to the severity of the flow, they distinguish between mild, moderate and severe forms, downstream - acute and protracted. Chronic forms of hepatitis A are not observed.
Etiology
The causative agent - Hepatitis A virus (HAV) - belongs to the family Picornaviridae, the genus Hepatovirus.
Opened in 1973 by S. Feinstone. HAV is a small virus containing ribonucleic acid (RNA), has one specific Ag (HAAg), which is highly immunogenic. There are four known HAV genotypes that belong to the same serotype, which is the reason for the development of cross-immunity.
Anti-HAV IgM circulate in the blood from the first days of illness a short time(2-4 months), and HAV IgG appearing later remain in the body for a long time. The hepatitis A virus is highly persistent in the environment, but is susceptible to ultraviolet irradiation and boiling (dies after 5 minutes).
Pathogenesis
The entrance gate is the mucous membranes of the gastrointestinal tract. In the vascular endothelium of the small intestine and mesenteric lymph nodes, the primary replication of the virus occurs. followed by viremia clinical picture manifested by intoxication syndrome), followed by dissemination of the pathogen into the liver (a consequence of the hepatotropic nature of the virus). HAV replication in hepatocytes leads to dysfunction of cell membranes and intracellular metabolism with the development of cytolysis and dystrophy of liver cells. Simultaneously with the cytopathic effect of the virus (leading in hepatitis A), a certain role is assigned to immune damaging mechanisms. As a result, clinical and biochemical syndromes characteristic of hepatitis develop - cytolytic, mesenchymal-inflammatory, cholestatic. The pathogenesis of complications of gestation.
The pathogenesis of complications of gestation in hepatitis A has not been studied enough, including because of their great rarity.
Clinical picture
Hepatitis A is characterized by polymorphism of clinical manifestations and self-limiting nature with reversible structural and functional changes in the liver.
The inapparent form prevails in frequency, its diagnosis is possible only with the help of enzyme immunoassay when examining contact and sick persons (in epidemic foci). Manifest forms proceed with a successive change of periods: incubation, prodromal (preicteric in the icteric form of the disease), peak (icteric in the presence of jaundice), convalescence. Infrequently, but relapses and complications of infection are possible. The duration of the incubation period averages 15-45 days. prodromal period lasts 5-7 days, proceeds with a variety of clinical symptoms. According to the leading syndrome, it is customary to distinguish influenza-like (feverish), dyspeptic, asthenovegetative, and the most frequently observed mixed variant of the prodrome with the corresponding clinical manifestations. 1-4 days after the first signs of the disease, the color of the urine changes (up to Brown color varying intensity), feces (acholia) become discolored, acquiring the consistency and color of white (gray) clay. Already in the prodromal period, hepatomegaly is possible with liver tenderness on palpation. Sometimes the spleen is slightly enlarged. The peak period lasts an average of 2-3 weeks (with fluctuations from 1 week to 1.5-2 months, with the development of relapse - up to 6 months or more). The beginning of this period in the icteric form is marked by icteric staining of the visible mucous membranes and skin. At the same time, the well-being of patients noticeably improves, the signs of the prodromal period soften or disappear altogether. At the same time, the enlargement of the liver may continue - patients are concerned about heaviness and fullness in the epigastric region, moderate pain in the right hypochondrium. In 1/3 of cases during this period, splenomegaly is noted.
With the disappearance of jaundice, the restoration of the normal color of urine and feces, a period of convalescence begins. Its duration ranges from 1-2 to 812 months (depending on the presence or absence of relapses, exacerbations and the course of the disease). Erased and anicteric forms of hepatitis A usually proceed easily, with few symptoms, with a quick recovery. The frequency of protracted manifest forms does not exceed 5-10%, in these cases, an increase in either the peak period or the convalescence period (with or without relapses, exacerbations) is noted, followed by clinical and laboratory recovery. Hepatitis A in pregnant women proceeds in the same way as in non-pregnant women. There is no risk of antenatal transmission of the pathogen.
Complications of gestation
In rare severe and prolonged forms of hepatitis A, premature birth, in isolated cases - spontaneous miscarriages. There may be a threat of abortion, premature or early rupture of amniotic fluid. In pregnant women with hepatitis A, as in other extragenital diseases, somewhat more often than in the population, early toxicosis, preeclampsia develop (including during childbirth).
Diagnostics
Anamnesis
The diagnosis of hepatitis is established on the basis of epidemiological conditions (contact with a patient with hepatitis A), anamnestic data (symptomatic complexes of the prodromal period), indications of dark urine and fecal acholia.
Physical examination
During an objective examination, the main symptoms are icterus of the visible mucous membranes (the frenulum of the tongue, sclera), skin, slight or moderate enlargement and sensitivity / tenderness of the liver on palpation, much less often - slight splenomegaly.
Laboratory research
The most constant and diagnostically significant biochemical sign of hepatitis is an increase in the activity of the hepatocellular enzyme alanine aminotransferase by 10 times or more compared to the norm. Hypertransferasemia is the main marker of cytolysis syndrome. An increase in the activity of alanine aminotransferase begins already at the end of the prodromal period, reaches a maximum during the height of hepatitis, gradually decreases and normalizes during the convalescence period, indicating recovery. Hyperfermentemia is characteristic not only of icteric, but also anicteric forms of hepatitis. Violation of pigment metabolism is marked by the appearance of urobilinogen and bile pigments in the urine, an increase in the content of bilirubin in the blood, mainly conjugated (bound, direct bilirubin). The mesenchymal-inflammatory syndrome is revealed by the determination of protein sedimentary samples. In hepatitis, the thymol test rises, and the sublimate titer decreases. The degree of their deviation from the norm is proportional to the severity of the infection. In many cases, hypocholesterolemia is noted due to a decrease in its synthesis by damaged hepatocytes. For hepatitis occurring without bacterial layers, leukopenia, neutropenia, relative and absolute lymphocytosis and monocytosis, normal erythrocyte sedimentation rate (often 23 mm / h) are characteristic. Verification of hepatitis A is achieved using enzyme immunoassay. The diagnosis of hepatitis A is considered confirmed by the determination of anti-HAV IgM in the blood serum during the prodromal period and during the peak period. Anti-HAV IgG is usually detected already during convalescence.
Instrumental Research
When performing an ultrasound scan, sometimes determine diffuse changes liver and increase its echogenicity. There are no characteristic signs of hepatitis on ultrasound.
Differential Diagnosis
Hepatitis A is differentiated primarily from other etiological forms of hepatitis (B and C, mixed hepatitis), since in 40-70% of cases of jaundice in pregnant women they have viral nature. The basis of their differentiation is the use and correct interpretation of the results of enzyme immunoassay. Sometimes it becomes necessary to differentiate viral hepatitis, including hepatitis A, from the so-called satellite hepatitis (with infectious mononucleosis, pseudotuberculosis, intestinal yersiniosis, leptospirosis, etc.). In these cases, the basis for distinguishing liver damage is the correct assessment of symptoms that are not just associated with satellite hepatitis, but determine the clinical appearance of diseases. The final solution to the problem of differentiation of viral hepatitis and other infectious lesions of the liver is the use of appropriate specific bacteriological and serological research methods.
In some cases, the differential diagnosis of viral hepatitis and jaundice directly related to pregnancy is more difficult. In chronic granulomatous disease, itching of varying intensity comes to the fore with usually mild jaundice. There is no hepatosplenomegaly in chronic granulomatous disease, as well as intoxication. Hepatosis is characterized by leukocytosis and an increase in the erythrocyte sedimentation rate. The content of conjugated bilirubin in serum increases slightly, hyperfermentemia in most cases is absent. However, in some pregnant women, activity is still increased - such options are the most difficult for differential diagnosis. The cholesterol content is usually elevated. Finally, in chronic granulomatous disease, there are no markers of viral hepatitis (exceptions to this rule are possible if chronic granulomatous disease develops against the background of chronic hepatitis B and C, that is, with comorbidity, the frequency of which has been increasing everywhere in recent years).
The greatest difficulties arise when distinguishing between severe forms of hepatitis (usually hepatitis B) and Sheehan's syndrome - acute fatty hepatosis of pregnant women. Their clinical similarity can be very significant. The correct differentiation of hepatitis and acute fatty preeclampsia in pregnant women is most facilitated by a detailed biochemical study, especially with indications for the treatment of a pregnant woman with tetracycline antibiotics in large doses in the third trimester of gestation. The liver in acute fatty gestosis of pregnant women is usually not enlarged, signs of DIC, hypoproteinemia (often with ascites), azotemia, and high leukocytosis are noted. The content of direct (conjugated) bilirubin increases moderately or slightly, the activity of cytolysis markers is low. The activity of alkaline phosphatase is increased, the sublimate test is reduced, however, these indicators have no differential diagnostic value, since they are also characteristic of hepatitis, as well as a decrease in prothrombin. On the contrary, hypoglycemia, which is almost not amenable to correction, and decompensated metabolic acidosis, which are characteristic of acute fatty hepatosis of pregnant women and are uncharacteristic of hepatitis, are highly informative. Hepatitis markers are absent, unless it is a comorbidity.
Currently, a rare variant of differential diagnosis is hepatitis and preeclampsia with liver damage. The latter is the extreme severity of preeclampsia with all its manifestations, steadily increasing over time with inadequate therapy for severe preeclampsia. Biochemical signs of cytolysis, pigmentary disorders are moderately or slightly expressed in preeclampsia and do not correlate with the severity of other manifestations of pregnancy complications and the general condition of the patient. Occasionally, errors in the diagnosis of viral hepatitis, primarily hepatitis A, occur in pregnant women with jaundice that occurs with severe early toxicosis. In this case, repeated "excessive" vomiting and dehydration come to the fore. The course of the complication, unlike hepatitis, does not have a cycle, jaundice is mild, the intoxication syndrome is insignificant, the liver and spleen remain within normal sizes.
The content of bilirubin rarely exceeds the norm by more than 2 times and usually increases due to the non-conjugated (indirect, unbound) fraction. There is usually no increase in the activity of alanine aminotransferase, as well as no DIC. Often, toxicosis develops acetonuria, which does not happen with hepatitis. Finally, with early toxicosis, immunoserological markers of hepatitis are not determined.
When differentiating hepatitis A (and other hepatitis) with HELLP-syndrome, the reference points are considered to be the presence in the latter hemolytic anemia, thrombocytopenia, increased levels of unconjugated (indirect, free) bilirubin. Arterial hypertension can help in the differential diagnosis, since hepatitis A tends to hypotension (if the patient does not suffer from hypertension or renal pathology). Hepatitis A does not aggravate the course of the HELLP syndrome.
With the appearance of jaundice syndrome (icteric staining of visible mucous membranes and skin, darkening of urine, fecal acholia, elevated bilirubin), hepatomegaly, splenomegaly, intoxication syndrome and fever, increased activity of hepatocellular enzymes (alanine aminotransferase) against the background of leukopenia and normal / reduced the erythrocyte sedimentation rate shows the consultation of the infectious disease specialist and his joint observation of the pregnant woman with the obstetrician.
Diagnosis example
Viral hepatitis A, icteric form, severe course. Pregnancy 32 weeks.
Treatment
Non-drug treatment
Most patients with hepatitis A, including pregnant women, do not need active drug therapy. The sparing regimen is considered the basis for the treatment of patients. rational diet. During the height of the infection, bed rest is indicated. The volume of fluid consumed is important (preferably alkaline mineral) - at least 2 liters per day. Within 6 months after recovery, limit physical exercise and recommend a sparing (mechanically and thermally) diet with the exception of spicy, fatty foods and alcohol.
Medical treatment
With severe intoxication, intravenous detoxification is carried out (saline solutions, dextrans, albumin). A good effect is given by detoxifiers for oral administration. During the period of convalescence, multivitamins and hepatoprotectors are prescribed to restore disturbed metabolism. With posthepatitis biliary dyskinesia, antispasmodics and choleretic agents are prescribed.
Surgery
Surgical treatment of hepatitis A is not carried out. Termination of pregnancy in hepatitis is not indicated, as it can worsen the prognosis of the disease. Exceptions - the occurrence of placental abruption with bleeding, the threat of uterine rupture.
Hospitalization of patients with hepatitis A is optional. Patients can stay at home under the supervision of an outpatient doctor (with the exception of persons living in hostels, which is dictated by anti-epidemic considerations). As for pregnant women with hepatitis A, they should be hospitalized in an infectious diseases hospital to monitor and timely identify the threat of complications of gestation and prevent adverse pregnancy outcomes. In the hospital, the pregnant woman should be observed by two attending physicians - an infectious disease specialist and an obstetrician.
Complications of gestation that have arisen in a patient with hepatitis A in any trimester are corrected according to the principles adopted in obstetrics by appropriate methods and means. This also applies to complications during childbirth and the postpartum period. Indications for hospitalization Pregnant women with hepatitis, including hepatitis A, are hospitalized in an infectious diseases hospital according to clinical indications(for monitoring the course of gestation, prevention and timely correction of possible complications of pregnancy).
Evaluation of the effectiveness of treatment
Therapy for hepatitis A is well developed, most patients recover completely. Mortality does not exceed 0.2-0.4% and is associated with severe concomitant pathology. With adequate management of a pregnant woman and proper joint supervision of an obstetrician and an infectious disease specialist, pregnancy outcomes in women with hepatitis A are also favorable (for the mother, fetus and newborn).
The best tactic in relation to delivery of a patient with hepatitis A is considered urgent delivery through the natural birth canal.
Information for the patient
Hepatitis A is an acute intestinal infection, therefore, one of the main conditions for self-protection against it is strict observance of personal hygiene rules. In order to avoid sexual infection (very rare), it is necessary to exclude oral-anal sexual intercourse. With the development of the disease in a pregnant woman, hospitalization is mandatory. Determination of anti-HAV IgM in a newborn for 3 months does not indicate its infection, since they are transmitted from the mother. Breastfeeding is permitted provided that all hygiene rules (nipple care, etc.) are observed. The use of hormonal contraceptives is permissible no earlier than 8-2 months after the disease. There are no contraindications for other contraceptives. Re-pregnancy is possible 1-2 years after hepatitis.
Hepatitis E
Hepatitis E is an acute viral intestinal infection with liver damage, occurring cyclically, prone to epidemic spread, mainly in regions with a tropical and subtropical climate; characterized by particular severity and high frequency of adverse outcomes in pregnant women.
Synonyms
Hepatitis E; Hepatitis is neither A nor B with a fecal-oral mechanism of infection.
Epidemiology
The epidemiology of hepatitis E shares many similarities with the epidemiology of hepatitis A (see above). Reservoirs of the causative agent of hepatitis E can be rodents, pigs. The main route of transmission of the hepatitis E virus is water, less often alimentary (including the use of raw or poorly thermally processed mollusks and crustaceans). The contact-household way is noted very rarely. The infectious dose of the hepatitis E pathogen is 2 times higher than the hepatitis A virus. Susceptibility is universal. More often people aged 15-0 get sick, and among them - men, residents countryside. Large outbreaks and epidemics are possible, mainly in autumn, in the tropics - during the rainy season. It is possible to bring the infection into the middle zone (“travelers' hepatitis”, however, it is not accompanied by the spread of the disease and outbreaks.
Classification
There are inapparent and manifest forms, as in hepatitis A. In pregnant women who become infected after 24 weeks of gestation, fulminant (fulminant) forms are possible with high mortality (20-5%); Outbreaks with lethality in 40-80% of cases are described. According to the severity of the course in pregnant women, mild (up to 4%), moderate (about 70%) and severe (25-28%) forms are distinguished. There are no chronic forms of hepatitis E.
Etiology
The causative agent of Hepatitis E virus (HEV), RNA-containing. Three genotypes are known, isolated in different regions. HEV is less stable in the environment than HAV.
Pathogenesis
In general terms, it is similar to the pathogenesis of hepatitis A. The main link is the direct cytopathic effect of HEV with cytolysis of hepatocytes. Immunopathological processes do not play a significant role. The immune response occurs quickly, which leads to the relief of the disease. Like hepatitis A, hepatitis E is a self-limiting infection. The causes and mechanism of the particularly severe course of hepatitis E in pregnant women have not been studied. In fulminant forms of hepatitis E in pregnant women, massive or submassive liver necrosis is noted. Pathogenesis of complications of gestation
The pathogenesis of gestational complications in hepatitis E is not known in detail. With a fulminant course of infection in the first days of the disease (no later than the 17th day of the disease), acute liver failure develops up to hepatic coma; almost half of pregnant women develop and progress at the same time renal failure. DIC as a component of liver failure contributes to bleeding and large blood loss during childbirth. Against this background, spontaneous abortion, antenatal fetal death, and stillbirth often occur. Children born alive have signs of severe hypoxia, fetal growth retardation, they are not adapted to extrauterine life and usually die in the first three months after birth.
Clinical picture
The incubation period ranges from 20 to 80 days. The duration of the prodromal period is usually 3-7 days and clinically proceeds as in hepatitis A. Some patients complain of arthralgia and diarrhea. At the height of hepatitis E, when jaundice appears, the state of health, unlike hepatitis A, usually does not improve. In men and non-pregnant women, hepatitis E occurs with the same symptom complex as in hepatitis A. As a rule, hepatomegaly is noted; splenomegaly is very rare. The manifestation of the disease lasts 3 weeks and ends with recovery (in the vast majority of cases). The convalescence period is longer than with hepatitis A.
Complications of gestation
A high risk of pregnancy complications for the mother and fetus, often with a fatal outcome, is noted in severe and especially fulminant forms of hepatitis E. The most dangerous cases are when a pregnant woman becomes infected with HEV in the second half of gestation (later than 24 weeks). In these forms of hepatitis E, the clinical picture is more reminiscent of the most severe forms of hepatitis B. Jaundice is steadily increasing, fever is increasing, liver and kidney failure is rapidly developing, and signs of DIC are intensifying. With hepatitis E, pregnant women often experience increased hemolysis of red blood cells with hemoglobinuria, which exacerbates renal failure. Hemoglobinuria is an early sign of a beginning deterioration in the condition of a pregnant woman and a difficult prognosis for her life and health. In case of spontaneous abortion, the woman's condition deteriorates sharply, and death is possible. In childbirth, the likelihood of massive bleeding is extremely high, as well as in the postpartum period. Some authors do not exclude the possibility of vertical transmission of the pathogen. The most severe complication of gestation is also ante-, intra- and postnatal death of the fetus. The probability of having a healthy child is practically non-existent, the possibility of a newborn's survival is very low.
Diagnostics
Anamnesis
Recognition of hepatitis E is possible taking into account the epidemiological history (stay in areas endemic for hepatitis E), the history of the disease.
Laboratory research
Verification of hepatitis E is carried out by detecting anti-HEV IgM in the blood in enzyme immunoassay. These antibodies appear in the blood on the 10-12th day of illness and circulate for 1 month. In the early stages of infection, detection of HEV RNA in blood and feces is possible using a polymer chain reaction. Occasionally, HEV is isolated from faeces and detected in liver biopsies by immunofluorescence.
Differential Diagnosis
It is carried out with other etiological forms of viral hepatitis and liver damage associated with the actual pregnancy.
Medical treatment
Etiotropic (antiviral) drugs are absent. Therapy, as a rule, is pathogenetic, aimed at stopping intoxication and (in case of fulminant forms) at fighting in resuscitation mode with acute liver and kidney failure, bleeding, and the threat of miscarriage.
Surgery
Termination of pregnancy in any way with hepatitis E is strictly contraindicated. Only in the early stages of gestation is an artificial termination of pregnancy possible, but only during the period of convalescence.
Prevention and prediction of complications of gestation
In the usual course of hepatitis E, treatment is carried out in a hospital using a comprehensive examination of the mother and fetus to determine early signs of trouble and correct them. With fulminant forms, the same measures are carried out in the mode of intensive observation and resuscitation, but, unfortunately, they are ineffective.
Features of the treatment of complications of gestation The main place in the treatment of complications of gestation belongs to the obstetrician, who uses all the necessary studies to predict pregnancy and improve the condition of the fetus. At the same time, an infectious disease specialist and a resuscitator should work with him, providing detoxification and therapy for hepatic coma, renal failure. The joint efforts of doctors are directed to combat bleeding. If necessary, nephrologists and a hematological team of doctors take part in saving pregnant women.
Indications for hospitalization
Pregnant women with hepatitis E should be hospitalized in an infectious diseases hospital, where there is an obstetric department (wards), without fail.
Evaluation of the effectiveness of treatment
In the general population, the effectiveness of therapy is good, recovery occurs in the vast majority of patients. The therapy of hepatitis E in pregnant women is unsatisfactory, every fourth or fifth woman who falls ill after 24 weeks of gestation dies. Outbreaks and epidemics with mortality in pregnant women in 40-80% of cases are described.
Choice of term and method of delivery
It is necessary to ensure that a pregnant woman with hepatitis E stays in the obstetric department (ward) of an infectious disease hospital with all measures to prolong pregnancy until term delivery.
VIRAL HEPATITIS WITH HEMOCONTACT TRANSMISSION
Hepatitis B
Hepatitis B is a viral infection that occurs with a predominant liver lesion and a polymorphism of clinical manifestations from virus carriers and acute hepatitis to progressive chronic forms and outcome in liver cirrhosis and hepatocarcinoma.
Epidemiology
Hepatitis B - acute anthroponosis. The reservoir of the pathogen and the source of infection are patients with acute and chronic forms of hepatitis B, virus carriers (these are also patients with inapparent forms of the disease, the number of which is 10-100 times more than patients with manifest forms of infection). The latter represent the greatest epidemiological danger to others. In acute hepatitis B, the patient is contagious from the middle of the incubation period to the peak period and the complete release of the body from the virus. In chronic forms of the disease, when lifelong persistence of the pathogen is noted, patients present a constant danger as sources of infection.
The mechanism of infection is hemocontact, non-transmissible. Distinguish between natural and artificial paths infections. Natural ways - sexual and vertical. The sexual route makes hepatitis B a sexually transmitted infection. The vertical pathway is realized mainly during childbirth, about 5% of fetuses are infected in utero. When a woman is infected in the third trimester of pregnancy, the risk of infecting a child reaches 70%, with an HBSAg carrier - 10%. The greatest risk of transmission of the virus from mother to fetus is observed in cases of simultaneous presence of HBSAg and HBEAg in the blood of a pregnant woman (replicative phase of infection), a high degree of viremia. Household blood-borne transmission of the virus is possible (sharing razors, scissors, toothbrushes and other items when contact with the patient’s blood can occur). Artificial (artificial) routes of transmission of hepatitis B include transfusion of blood and its components (the value of this route has been falling in recent years ), diagnostic and therapeutic invasive manipulations performed with poorly sterilized instruments, that is, contaminated with blood. In recent decades, non-medical parenteral interventions have come to the fore - intravenous injections drugs and their surrogates. Tattoos are a big risk different kind notches, cutting, etc.
The main factor in the transmission of the hepatitis B virus is blood; for infection from a patient, it is enough for a susceptible person to enter the body of a minimal infectious dose of blood (7-10 ml). The causative agent of hepatitis B can also be found in other biological fluids (removable genital tract) and tissues. Susceptibility to hepatitis B is high in all age groups. High-risk groups for infection include:
- recipients donated blood(patients with hemophilia, other hematological diseases; patients on chronic hemodialysis; patients who received organ and tissue transplantation; patients with severe comorbidities who had numerous and varied parenteral interventions);
- users of intravenous drugs;
- men with homo- and bisexual orientation;
- representatives of commercial sex;
- persons who have numerous and promiscuous sexual relations (promiscuity), especially with patients with sexually transmitted infections;
- children of the first year of life (as a result of possible infection from the mother or due to medical manipulations);
- medical workers who have direct contact with blood (the risk of occupational infection reaches 10-20%).
Seasonal fluctuations for hepatitis B are not typical. The spread of the infection is ubiquitous. The incidence varies widely. Russia belongs to the territory of moderate intensity of the spread of hepatitis B. More than 2/3 of all those infected with hepatitis B live in the Asian region.
Classification
Hepatitis B has a wide range of clinical manifestations. Distinguish: acute cyclic (self-limiting) hepatitis B (subclinical, or inapparent, anicteric, icteric form with a predominance of cytolysis or cholestasis); acute acyclic progressive hepatitis B (fulminant, or fulminant, malignant form).
According to the severity of the course, mild, moderate and severe forms are distinguished. Chronic hepatitis B can have two phases - replicative and integrative with varying degrees of morphological and clinical and biochemical activity. Chronic hepatitis B also includes cirrhosis of the liver and primary hepatocellular carcinoma. Some authors prefer to refer to the last two forms as outcomes of chronic hepatitis B.
Etiology
The causative agent of Hepatitis B virus (HBV) is a DNA-containing virus (virion - Dane particle) that has a complex antigenic structure. Virion antigenic systems have been isolated: HBSAg (surface antigen) (found in blood, hepatocytes, semen, vaginal secretion, cerebrospinal fluid, synovial fluid, breast milk, saliva, tears, urine); HBcAg (core antigen) (determined in the nuclei and perinuclear zone of hepatocytes, it is not in the blood); HBsAg (infectivity antigen) is found in the blood and confirms the presence of HBcAg in liver cells. Various antigenic variants of HBV have been described, including mutant strains of the pathogen resistant to antiviral therapy. The hepatitis B virus is stable in the environment. It is inactivated by autoclaving (30 min), dry steam sterilization (160 °C, 60 min).
Pathogenesis
From the portal of entry, the hepatitis B virus enters hematogenously into the liver, where the pathogen and its Ag replicate. does not possess, unlike HAV and HEV, direct cytopathic action; liver damage occurs immune-mediated, its degree depends on many factors related to the infectious dose, virus genotype, virulence, as well as the immunogenetic status of the organism, interferon activity and other elements of specific and nonspecific protection. As a result, necrobiotic and inflammatory changes corresponding to mesenchymal-inflammatory, cholestatic syndromes, and cytolysis syndromes. The acute cyclic form of hepatitis B corresponds to a normal response to pathogen aggression. The disappearance of the virus from the body and, consequently, recovery is the result of the destruction of all infected cells and the suppression of all phases of pathogen replication by interferon. At the same time, antibodies to Ag of the hepatitis B virus accumulate. The resulting immune complexes of the virus, antibodies to them, the C3 component of complement) are phagocytosed by macrophages, as a result of which the pathogen leaves the patient's body.
Fulminant (acyclic, malignant) forms of hepatitis B are provided primarily by a genetically determined hyperergic reaction of immune cells to antigenically alien viruses with a low interferon response.
The mechanisms of progression and chronicity are associated with an inadequate immune response against the background of high replicative activity of the virus or low replication activity with the integration of the HBV genetic material into the hepatocyte genome; mutation of the virus, a decrease in the synthesis of a-interferon, autoimmune reactions, features of constitutional immunity. The autoimmune mechanisms that develop in some cases are associated with the interference of virus-specific proteins of the virus and structural subunits of hepatocytes.
With the progression of severe forms of acute and chronic hepatitis B, it is possible to develop toxic dystrophy, massive and submassive necrosis of the liver with acute liver failure, in which all types of metabolism suffer ("metabolic storm". As a result, encephalopathy develops, massive hemorrhagic syndrome, which become the cause death of patients.
Another option for the progression of hepatitis B is the development of liver fibrosis against the background of varying degrees of hepatitis activity with further evolution to liver cirrhosis, and then to primary hepatocellular carcinoma. polymer chain reaction).
The pathogenesis of complications of gestation
Severe metabolic disorders in severe hepatitis B are the main cause of gestational complications. The most frequent of them are the threat of miscarriage and early spontaneous abortion, especially at the height of the disease and in the third trimester of pregnancy. Premature birth with hepatitis B is noted 1.5 times more often than with hepatitis A. Hepatitis B, like other hepatitis, can provoke or aggravate the course of preeclampsia in a pregnant woman, premature or early rupture of amniotic fluid, preeclampsia during childbirth. Special observation requires the fetus of a sick mother because of the possibility of hypoxia, delayed fetal development. At birth in the midst of hepatitis B, newborns are less adapted to extrauterine life, they tend to have lower Apgar scores. During childbirth during the period of hepatitis B convalescence, there are practically no complications of gestation. This applies to the mother, the fetus, and the newborn. In chronic hepatitis, the frequency and severity of complications of gestation is significantly lower.
Clinical picture
The most frequent among the various manifest forms of hepatitis B is acute cyclic icteric hepatitis with cyclic syndrome. The incubation period for this form of hepatitis B ranges from 50 to 180 days and has no clinical signs. The prodromal period (preicteric) lasts an average of 4-10 days, very rarely increases to 3 weeks. The symptoms of this period are basically the same as in hepatitis A. Features - a less frequent febrile reaction in hepatitis B, the frequent development of arthralgia (an arthralgic variant of the prodrome). There is also a latent variant of this period (5-7%), when jaundice becomes the first clinical manifestation of the disease. At the end of the prodrome, the liver and, less often, the spleen increase; urine darkens, feces become discolored, urobilirubin appears in the urine, sometimes bile pigments, an increase in HBSAg and alanine aminotransferase activity is determined in the blood.
The icteric period (or peak period) lasts, as a rule, 2-6 weeks with possible fluctuations. It proceeds as in hepatitis A, but intoxication in most cases not only does not disappear or softens, but may increase. The liver continues to grow, so heaviness and pain in the right hypochondrium persist. In the presence of a cholestatic component, itching may occur.
A dangerous symptom is a reduction in the size of the liver (to the degree of “empty hypochondrium”, which, while maintaining jaundice and intoxication, indicates an onset of acute liver failure. Gradual thickening of the liver, sharpening of its edge with ongoing jaundice may be indications of chronic hepatitis B.
The period of convalescence proceeds differently: from 2 months with a smooth course of infection to 12 months with the development of clinical, biochemical or biochemical relapses. In pregnant women, hepatitis B proceeds in the same way as in non-pregnant women, but they have a severe form of the disease (10-11%) more often.
by the most dangerous complication severe forms of hepatitis B, both outside and during pregnancy, are acute liver failure, or hepatic encephalopathy. There are four stages of acute liver failure: precoma I, precoma II, coma, deep coma with areflexia. Their total duration ranges from several hours to several days.
The first symptoms that threaten the development of acute liver failure are progressive hyperbilirubinemia (due to the conjugated fraction and an increase in the fraction of indirect, free bilirubin) with a simultaneous decrease in the activity of alanine aminotransferase, a sharp (below 45-50%) decrease in prothrombin and other blood coagulation factors, increasing leukocytosis and thrombocytopenia. Acute liver failure completely dominates the clinical picture of the fulminant form of hepatitis B, which begins and develops rapidly and ends with the death of patients within 2 weeks.
In 10-15% of patients with acute hepatitis B, chronic hepatitis develops, which is usually diagnosed after 6 months of clinical and biochemical manifestations of the disease. In some cases (with an unrecognized acute period of the disease, with inapparent, anicteric forms of hepatitis B), the diagnosis of chronic hepatitis is established already at the first examination of the patient.
Chronic hepatitis in many patients is asymptomatic; it is often detected during examination on the occasion of an "unclear diagnosis" according to the results of biochemical analysis (increased ALT activity, proteinemia, HBV markers, etc.). With an adequate clinical examination in such patients, it is possible to determine hepatomegaly, a dense consistency of the liver, and its pointed edge. Sometimes splenomegaly is noted. With the progression of the disease, extrahepatic signs appear - telangiectasia, palmar erythema. Hemorrhagic syndrome gradually develops (hemorrhages into the skin, first at the injection sites; bleeding gums, nose and other bleeding).
When autoimmune mechanisms are activated, vasculitis, glomerulonephritis, polyarthritis, anemia, endocrine and other disorders develop. As chronic hepatitis B develops, signs of the formation of liver cirrhosis appear - portal hypertension, edematous-ascitic syndrome, hypersplenism, etc.
The so-called carriage of HBsAg is considered a variant of chronic hepatitis B with minimal activity of the pathological process, a subclinical course in the integrative phase of infection. Exacerbation of chronic hepatitis B is manifested by intoxication, usually with an increase in body temperature to subfebrile values, asthenovegetative symptoms, jaundice (moderate in most cases), hemorrhagic syndrome, and increased extrahepatic signs. 30-40% of cases of hepatitis B in the replicative phase end in cirrhosis and primary liver cancer, while HBV markers can be detected in the blood and liver tissues. At any stage of chronic hepatitis B, the development of acute liver failure, portal hypertension, bleeding from varicose veins of the esophagus, often the addition of bacterial flora with the development, in particular, intestinal phlegmon, is possible.
In pregnant women, chronic hepatitis B proceeds in the same way as in non-pregnant women, with the same complications and outcomes. The main cause of death in pregnant women with hepatitis B is acute liver failure, or rather, its terminal stage- hepatic coma. The lethality of pregnant women with acute hepatitis B is 3 times higher than in non-pregnant women, and is more common in the third trimester of gestation, especially against the background of already existing obstetric complications of pregnancy.
Complications of gestation
The nature and range of complications of gestation in hepatitis B are the same as in other hepatitis. The most dangerous are intrauterine fetal death (at the height of intoxication and jaundice in the mother), stillbirth, miscarriage and premature birth, which can lead to a critical deterioration in the condition of a patient suffering from a severe form of hepatitis B. In chronic hepatitis B, miscarriage is rarely observed. In childbirth at the height of the disease, the likelihood of massive bleeding is high, as in the postpartum period. In the case of vertical transmission of HBV from mother to fetus, 80% of newborns develop chronic hepatitis B.
Diagnostics
The recognition of hepatitis B is facilitated by a correctly and carefully collected epidemiological history, which makes it possible to classify a patient, including a pregnant woman, as a high-risk group for hepatitis B infection. The anamnestic method is of great importance, which makes it possible to determine the frequency of development of the disease and complaints characteristic of each period of the disease. Physical examinations
The presence of hepatitis in a patient is confirmed by the appearance of jaundice, hepatomegaly, liver tenderness on palpation, splenomegaly. In chronic hepatitis B, the diagnosis is based on the definition of hepatosplenomegaly, features of the consistency of the liver, the state of its edge, asthenovegetative syndrome, jaundice, telangiectasia, palmar erythema, and in advanced stages - portal hypertension, edematous-ascitic syndrome, hemorrhagic manifestations.
Laboratory studies Violation of liver function is determined by biochemical methods (characterized by increased activity of alanine aminotransferase, an increase in the concentration of conjugated bilirubin, a decrease in the content of total protein and albumin, dysproteinemia, hypocholesterolemia, disorders of the blood coagulation system).
Verification of hepatitis B is carried out using the reaction of damage to granulocytes, the reaction of indirect hemagglutination, counter immunoelectrophoresis, and currently most often linked immunosorbent assay. Allocate chronic hepatitis B with high and low replicative activity, which determines the nature and pace of development of the pathological process in the liver. Prolonged circulation of HBEAg indicates active replication of the virus. In these cases, HBSAg, anti-HBC IgM, HBV DNA (in polymer chain reaction) are detected in the blood. The chronic replicative type of hepatitis B is often characterized by either steady progression or alternation of clinical and biochemical exacerbations and remissions with moderate or significant activity of the pathological process in the liver (according to the study of intravital biopsy specimens).
In chronic hepatitis B with low replicative activity in the blood, HBSAg, anti-HBE IgG and anti-HBC IgG are determined. All this gives grounds (especially with normal or slightly increased activity of alanine aminotransferase) to diagnose the integrative type of chronic hepatitis B, which proceeds benignly. However, even in such circumstances, tumor transformations and the development of primary hepatocellular carcinoma are possible in the liver. In 10-15% of cases, the integrative phase of chronic hepatitis B can transform into a replicative phase. A laboratory study of the blood of HBsAg carriers reveals functional liver failure (hyperbilirubinemia, a decrease in the pro-thrombin index, hypo- and dysproteinemia with hyperbilirubinemia, hypocholesterolemia, etc.) . In the liver tissue (biopsy, autopsy material), HBV virions, as well as HBcAg and other antibodies of the virus, can be detected by immunofluorescence or electron microscopy. Using the in situ complement fixation reaction, HBV DNA is determined.
Differential Diagnosis
Differential diagnosis is carried out in the same way as for other viral hepatitis. In recent years, the need for differential diagnosis of hepatitis B with toxic liver damage (alcohol surrogates, other poisons) has been actualized. To distinguish between these liver lesions, an important role is played by the informal collection of anamnestic information, the regular development of signs of nephropathy of toxic origin against the background of clinical and laboratory symptoms of functional liver failure, and often the detection of encephalopathy. Indications for consultation of other specialists Indications for consultation of other specialists are the same as for other viral hepatitis.
Diagnosis example
Pregnancy 32 weeks. The threat of abortion. Acute hepatitis B, icteric form, severe course, replicative phase of infection.
Treatment
Treatment Goals
Therapy for hepatitis B depends on the severity of the infection, its phase, the presence or absence of advanced stages of chronic hepatitis B. The goals of therapy are the same as for other hepatitis.
Medical treatment
In recent years, etiotropic antiviral chemotherapy drugs and interferon alfa have been widely used to treat patients with hepatitis B, but they are contraindicated during pregnancy. In these cases, the dominant pathogenetic therapy aimed at reducing intoxication, combating hemorrhagic and edematous-ascitic syndromes. Surgical treatment
Surgery with hepatitis B is not carried out.
Prevention and prediction of complications of gestation Prevention and prediction of complications of gestation, aimed at careful monitoring of the condition of the mother and fetus, is carried out in an infectious diseases hospital with the presence of an obstetric department (wards).
Features of the treatment of complications of gestation
Therapy of complications of gestation in pregnant women with hepatitis B has no special features. Pregnant women in the third trimester of pregnancy require the greatest attention. In childbirth and the postpartum period, special alertness is necessary regarding possible massive bleeding in cases of severe disease.
Indications for consulting other specialists
Indications for consultation of other specialists arise with the development of acute liver failure, when resuscitators, obstetricians and infectious disease specialists should participate in rescuing the patient. With massive bleeding, it is necessary to involve hematologists in therapy.
Indications for hospitalization
All patients with all forms of hepatitis B, pregnant and non-pregnant, undergo a course of examination and treatment in an infectious diseases hospital and without fail.
Evaluation of the effectiveness of treatment
In mild and moderate forms of acute hepatitis B, the effect of therapy is good, in severe forms it is doubtful. The effectiveness of chronic hepatitis B at different stages of the pathological process is different, but always requires perseverance and adequate monitoring. With the development of liver transplantation, noticeable success can be achieved even in advanced stages of the disease.
Choice of term and method of delivery
Artificial termination of pregnancy is possible (at the request of the mother) only during the period of convalescence of acute hepatitis B. The best tactic is to prolong the pregnancy until term delivery through the natural birth canal. The same is true for chronic hepatitis B. The rationale and safety of antivirals during pregnancy and the rationale for passive and active immunization to reduce the risk of perinatal transmission of HBV infection
During pregnancy, HBSAg-positive women usually do not experience exacerbations of chorionic hepatitis B, and liver enzyme levels often normalize if initially elevated. However, there are several reports of the development of exacerbations of chronic hepatitis B during pregnancy, up to the development of fulminant liver failure. A number of women experience exacerbations of hepatitis in the first months after childbirth. Cases of fulminant hepatitis have also been described in children born to women with chronic hepatitis B.
The implementation of the universal screening program for pregnant women and passive-active immunoprophylaxis of newborns has reduced the transmission of HBV infection by 5-10%. However, up to 30% of children born to mothers who are carriers of the hepatitis B virus with a high level of viremia are resistant to ongoing immunoprophylaxis. The results of a recent large-scale study including 1043 observations showed that there is a linear correlation between the level of maternal hepatitis B virus DNA and the failure rate of immunoprophylaxis. Ineffective immunoprophylaxis is more often recorded when the level of viremia in the mother is more than 200,000 IU / ml.
In such cases, antiviral therapy should be recommended to the pregnant woman to reduce the risk of perinatal mother-to-child transmission of hepatitis B virus. Despite the relatively small number of non-randomized studies on this issue, and the low level of evidence for each of them separately, one can rely on a meta-analysis of studies conducted on the results of a combination of antiviral therapy (lamivudine or telbivudine) in the third trimester of pregnancy and passive-active immunization of newborns, which demonstrated that this approach reduces the likelihood of transmission of the hepatitis B virus to the newborn and does not cause additional harm to the newborn. Currently, new data have been obtained on the safety of the use of antiviral drugs of the nucleoside (t) analogs group during pregnancy, which formed the basis of the European recommendations (EASL, 2012) for the management of pregnant women with chronic hepatitis B and the prevention of neonatal infection.
Adverse effects reported with the use of nucleoside(tide) analogues during pregnancy include lactic acidosis and acute fatty liver disease. Fatal lactic acidosis has only been reported in infants whose mothers took antiretroviral drugs during pregnancy. Such cases have not been observed in infants born to mothers with chronic hepatitis B who are taking antiviral therapy for hepatitis B.
According to the FDA classification of drugs for the risk of exposure to the fetus, lamivudine and entecavir are classified as category C, telbivudine and tenofovir are classified as category B. Data from studies show that the proportion of birth defects associated with the use of lamivudine and tenofovir during pregnancy was comparable with that in the general population.
There are data on the safety of the use of telbivudine and lamivudine in 700 pregnant women compared with a group of pregnant women who did not receive antiviral treatment for chronic hepatitis B. It was shown that among women treated with tel-bivudine and lamivudine, no more children were born with congenital defects than in the control group (0.97% and 1.7%, respectively, p>0.05). It should be emphasized that in the absence of antiviral treatment, 8% of children were born HBSAg-positive with positive DNA of the hepatitis B virus in the blood. The safety of entecavir during pregnancy has not been well studied.
Thus, the currently available data clinical observations indicate that to prevent intrauterine and perinatal transmission of hepatitis B virus to a child in the presence of a high level of viremia in a pregnant woman suffering from chronic hepatitis B, the use of lamivudine, telbivudine and tenofovir in the third trimester of pregnancy in combination with passive and active immunization of the newborn is safe and justified. The use of interferon preparations is contraindicated during pregnancy. Tactics of managing pregnant women with a high level of hepatitis B virus DNA who did not receive antiviral therapy before pregnancy.
European guidelines (EASL, 2012) recommend the use of antiviral drugs to prevent mother-to-child transmission of HBV infection at HBV DNA levels of 10 67 IU/ml in the third trimester of pregnancy (A), especially in the presence of HBeAg-positive chronic hepatitis B, since with this combination there is a 10% risk of transmission of infection to the newborn despite the introduction of a specific immunoglobulin and a vaccine. Mothers with a high level of viremia should be informed that the use of nucleoside analogues reduces the level of viral load and may enhance the preventive effect of vaccination and the use of immunoglobulin. However, it should be taken into account that HBV carriers with a high level of viremia may need long-term antiviral therapy (after delivery) due to indications for the treatment of active hepatitis, so the choice of the drug should be made taking into account the risk of developing drug resistance.
The risk of developing resistance to antiviral therapy is highest with lamivudine, much less with telbivudine, and minimal with tenofovir. In this regard, when planning long-term therapy, tenofovir should be the drug of choice, since, in addition to the indicated advantage, this drug has a high antiviral activity and its use in pregnant women has been demonstrated to be safe.
Indications for the appointment of antiviral therapy in patients in the phase of immune tolerance of chronic hepatitis B, which was already diagnosed before pregnancy, are: the level of maternal hepatitis B virus DNA is more than 10 6 IU / ml at the end of the second trimester of pregnancy, the birth of a child, infected virus hepatitis B, with previous ineffective immunoprophylaxis, a history of premature birth. It should be borne in mind that in this case, antiviral therapy is prescribed solely for the prevention of infection of the newborn and will be canceled after delivery. Tenofovir, telbivudine, or lamivudine may be used as monotherapy. Optimal time the beginning of antiviral therapy - the end of the second - the beginning of the third trimester of pregnancy - so that there is enough time (4-6 weeks) to reduce the level of viremia by the time of delivery.
Treatment may be discontinued at 4 weeks postpartum or earlier if breastfeeding is necessary. In addition, it is necessary to control the activity of serum transaminases every 4-6 weeks of the postpartum period for at least 12 weeks after the end of antiviral therapy to exclude the transition of the disease to the immunoactive phase.
When markers of hepatitis B infection are detected for the first time during pregnancy, it is necessary to conduct the most complete examination in order to establish whether there are indications for treating the pregnant woman due to hepatitis B activity or whether antiviral treatment is necessary only to prevent infection of the newborn. Acute hepatitis B should be ruled out. The examination should include the determination of anti-HBcor IgM, HBEAg, anti-HBe, anti-HDV IgG and IgM in the blood, the level of hepatitis B virus viremia. Additional tests should include a complete clinical and biochemical analysis of blood. Even minor indications of the possibility of liver cirrhosis require an ultrasound examination of the abdominal organs. It is necessary to establish the feasibility of antiviral therapy in this phase of the disease and assess the likelihood of long-term therapy, which will determine the choice of an antiviral drug.
If an unplanned pregnancy occurs during antiviral therapy for chronic hepatitis B, treatment tactics should be reviewed. Patients with advanced liver fibrosis should continue antiviral therapy, but the choice of drugs used medicines should be determined by their safety to the fetus. Treatment with pegylated interferon should be discontinued and nucleoside analogs given. The drug of choice in this case is tenofovir. If the patient has already received tenofovir, treatment may be continued. If the patient was treated with lamivudine or telbivudine, treatment may be continued with the same drug if HBV DNA is not detected in the blood. If hepatitis B virus replication is not completely suppressed, switching to tenofovir treatment is preferable to prevent exacerbation of hepatitis during pregnancy. If the patient was receiving entecavir, it is reasonable to switch to tenofovir treatment.
In the absence of severe liver fibrosis, treatment with nucleoside (ti) analogues can be interrupted for the first 2 trimesters of pregnancy, further prescribed according to indications (with the return of viremia and its high level) in the third trimester of pregnancy or interrupted until the moment the woman finishes breastfeeding the baby. It is very important to study the level of ALT activity and the level of viremia at 1, 3 and 6 months after the interruption of antiviral therapy, given the possible risk of exacerbation of chronic hepatitis B, especially after childbirth.
Antiviral therapy for chronic hepatitis B and breastfeeding
Although HBSAg has been found in breast milk, breastfeeding does not increase the risk of transmission of HBV infection compared to formula-feeding. The results of studies have not demonstrated an association between natural feeding of infants by HBV-positive mothers and the development of chronic hepatitis B in them. Thus, newborns who received immunoglobulin and received the first stage of hepatitis B vaccination can be breast-fed. If it is necessary to continue antiviral therapy in the postpartum period, breastfeeding is not recommended due to the lack of information on the safety of the drugs taken on the development of the newborn.
Information for the patient
When planning a pregnancy, a woman, on the advice of an obstetrician, should be vaccinated against hepatitis B. Chronic hepatitis B is not a contraindication to pregnancy. If the patient has antibodies to HBV (vaccinated), breastfeeding is possible with proper nipple care and strict personal hygiene. If markers of hepatitis B replication activity are present, breastfeeding should be avoided. A woman who gives birth to a child without HBSAg in the blood is required to consent to the vaccination of the newborn against hepatitis B.
Hepatitis D
Hepatitis D has no independent significance: its causative agent HDV is not capable of replication in the absence of HBV, since it forms its shell from HBSAg. It exists exclusively as a coinfection or superinfection with hepatitis B. This kind of mixed infection (hepatitis B + hepatitis D) tends to be severe and chronic.
Epidemiology
It is often found in regions with a hot and warm climate, often in European countries. The possibility of infection in the middle lane is low.
Hepatitis C
Hepatitis C is a viral anthroponotic infection with a predominant lesion of the liver, prone to a long chronic low-symptomatic course, and outcome in liver cirrhosis and primary hepatocellular carcinoma.
Epidemiology
The source and reservoir of hepatitis C is a patient with an acute or chronic infection. HCV-RNA can be detected in the blood very early, as early as 1 week after infection. In epidemiological terms, the most unfavorable are inapparent (subclinical) forms of hepatitis C, which predominate in this disease. The prevalence of infection to a certain extent characterizes the infection of donors: in the world it ranges from 0.5 to 7%, in Russia it is 1.2-8%.
Hepatitis C, like hepatitis B, has a blood-borne route of infection, they have the same transmission factors and high risk groups for infection. The infectious dose of HCV is several times higher than that of HBV: the probability of contracting hepatitis C with a needle prick contaminated with the pathogen reaches 3-10%. Contact of infected blood with intact mucous membranes and skin does not lead to infection. Vertical transmission of HCV is rare and is denied by some authors. The probability of domestic and professional infection is low, however, the incidence of hepatitis C in medical workers is still higher (1.5%) than in the general population (0.3-0.4%). The leading role in risk groups belongs to drug users (hepatitis of drug addicts). The role of sexual and family contacts in hepatitis C infection is insignificant (about 3%). For comparison: the risk of sexual transmission of HBV - 30%, HIV - 10-5%. In the case of sexual transmission, transmission of the pathogen occurs more often from a man to a woman. Hepatitis C is ubiquitous. It is believed that at least 500 million people are infected with HCV in the world, i.e., there are significantly more infected with HCV than carriers of HBSAg.
7 genotypes and more than 100 subgenotypes of the hepatitis C virus have been identified. In Russia, one genotype dominates, three genotypes occur. The increase in the incidence in the world and the country is partly of a registration nature (improvement in diagnosis throughout the country with the start of mandatory registration of hepatitis C in 1994), but there is also a true increase in the number of patients.
Etiology
The causative agent of hepatitis C (HCV) is an RNA-containing virus. It is characterized by extreme variability, which prevents the creation of a vaccine. Structural proteins are distinguished in the virus: core (heart-shaped), E1 and E2 and non-structural proteins (NS2, NS3, NS4A, NS4B, NS5A and NS5B), on the detection of which the verification of the diagnosis of hepatitis C is based, including its forms (phases ).
Pathogenesis
Once in the human body through the entrance gate, the pathogen enters the hepatocytes, where it replicates. The direct cytopathic effect of HCV has been proven, but the hepatitis C virus has a weak immunogenicity, so the elimination of the pathogen does not occur (just like HAV, which has a direct cytopathic effect). Antibody formation in hepatitis C is imperfect, which also prevents the neutralization of the virus. Spontaneous recovery is rare. In 80% or more of those infected with HCV, chronic hepatitis develops with long-term persistence of the pathogen in the body, the mechanism of which is different from the persistence of HBV. With hepatitis C, there are no integrative forms due to the special structure of the virus (it has neither matrix nor intermediate DNA). Persistence of the pathogen in hepatitis C is explained by the fact that the rate of mutation of viruses significantly exceeds the rate of their replication. The resulting antibodies are highly specific and cannot neutralize rapidly mutating viruses (“immune escape”. The proven ability of HCV to replicate outside the liver also contributes to long-term persistence: in the cells of the bone marrow, spleen, lymph nodes, and peripheral blood.
Hepatitis C is characterized by the inclusion of autoimmune mechanisms, which entail numerous extrahepatic manifestations of chronic hepatitis C. Hepatitis C differs from other viral hepatitis by a torpid subclinical or asymptomatic course and at the same time asymptomatic, but steady progression of the pathological process in the liver and other organs, especially in older people (50 years or more), suffering from comorbidities, alcoholism, drug addiction, protein-energy malnutrition, etc.
Most researchers believe that the genotype of the virus does not affect the progression of the disease and its rate. An immunogenetic predisposition to hepatitis C is possible. Chronic hepatitis C usually occurs with minimal or weak activity of the pathological process and mild or moderate fibrosis (according to the results of intravital liver biopsies), but often the pace
Kuzmin V.N., Adamyan L.V., Kharchenko E.I.
Moscow State University of Medicine and Dentistry named after A.I. Evdokimov” of the Ministry of Health of Russia, Moscow, Russia
Purpose of the study. Determination of the role of hepatotropic (HAV, HBV, HCV, HDV) and conditionally hepatotropic (HGV, CMV, EBV, HSV types 1, 2 and 6) viruses in the etiological structure of diseases in pregnant women accompanied by increased activity of ALT and AST in blood.
Materials and methods. 211 pregnant women were examined, including 123 patients with chronic viral hepatitis, 74 patients with increased ALT activity in the blood in the absence of viral hepatitis markers (PALAT-OMVG) and 14 patients with acute viral hepatitis. The study was carried out using modern test systems by enzyme immunoassay, chemiluminescence and polymerase chain reaction.
Results. Among pregnant women with chronic HBV and HCV infections, in most cases, HBV DNA and RNA were detected in the blood, respectively, both against the background of normal and against the background of increased activity of transaminases in the blood. In the PALAT-OMVG group, none of the conditionally hepatotropic viruses was detected in more than 7% of cases. In 10 patients with hepatitis of unspecified etiology, the genetic material of the HAV, HBV, HCV, HDV, HGV, CMV, EBV, HSV types 1, 2, and 6 viruses was not detected in the blood.
Conclusion. In the absence of serological data confirming the presence of an infectious pathology, PCR blood testing for the presence of conditionally hepatotropic viruses in pregnant women in case of hepatitis of unspecified etiology is of little information. However, given that the range of conditionally hepatotropic viruses is not limited to those included in this study, it is advisable to additionally examine pregnant women with increased ALT and AST activity in the blood for the presence of TTV, B19V, HSV type 8 viruses, SEN and NV-F.
Literature
About the authors / For correspondence
The thymol test usually does not increase.
There are no significant abnormalities in the peripheral blood. the number of leukocytes is normal or low.
The recovery period can last up to six months. Clinical and biochemical changes disappear slowly. The content of bilirubin in the blood serum normalizes relatively quickly (within 2-4 weeks), and the increased activity of enzymes persists from 1 to 3 months. In a number of patients, a wave-like nature of hyperenzymemia can be observed during the period of convalescence. It should be taken into account that the recurrence of the disease with enzymatic exacerbation and hyperbilirubinemia requires the exclusion of HDV infection.
Clinical variants of HBV can be very diverse: icteric, anicteric, erased, inapparent (subclinical). It is difficult to judge the frequency of each of them, since usually only the icteric variant is diagnosed and, accordingly, recorded. Meanwhile. according to epidemiological studies, the anicteric variant is found much more often than the icteric one.
One of the features of the icteric variant of HBV is the severity of the cholestatic syndrome in some cases. At the same time, intoxication is insignificant, the main complaint of patients is itching of the skin; jaundice is intense, with a greenish or gray-green tint of the skin, persists for a long time. The liver is significantly enlarged, dense. Acholic feces, dark urine for a long time. In the blood serum - high bilirubinemia. elevated cholesterol and alkaline phosphatase activity. and the level of hyieralatemim is relatively low (5-10 norms). The icteric period can be delayed up to 2-4 months, the full normalization of biochemical changes occurs even later.
HBV can be mild, moderate, or severe.
The most informative for assessing the severity of viral hepatitis is the syndrome of hepatic intoxication, which is manifested by weakness, adynamia, loss of appetite, vegetovascular disorders, and in some cases, impaired consciousness. It is the severity of intoxication (in combination with the results of laboratory tests, primarily prothrombin activity) that characterizes the severity of hepatitis.
Hepatic transaminases in the blood material are ALT and AST. They contribute to the movement of amino groups, which will later be converted into amino acids. Most of their action takes place in the liver. Quantitative indicators of tests may differ depending on the patient's gender, body weight and age.
01 Value of transaminases and reasons for fluctuations
The blood of a healthy person does not show the activity of transaminases, an increase in their number is referred to as alarm bells. As a rule, a deviation from the norm in a big direction is not always provoked by liver diseases. Often, AST is used as a marker that shows problems with the heart muscle in myocardial infarction. In addition, an increase in concentration is provoked by a severe attack of angina pectoris.
There is an increase in transaminases with burns, sepsis, shock, a strong inflammatory process in the pancreas or gallbladder, and skeletal injuries.
The indicator of enzyme activity in this case does not differ in the specifics of the tests. However, fluctuations in AST and ALT are considered reliable indicators with high sensitivity. They determine liver damage, subject to the manifestation of clinical symptoms. When is a jump in the activity of hepatic transaminases observed in liver defects? This happens in the following cases:
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02 How are the symptoms of deviations expressed?
A very low percentage of the population constantly monitors their health by regularly undergoing a series of procedures. AST and ALT look at the blood material, which means that you will have to go to the doctor for a referral. Particular attention should be paid to patients who have a history of symptoms of liver disease.
The incredible value of such tests for the study of enzyme activity lies in the anticipation of an increase in transaminases. That is, in the presence of viral hepatitis A, a jump in ALT and AST is observed in a patient even in the preicteric stage. The patient still has a few weeks before the onset of symptoms of the disease, and the blood has already shown changes.
A patient with a history of hepatitis B is characterized by hyperfermentemia already 3 weeks before the visual manifestation of the disease. Early diagnosis of a serious illness suggests the absence of complications. If you do not take into account the abundance of causes, almost all liver diseases are characterized by similar symptoms:
1. Nausea and vomiting. Urges are noted without relationship with meals. 2. Aversion to certain food groups, refusal to eat, almost no appetite. 3. Sluggish state of health, weakness. The sensations may pass or be permanent. 4. The abdomen increases significantly in size, saphenous veins rendered as a grid. 5. Mucous membranes bleed. There are discharges from the nose, mouth and intestines. 6. Skin itching is debilitating, worse at night. 7. Natural discharge changes normal color, feces are discolored, and urine is unnecessarily dark. eight. Painful sensations on the right side, in the epigastric zone. There is tingling in the intercostal space.
It is quite easy to determine that the norm of transaminases is exceeded by these symptoms. It is important not to self-medicate, but immediately seek medical help.
03 Significance in diagnosing various diseases
Peak values of enzyme activity in the presence of acute viral hepatitis are observed during the 3rd week of the disease. A month later, experts note a decrease in ALT and AST to a normal amount.
If a patient has a 1.5-fold increase in transaminases, then we are talking about a moderate degree of hyperenzymemia. When fluctuating from 6 to 10 times, an average degree is assumed. The most severe option, when the degree becomes high, is fluctuations in values more than 10 times higher than the norm.
If the disease has a chronic course, then outside the exacerbation phase, there is no sharp fluctuation of enzymes in the blood material. Sometimes there is moderate change to the big side. An interesting fact, but the latent phase of cirrhosis proceeds with normal ALT and AST.
Most often, experts look not only at the level of hepatic transaminases, but also at the state of other indicators. bilirubin changes, alkaline phosphatase and a number of other biochemical values will narrow the search for pathology.
Acute liver failure and obstructive jaundice suggest the detection of high levels of bilirubin. During this period, the concentration of ALT and AST will be below the mark. This pathology is called bilirubin aminotransferase dissociation.
Jumps in indicators in children are due to the presence of the hepatitis virus or damage to the organ due to drug exposure. Doctors are always afraid of Reye's syndrome, a pathology that can take the life of the patient. It usually occurs when acute hepatic encephalopathy develops after the use of Aspirin.
For a deeper study of the analyzes, the ALT and AST values are compared, deriving the de Retis coefficient. Usually it fluctuates around the mark of 1.33, but when the figure drops, it is worth talking about possible inflammation in the liver or its infection. With necrosis of the heart muscle or possible hepatitis due to alcohol, the coefficient exceeds 2 units. But acute hepatitis of the viral type is diagnosed with a result of 0.55.
04 How important are liver transaminases?
Regardless of the patient's condition, an excess of transaminases indicates destructive processes in the liver. Hyperfermentemia can give a relapse after stabilization of the condition and the normal values of ALT and AST in the blood. Often this is due to the emergence of a new pathological process or exacerbation of an existing defect.
A decrease in transaminases can be achieved only if real reason their growth. Normal indicators return subject to high-quality diagnostics and the appointment of adequate therapy. Usually, specialists allow patients to undergo treatment at home or at a day hospital. However, if too high rates are detected, hospitalization and a more detailed examination are suggested.
For a thorough diagnosis, the results of electrocardiography, ultrasound or CT of the abdominal organs, and a detailed biochemical blood test will be required. Sometimes experts suggest the appointment of an ELISA to find antibodies to the hepatitis virus. As an alternative, PCR is carried out, DNA and RNA of the existing virus are already removed here.
It is noted that the cost of these tests is quite high, so they are carried out only when necessary. Usually the reason is reliable data from previous studies. Since the tests are sensitive to various changes in the liver, using laboratory analysis it is possible to determine the effect of therapy on the patient's body by adding several more instrumental techniques to it.
05 Treatments to lower ALT and AST
First of all, doctors prescribe a drug from the group of hepatoprotectors to the patient. This measure contributes to the correction of processes in the affected liver. Medicines from this area include all products containing ursodeoxycholic acid. The most popular names are Ursodez, Ursosan or Ursofalk.
There are more gentle drugs containing phospholipids, Rezalut or Essentiale Forte. Sometimes they are replaced by Karsil, especially often it is prescribed to elderly people. Heptral or Heptor have proven themselves well, the drug contains ademetionine. When using it, patients showed a rapid improvement in their condition. The results of control studies were always positive.
The appointment of funds occurs according to an individual method, the specialist is repelled by the patient's indicators. Some may be allergic to components or not respond to therapy. In such cases, the treatment is adjusted with a subsequent examination. Repeated therapy suggests early control of hepatic transaminases.
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Liver dysfunction can go unnoticed for a long time. Symptoms of diseases often appear in the later stages, which makes treatment difficult and obviously reduces its effectiveness. Determination of liver transaminase activity is one of the most accurate laboratory tests performed to assess the condition of the liver.
What are transaminases
Transaminases, or transferases, are enzymes that catalyze the chemical reactions of nitrogen metabolism, the main task of which is the transport of amino groups to form new amino acids. Biochemical processes requiring their participation are carried out mainly in the liver.
The transit movement of transaminases in the blood normally does not affect the result of the tests; in quantitative terms, their concentration for women and men, respectively, is up to 31 and 37 U/l for ALT and 31 and 47 U/l for AST.
Hepatic transferases determined during standard laboratory tests:
alanine aminotransferase, or alanine transaminase (ALT); aspartate aminotransferase, or aspartic transaminase (AST).
The level of enzymes in a healthy liver is influenced by such characteristics as age (increased value in newborns), gender (the norm of transaminases in the blood in women is lower than in men), overweight (there is a slight increase in transaminases).
Causes of fluctuations in AST, ALT
Transaminases in the blood of a healthy person do not show activity; a sharp increase in their level is an alarm signal. It is worth knowing that the growth of indicators is not always provoked by liver disease. AST is used as a marker of cardiac muscle damage in myocardial infarction; increases concentration and with a severe attack of angina pectoris.
Transaminases are elevated in skeletal trauma, burns, acute inflammation of the pancreas, or gallbladder, sepsis and shock states.
Therefore, the determination of the enzymatic activity of transaminases cannot be attributed to specific tests. But at the same time, AST and ALT are reliable and sensitive indicators of liver damage in the presence of clinical symptoms or history of the disease.
An increase in the activity of hepatic transaminases applicable to liver pathology is observed in the following cases:
1. Necrosis of hepatocytes (liver cells).
Necrosis is an irreversible process during which a cell ceases to exist as a structural and functional unit of tissue. The integrity of the cell membrane is violated and the cellular components come out, which leads to an increase in the concentration of biologically active intracellular substances in the blood.
Massive necrosis of hepatocytes provokes a rapid and multiple increase in hepatic transaminases. For the same reason, significant cirrhosis of the liver is not accompanied by enzymatic hyperactivity: there are too few functioning hepatocytes for their destruction to cause an increase in AST and ALT.
The transaminase values correspond to the norm, although the process is already in the stage of decompensation. ALT is considered a more sensitive indicator in liver diseases, therefore, with appropriate symptoms, first of all, attention is paid to its level.
Necrotic changes in the liver tissue are observed in acute and chronic hepatitis of various etiologies: viral, toxic (in particular, alcoholic and medicinal), acute hypoxia, which occurs as a result of a sharp drop in blood pressure during shock.
The release of enzymes directly depends on the number of affected cells, therefore, the severity of the process before conducting specific studies is estimated by the quantitative level of AST and ALT transaminases and an increase compared to the norm.
However, to determine further tactics, it is necessary additional examination along with a biochemical blood test in dynamics.
2. Cholestasis (stagnation of bile).
Despite the fact that a violation of the outflow of bile can occur for various reasons, its prolonged stagnation in conditions of preserved secretion by hepatocytes leads to overstretching, metabolic disorders, and, at the end of the pathological chain, to necrosis.
3. Dystrophic changes.
Dystrophy is a violation of tissue metabolism. It somehow accompanies inflammation; how its variety can be considered substitution connective tissue necrotic areas, which is the pathogenetic basis of liver cirrhosis.
Among the reasons for the increase in transaminases, fatty degeneration of the liver (alcoholic fatty hepatosis) is indicated.
Genetic diseases are also important, for example, Wilson-Konovalov disease (hepatolenticular degeneration), characterized by excessive accumulation of copper.
Liver tumors, both benign and malignant, in the process of growth destroy the surrounding tissues, which causes inflammation. This is reflected in a persistent increase in liver transaminases.
A similar effect is exerted by metastases - tumor cells brought with the blood or lymphatic fluid, forming secondary tumor foci in the liver tissue.
6. Medicinal effect.
To date, science has the data of numerous studies that have proven that drugs cause elevated transaminases. These include:
antibacterial agents (tetracycline, erythromycin, gentamicin, ampicillin); anabolic steroids (decanabol, eubolin); non-steroidal anti-inflammatory drugs (acetylsalicylic acid, indomethacin, paracetamol); monoamine oxidase inhibitors (selegiline, imipramine); testosterone, progesterone, oral contraceptives; sulfa drugs (biseptol, berlotsid); barbiturates (secobarbital, reposal); cytostatics, immunosuppressants (azathioprine, cyclosporine); preparations containing copper, iron.
The increase in transaminases does not depend on the form of the drug; tablets, as well as intravenous infusions, can adversely affect the liver or cause false activity of AST and ALT, which is due to the specifics of their determination in blood serum.
Symptoms
Despite the variety of causes, liver diseases have a number of similar symptoms, accompanied by an increase in liver transaminases:
weakness, lethargy, which appeared suddenly or persisted for a long time; nausea, vomiting, regardless of whether there is a connection with food intake; loss of appetite or its complete absence, aversion to certain types of food; pain in the abdomen, especially when localized in the right hypochondrium, epigastrium; an increase in the abdomen, the appearance of an extensive network of saphenous veins; icteric coloration of the skin, sclera of the eyes, visible mucous membranes of any degree of intensity; painful obsessive skin itching, aggravated at night; discoloration of discharge: darkening of urine, acholic (discolored) feces; bleeding of mucous membranes, nasal, gastrointestinal bleeding.
The value of the study of enzymatic activity explains the proactive clinical symptoms of an increase in AST and ALT transaminases in viral hepatitis A - already in the preicteric period, 10-14 days before the onset of icteric syndrome.
In hepatitis B, predominantly alanine transaminase is increased, hyperenzymemia is observed several weeks before the onset of signs of the disease.
Significance in diagnosis
To determine the characteristics of liver pathology according to the level of hyperenzymemia, a special scale is used. The degree of increase in hepatic transaminases is divided as:
Moderate (up to 1–1.5 norms or 1–1.5 times). Average (from 6 to 10 norms or 6-10 times). High (more than 10-20 norms or more than 10 times).
The peak of transaminase activity in acute viral hepatitis is observed in the second or third week of the disease, after which it decreases to normal ALT and AST values within 30–35 days.
At chronic course out of exacerbation, hyperfermentemia is not characterized by sharp fluctuations, and remains within a moderate or slight increase. In the latent (asymptomatic) phase of liver cirrhosis, transaminases are most often within the normal range.
It is important to pay attention to whether hepatic transaminases are elevated in isolation or in combination with other indicators of the biochemical spectrum: bilirubin, gamma-glutamyl transpeptidase, alkaline phosphatase, since the combination of an increase in indicators indicates a specific pathology or narrows the range of probable causes.
So, elevated transaminases are detected in carriers of hepatitis B, despite the absence of symptoms.
Subhepatic (mechanical) jaundice, acute liver failure may be accompanied by an increase in the level of bilirubin with a simultaneous normal or low concentration of AST and ALT. This phenomenon is called bilirubin aminotransferase dissociation.
An increase in transaminases in children is often due to infection with the hepatitis virus, drug-induced liver injury. A dangerous pathology that occurs in childhood is Reye's syndrome. Acute hepatic encephalopathy, a life-threatening condition, develops as a result of the use of acetylsalicylic acid (aspirin).
For the purpose of in-depth diagnostics, the de Ritis coefficient is used, which is the ratio of the AST and ALT transaminases. Normally, it is 1.33. If the de Ritis coefficient is less than 1, this is regarded as a sign of an infectious-inflammatory lesion of the liver.
For acute viral hepatitis, for example, it is 0.55-0.83. Achieving a level equal to 2 or higher suggests presumptive alcoholic hepatitis or necrosis of the heart muscle.
Significance in therapy
An increased content of transaminases in the blood is in most cases an unfavorable sign, evidence that liver cells are being destroyed.
Hyperenzymemia can be detected again some time after the normalization of indicators. As a rule, this indicates the beginning of a new or recurrence of an existing pathological process and renewed necrosis of hepatocytes.
How to lower transaminases? The level of AST and ALT is only a reflection of the presence of the disease; so get back to normal values possible only when adequate diagnosis and treatment of the detected pathology. High and extremely high levels of enzymes necessitate hospitalization and immediate additional examination.
It includes general clinical blood tests, a detailed biochemical blood test with the determination of electrolytes, glucose, as well as instrumental methods- electrocardiography, ultrasound and / or computed tomography of the abdominal organs.
If necessary, ELISA (enzyme-linked immunosorbent assay) is performed to search for antibodies to hepatitis viruses or PCR (polymerase chain reaction) to determine the DNA or RNA of viruses.
Given the high cost, it is not economically feasible to perform them without proper clinical justification or reliable anamnestic data.
The test for the determination of transaminases is sensitive to changes in the liver, so it can be used to assess the effectiveness of therapy in combination with other laboratory and instrumental methods.
hyperenzymemia
Universal Russian-English Dictionary. Akademik.ru. 2011 .
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What indicators of ALT and AST in hepatitis C are the norm?
Hepatitis C is a dangerous infectious disease leading to irreversible liver damage and severe life-threatening consequences. The indicators of ALT and AST in hepatitis C reflect the state of the enzymatic function of the liver and the degree of its damage and make it possible to detect adverse changes. This allows you to start timely treatment, which will slow the progression of the disease and help prevent serious complications.
What are ALT and AST?
Infection with viral hepatitis C is possible only through contact with blood, that is, by the parenteral route. Often, infection occurs during medical procedures (injections, blood transfusions), if the rules of sterility are violated and the virus enters the body along with infected blood.
In the diagnosis of hepatitis C, the study of aminotransferases, liver enzymes that are present in the liver and muscle tissue of other organs, plays a key role. Two of them are of clinical importance - alanine (ALT) and aspartic (AST). They are determined during a biochemical blood test. Tracking such indicators in dynamics allows assessing the effectiveness of treatment and, in the absence of positive dynamics, taking measures to correct it.
Indicators in normal and pathological conditions
ALT and AST are found in the liver and muscle tissue of the skeletal muscles and heart. It is there that they perform their function, and only a small part of them enters the blood, where they are determined during biochemical analysis. When these organs are damaged, the content of enzymes in the blood increases. Since ALT is more often elevated in liver disease, it is called "hepatic aminotransferase", and AST, respectively, "cardiac".
In fact, this division is very arbitrary, since both enzymes increase during pathological processes. Sometimes an increase in their concentration in the blood can provoke the use of certain medications (for example, oral contraceptives, anticoagulants, or medicines from the NSAID group).
More detailed information the doctor receives by comparing data on changes in the concentration of other enzymes, as well as the results of other tests. Normally, the content of these enzymes has the following meaning:
An increase in the amount of one or another enzyme in the blood is called hyperenzymemia. It is classified according to severity:
- mild (increased concentration up to 5 times);
- medium (6-10 times);
- severe (enzyme concentration exceeded by more than 10 times).
In hepatitis C, moderate hyperenzymemia is most often observed, which can decrease to mild or increase to severe. If hepatitis is complicated by cirrhosis, then hyperfermentemia gradually increases, moving from moderate to high severity. Often, laboratory blood changes in hepatitis are asymptomatic and imperceptible to the patient. Therefore, you will have to donate blood for analysis regularly in order to track the dynamics of the development of the disease.
What diseases cause hyperfermentemia?
An increase in the content of aminotransferases in the blood occurs with liver diseases (hepatitis, cirrhosis), myocardial infarction and muscle injuries. In the case of injuries, biochemical parameters are not of great diagnostic value, since other symptoms come to the fore.
In the case of myocardial infarction, the increase in the content of enzymes in the blood varies significantly with time and can accurately indicate how many hours have passed since the onset of the disease. In this case, AST is higher than ALT, which is why AST is called "cardiac aminotransferase". The determination of blood biochemical parameters in myocardial infarction is used to establish the possibility of thrombolysis in the first hours from the onset of an attack, as well as to assess the dynamics of the patient's condition and the effectiveness of the treatment. A decrease in aminotransferases to the norm or values close to it is a sign of the effectiveness of the therapy provided.
As a rule, in liver diseases, ALT is higher than AST, which is why the alanine enzyme is called "hepatic aminotransferase." The degree of enhancement can range from mild to high. In hepatitis C, the increase in the concentration of ALT and AST occurs in waves. The first increase occurs about two weeks after infection and often goes unnoticed. This is a slight increase, most often kept within the framework of mild hyperfermentemia, less often - medium. Then, for several years, biochemical parameters return to normal, sometimes the content of enzymes, more often ALT, is slightly higher than normal.
The next big wave of increase in fermentemia occurs 5-8 years after infection. ALT rises to figures corresponding to moderate hyperfermentemia, AST - mild or moderate. Indicators can vary, sometimes dropping almost to the norm, or, on the contrary, increasing. If the disease is complicated by cirrhosis, then hyperfermentemia becomes persistent and high. In the future, in the course of therapy, a biochemical blood test is done regularly. An indicator of the effectiveness of treatment will be the absence of fluctuations and a stable decrease in the level of ALT and AST in the blood. After treatment, biochemical parameters depend on what changes have occurred in the liver at the time of detection of the disease and the start of intensive therapy.
What to do with an increased concentration of enzymes?
An increase in the concentration of enzymes in the blood does not have pronounced symptoms that the patient might notice. Therefore, a person may not suspect for a long time that he has hepatitis C. Violations indicating infection are detected only in the laboratory, and all other symptoms of liver damage are caused by other causes.
However, patients are concerned about what to do if ALT and AST are elevated? In fact, nothing needs to be done to reduce the actual concentration of enzymes - it will decrease by itself if the treatment is effective. In hepatitis C, the change in these indicators is used only as one of the methods for assessing the patient's condition.
This is one of the fastest and most affordable ways to track changes in the patient's condition and adjust the treatment regimen in time. Given the high cost of drugs and examinations for hepatitis C, the method of biochemical blood analysis remains relevant and retains high clinical significance.
A method for diagnosing hyperenzymemia in violation of the exocrine function of the pancreas
The invention relates to medicine, namely to diagnostic methods. The essence of the method: the patient's blood serum is examined, applied to a glass slide, covered with a coverslip and dried at o C for 1.5-2 hours. The crystals formed in the patient's blood serum are compared with the crystals of model composites, which are previously obtained by enriching the blood serum of a healthy person with enzymes trypsin, amylase, lipase. In the presence of crystals in the form of cellular or dendritic networks, hypertrypsinemia is diagnosed, in the presence of subparallel lamellae - hyperamylasemia, in the presence of bubble chambers with processes - hyperlipasemia. The method provides high information content and reliability. 11 ill., 1 tab.
The invention relates to medicine and can be used in the treatment of diseases of the pancreas.
The timely determination of violations of pancreatic enzyme production, the diagnosis of hyperenzymemia (the release of lipase, amylase, trypsin) continue to cause difficulties in the practice of doctors of various specialties (therapists, gastroenterologists, surgeons, endocrinologists, etc.).
Often, an attack of acute pancreatitis is not recognized in a timely manner, but is interpreted as a clinic of an acute abdomen, due to perforation of a stomach ulcer, an attack of acute cholecystitis, acute appendicitis, intestinal obstruction. This leads to tactical errors (Henderson J. Pathophysiology of the digestive system. - St. Petersburg, 1997, p.). Violation of the external secretion of the pancreas (PG) can also be observed in chronic pancreatitis, as well as in other diseases of the gastrointestinal tract, in which the pancreas suffers for the second time, with the development of complications after operations on the pancreas and nearby organs. There are known cases of violation of the external secretion of the pancreas (primarily, an increase in the blood levels of lipase, amylase, trypsin enzymes) during cardiovascular bypass surgery, heart transplantation, kidney transplantation.
The increase in pain in acute pancreatitis and exacerbation of chronic pancreatitis is accompanied by an increase in the blood levels of the enzymes amylase, lipase, trypsin (Zimmerman Y.S. Chronic pancreatitis. Guidelines. - Perm, 1990; Loginov A.S., Speransky M.D., Astashenkova K.Yu. Screening methods for rapid diagnosis of diseases of the liver and pancreas. Guidelines. - M., 1987; Grigoriev P.Ya., Yakovenko E.P. Diagnosis and treatment of diseases of the digestive system. - M .: Medicine, 1996 ).
Diagnosis of hyperenzymemia provides valuable information about the violation of the external secretion of the pancreas. The most important in the diagnostic process is the study of the content of enzymes in plasma of blood serum (SC), the determination of the content of α-amylase, lipase, trypsin. -amylase is produced by the pancreas and salivary glands. Hyperamylasemia is observed in many diseases, but is most pronounced in acute pancreatitis.
Lipase catalyzes the breakdown of glycerides, higher fatty acids. It is produced in the pancreas, lungs, and intestines. An increase in the activity of serum lipase may be a consequence of the pathology of the pancreas, lungs, intestines, stomach, leukocyte blood germ.
Trypsin is produced in the pancreas, from which, as part of the pancreatic juice (in the form of trypsinogen), it enters the duodenum and is involved in the digestion of food proteins. When the pancreas is damaged, trypsin activity increases sharply, especially in acute pancreatitis.
Diagnosis of violations of the enzyme-forming function of the pancreas is carried out by quantitative determination of the content of enzymes in the blood serum - amylase, lipase, trypsin, as well as in other biological fluids. In this case, various methods for the quantitative determination of enzymes are used (Medical laboratory technologies. Handbook. T.2. - St. Petersburg, 1999; Biochemical methods of research in the clinic. - M., 1969).
Lipase activity is determined in most methods on the basis of a titrimetric determination of the amount of fatty acids released by the enzyme. These methods differ in the substrate used: olive oil, tween, terbutyrin (Biochemical research methods in the clinic. Handbook. - M., 1969, p.).
The disadvantage of these methods is their low specificity, tk. these substrates are hydrolyzed not only by lipase, but also by other hepatic esterases.
The titrimetric method for determining lipase is based on the titration of fatty acids released as a result of enzymatic hydrolysis, the photometric method is associated with the introduction of special reagents into the reaction mixture. As a unified method, turbidimetric is used, in which olive oil is used as a substrate (Handbook. Medical laboratory technologies. T.2. - St. Petersburg, 1999, p. 39-41).
Principle: Spectrophotometric determination of the change in turbidity of an olive oil suspension under the action of lipase.
Reagents: olive oil, aluminum oxide, copper sulfate, ethyl alcohol, sodium salt deoxycholic acid, hydrochloric acid.
Special equipment: spectrophotometer with temperature-controlled cuvette.
Determination course: Before determination, the studied blood serum and reagents are warmed up to the measurement temperature. 3 ml of a working emulsion of olive oil is poured into the cuvette, 0.1 ml of blood serum is added, mixed (without shaking) and placed in a thermostat at 30 o C or 37 o C, after 2 minutes the extinction (E1) is measured against distilled water or air at wavelength of 340 nm in a cuvette with an optical path length of 10 mm, then the cuvette is again placed in a thermostat at the same temperature and after 5 minutes the extinction (E2) is measured, calculating E in 1 min. The calculation of the activity of lipase produced by the formula Disadvantages of the method: - violation of the nativeness of the SC (heating, connection with the reagent); - the use of reagents requiring additional processing; - the use of expensive equipment; - indirect determination of the presence of lipase.
Trypsin is determined in blood serum by determining its activity according to Erlanger et al. in the modification of V.A. Shornikova (Biochemical methods of research in the clinic. - L., 1969, p.). The method is based on trypsin cleavage of a synthetic colorless substrate - benzoylarginine-p-nitroanilide - with the formation of colored p-nitroaniline, the amount of which is determined calibrimetrically.
The disadvantage of this method: - the use of reagents is accompanied by laboriousness and high cost of the method; - use of a spectrophotometer; - carrying out calculations;
The most common in recent years is the determination of trypsin using the Bio-LA CHEMA-test kit (Kasafirek E., Chavko M., Bartik M.: Coll. Czechisiov. Chem. Commum. 36, 4070, 1971) - by the photometric method. The method is based on the ability of trypsin to hydrolyze the chromogenic substrate. N-alpha-tosyl-L-arginine-4-nitroanilide. The resulting 4-nitroanilide is determined photometrically (kinetic method).
Reagents: Tris buffer 3.4 mmol, calcium chloride 1.7 mmol/vial, substrate L-pack 10 mmol/l, standard solution 4-nitroaniline 500 µmol/l.
The composition of the incubation mixture:
Tris buffer, pH 8.2 (25 o C) - 40.6 mmol / l,
L-TAPA - 0.94 mmol / l,
CaCl - 20.6 mmol / l.
The volume ratio of serum:incubation mixture is 1:16.
acetic acid solution - 1.75 mmol / l.
1. Prepare a buffer solution with a reagent.
2. Prepare a working solution (mix reagent - 1 share of reagent 2 and 9 shares of buffer solution).
Measure the optical density in the interval of seconds and calculate the change in optical density per minute (A).
Measure the absorbance of the standard against the blank (A2).
Formula calculation
1. Violation of serum nativeness.
2. Using a photometer.
3. Preparation of working and buffer solutions.
Method for determining α-amylase activity
The biological fluids are divided into three main groups:
1. Reductometric, based on the determination of sugars formed from starch.
2. Amyloclastic, based on determining the amount of undigested starch by its reaction with iodine.
3. Chromolytic, based on the use of substrate-dye complexes, which, under the action of α-amylase, decompose to form a water-soluble dye (Handbook. Medical laboratory technologies. V.2. - St. Petersburg, 1993, pp. 19 and 20).
Disadvantages of the above methods:
Violation of the nativeness of blood serum;
Use of an indirect reaction (starch + iodine);
Labor intensive and unreliable.
We used as a prototype a unified amyloclastic method with a persistent starch substrate (Karavey's method) (Handbook. Medical laboratory technologies. V.2. - St. Petersburg, 1999, pp. 20 and 21).
Principle: -amylase hydrolyzes the breakdown of starch with the formation of end products that do not give a color reaction with iodine. The activity of α-amylase is judged by the decrease in color intensity.
1. Benzoic acid.
3. Starch, soluble for nephelometry or Lintner (specially available as a substrate).
4. 154 mM (0.9%) sodium chloride solution: Dissolve 9 g of NaCl in a small amount of distilled water in a 1 L volumetric flask, then make up to the mark.
5. Substrate buffer solution, pH 7.0: 13.3 g of sodium hydrogen phosphate and 2 g of benzoic acid are dissolved in 250 ml of 154 mm sodium chloride solution and brought to a boil. Suspend 0.2 g of soluble starch in a small amount of cold distilled water and add to the boiling buffer solution. Boil for 1 minute, cool and dilute to 500 ml with distilled water. The substrate buffer solution should be clear and stable at room temperature during the days.
6. Potassium iodide (KI).
8. Potassium fluoride (KF).
9. Concentrated HCl.
10. 0.01 n. iodine solution: 0.036 g of KIO 3 + 0.45 g of KI are dissolved in 40 ml of distilled water and 0.09 ml of concentrated HCl is added slowly with stirring. Dissolve 5 g of potassium fluoride in 50 ml of distilled water, filter into a volumetric flask, add 40 ml of iodine solution and top up with distilled water to a volume of 100 ml. Store in a dark glass container. Valid for a month. If potassium fluoride is not added to the working solution of iodine, then it should be prepared daily from 0.1 N. solution I.
0.5 ml of the substrate-buffer solution is placed in a test tube, heated for 5 minutes at a temperature of 37 o C, add 0.01 ml of blood serum.
Incubate for 7.5 minutes at a temperature of 37 o C. The incubation time must be accurately counted by a stopwatch from the moment of adding biological fluid(blood serum) into a starch substrate. Immediately after incubation, add 0.5 ml of 0.01 N. iodine solution and bring the volume with distilled water to 5 ml.
Photometry is carried out in a cuvette with an optical path length of 10 mm at a wavelength of N (3.3-8.9 mg/s l)nm (red light filter) against distilled water.
The activity of α-amylase is expressed in milligrams or grams of 1 starch hydrolyzed with 1 liter of biological fluid for 1 s of incubation at 37 o C.
The calculation is made according to the formula
where A is the activity of β-amylase, mg/s l;
Ek - extinction of the control sample,
Eo - extinction of the experimental sample;
0.2 - the amount of starch introduced into the experimental and control samples, mg;
crossover coefficient per 1 liter of blood serum;
7, crossover ratio per 1 s incubation.
2. Use (preparation) of complex reagents.
3. Duration of the study.
4. Exposure to toxic substances.
5. Violation of the nativeness of the studied enzyme.
6. Use of a photometer (instrument complexity).
7. Unreliability of the definition.
1. Simplify the sample preparation method.
2. Increase information content by isolating microtypes of crystals characteristic of selective hyperenzymemia.
3. To improve the accuracy and quality of diagnosing disorders of the exocrine function of the pancreas.
The essence of the invention lies in the fact that in order to diagnose a violation of the exocrine function of the pancreas (hyperfermentemia), blood serum is applied to a glass slide, covered with a coverslip, dried at a temperature of o C, kept in the open air for 1.5-2 hours, then follow in transmitted light and in the presence of cellular or dendritic networks, hypertrypsinemia is diagnosed, subparallel lamellae - hyperamylasemia, bubble chambers with processes - hyperlipasemia.
The method is carried out as follows:
1. Blood is taken from a vein - 3.0 ml, centrifuged to obtain serum.
2. Serum in the form of drops with a volume of 0.01-0.02 ml each is applied to a glass slide, covered with a cover glass.
3. Dry in a thermostat at a temperature of o C for 1.5-2 hours.
4. Keep outdoors for 1.5-2 hours.
5. Under a microscope in transmitted light, the picture of crystallization is studied and, if there are crystals in the form of cellular or dendritic networks in the preparation, hypertrypsinemia is diagnosed, subparallel lamellae - hyperamylasemia, bubble chambers with processes - hyperlipasemia.
We previously examined the reference crystallograms, for which the blood serum of a healthy person, placed in a container of quartz, was enriched with enzymes - amylase, lipase, trypsin.
Photo 1 (a-d) shows the reference crystallograms (CG) of the blood serum of a healthy person, enriched with enzymes. KG is made with crystals in the form of a cellular mesh and a dendritic mesh when the blood serum (SC) is supersaturated with the enzyme trypsin; model composite of hypertrypsinemia, trypsin concentration was 1200 and 1800 mmol/l, respectively, photo 1 (a, b); crystals from subparallel lamellae upon supersaturation of SA with the enzyme amylase, model composite of hyperamylasemia, amylase concentration was 94 mmol/l h, photo 1c; crystals from bubble chambers with processes when supersaturation of SK with lipase enzyme, model composite of hyperlipasemia, lipase concentration - 5.4 c.u., photo 1 g. The method was tested on 800 patients.
Example 1, photo 2 (a, c). Patient I., medical history (IB) 1819. Diagnosis: acute pancreatitis. Photo 2 a-c shows CG of the blood serum of patient I., there are bubble chambers with processes (a, b), a dendritic mesh (c).
Technology: blood was taken from the vein of patient I. in the amount of 3 ml, the blood was centrifuged to obtain serum. Drops of SC (5) with a volume of 0.01 ml each were applied to a glass slide, each drop was covered with a cover slip and dried in a thermostat for 1.5 hours at a temperature of +37 o C. The drug was kept in the open air for 2 hours, then studied in a passing light under a microscope. Crystals were found, represented by bubble chambers with processes, a dendritic network. At the same time, the level of lipase and trypsin was determined in the patient's SC, which turned out to be elevated and amounted to 3.4 c.u., respectively. (norm 0.8 c.u.), 630 mmol/l (norm 220 mmol/l).
The suspected hyperenzymemia (hyperlipasemia and hypertrypsinemia) was confirmed.
Example 2, photo 3 (a, b). Patient Zh., medical history 9680. Diagnosis: chronic recurrent pancreatitis, pain form. Photo 3 a, b shows the CG of the blood serum of patient Zh., there is a dendritic network (a), subparallel lamellae (b).
Technology: 3 ml of blood was taken from the vein of patient Zh., which was centrifuged to obtain SC. Drops of SC (3) with a volume of 0.02 ml each were applied to a glass slide, each was covered with a cover slip and dried in a thermostat for 2 hours at a temperature of +38 o C. The preparation was kept in the open air for 1.5 hours, then microscoped. Crystals were found - a dendritic network and subparallel lamellae. At the same time, trypsin and amylase levels were determined in the patient's SC, which turned out to be elevated and, respectively, amounted to 780 mmol/l (norm 220 mmol/l) and 72 mmol/l.h. (norm 18.5 mmol / l. H.). The suspected hyperenzymemia (hypertripsinemia and hyperamylasemia) was confirmed.
Example 3, photo 4 (a, b). Patient G., case history 10620. Diagnosis: duodenal ulcer, complicated by cicatricial deformity of the bulb, suspicion of chronic pancreatitis. Photo 4 a, b shows the CG of the blood serum of patient G., there is a dendritic mesh (a) and a mesh mesh (b). Technology: 3 ml of blood was taken from the vein of the patient G., which was centrifuged. Drops of SC (4) with a volume of 0.02 ml each were applied to a glass slide, each was covered with a cover slip and dried in a thermostat for 2 hours at a temperature of +38 o C. The drug was kept in the open air for 1.5 hours, then studied in transmitted light . Crystals were found - a dendritic network and a cellular network. At the same time, the level of trypsin in the patient's SC was determined, which turned out to be elevated and amounted to 630 mmol/l (the norm is 220 mmol/l). The suspected hyperenzymemia was confirmed.
Example 4, photo 5 (a, b). Patient M., case history 10972. Diagnosis: chronic recurrent pancreatitis, stage of fading exacerbation, erosive reflux esophagitis, chronic gastroduodenitis.
Photo 5 a, b shows the CG of the blood serum of patient M., there are bubble chambers with processes.
Technology: 3 ml of blood was taken from the vein of patient M., the blood was centrifuged. Drops of SC (3) with a volume of 0.02 ml each were applied to a glass slide and dried in a thermostat for 2 hours at a temperature of +38 o C. The drug was kept in the open air for 2 hours, then microscoped. Found crystals in the form of bubble chambers with processes. At the same time, the level of lipase was determined in the SC, which turned out to be elevated and amounted to 2.1 c.u. (norm 0.8 c.u.). The alleged hyperenzymemia (hyperlipasemia) was confirmed.
Example 5, photo 6 (a, b). Patient O., case history 9418. Diagnosis: chronic gastroduodenitis, postcholecystectomy syndrome. Chronic pancreatitis, pain form. Photo 6 a, b shows the CG of the blood serum of patient O., there are subparallel lamellae (a) and a mesh (b).
Technology: 3 ml of blood was taken from the vein of patient O., which was centrifuged. Drops of SK (5) with a volume of 0.01 ml each were applied to a slide, each drop was covered with a slide and dried in a thermostat at a temperature of +37 o C for 2 hours. The preparation was kept in the open air for 1.5 hours, then microscoped. Crystals were found - subparallel lamellas and a cellular grid. At the same time, the content of amylase and trypsin was determined in the SC, which turned out to be elevated and, accordingly, amounted to 28.5 mmol/l. hours and 290 mmol / l. The suspected hyperenzymemia (hyperamylasemia and hypertrypsinemia) was confirmed.
Example 6, photo 7.
Patient V., medical history 1443. Diagnosis: chronic gastroduodenitis, chronic cholecystitis, suspicion of chronic pancreatitis. Photo 7 shows the CG of the blood serum of patient V., there is a dendritic mesh.
Technology: drops of SC from patient V. were applied to a glass slide (5 drops), each with a volume of 0.02 ml. Each drop was covered with a cover slip and dried in a thermostat for 1.5 hours at a temperature of +38 o C. The sample was kept in the open air for 1.5 hours and examined under a microscope. Crystals in the form of a dendritic network were found. At the same time, the level of trypsin was determined in the SC, which turned out to be elevated and amounted to 285 mmol/l (the norm is 220 mmol/l). The alleged hyperenzymemia (hypertripsinemia) was confirmed.
Example 7, photo 8 (a, b). Patient B., case history 9389.
Diagnosis: duodenal ulcer in the stage of incomplete remission. Catarrhal reflux esophagitis. Chronic recurrent pancreatitis, pain form. Photo 8 a, b shows CG of blood serum, there are bubble chambers with processes (a) and subparallel lamellae (b).
Technology: 4 drops of patient B.'s SC, each with a volume of 0.01 ml, were applied to a glass slide, each was covered with a coverslip and dried in a thermostat at a temperature of +37 o C for 1.5 hours. The sample was kept in the open air for 1.5 hours and microscoped. Crystals were found: bubble chambers with processes and subparallel lamellae. At the same time, the level of lipase and amylase was determined in the SC, which turned out to be elevated and amounted to 1.2 c.u., respectively. e. (norm 0.8 c.u.) and 39.8 mmol / l.h. (Norm 18.5 mmol / l.h.) The alleged hyperenzymemia (hyperamylasemia and hyperlipasemia) was confirmed.
Example 8, photo 9 (a, b). Patient Zh., medical history 13200. Diagnosis: chronic pancreatitis, period of exacerbation. Photo 9 (a, b) shows the CG of the blood serum of patient G., there are subparallel lamellae.
Technology: blood from a vein in the amount of 3 ml was taken from a patient Zh., centrifuged. Drops of SK (4) each with a volume of 0.01 ml were applied to a glass slide. Each drop was covered with a cover slip and dried in a thermostat for 1.5 hours at a temperature of +38 o C. The sample was kept in the open air for 1.5 hours, then examined under a microscope in transmitted light. Crystals in the form of subparallel lamellae were found. At the same time, the level of amylase in the SC was determined, which turned out to be elevated and amounted to 45 mmol/l.h. The alleged hyperfermentemia (hyperamylasemia) was confirmed, which indicates a violation of the exocrine function of the pancreas.
Example 9, photo 10 (a, b). Patient B., medical history 12228. Diagnosis: chronic pancreatitis, stage of incomplete exacerbation. Chronic erosive gastritis, catarrhal bulbitis. Photo 10 a, b shows the CG of the blood serum of patient B., subparallel lamellae (a) and bubble chambers with processes (b) are visible. Technology: drops of SC (3) of patient B. were applied to a glass slide, each with a volume of 0.01 ml. Each drop was covered with a cover slip and dried in a thermostat at a temperature of +37 o C for 1.5 hours. The sample was kept in the open air for 2 hours and microscoped. Subparallel lamellae and bubble chambers with outgrowths were found. At the same time, the level of amylase and lipase was determined in the patient's SC, which turned out to be elevated and, respectively, amounted to 78 mmol/l.h. and 3.8 c.u. (norm of amylase - 18.5 mmol / l.h. and lipase - 0.8 y. e.). The expected hyperenzymemia (hyperamylasemia and hyperlipasemia) was confirmed.
Example 10, photo 11. Patient Sh., medical history 10767. Diagnosis: duodenal ulcer with localization of the ulcer on the back wall of the duodenal bulb, HP-associated, stage of exacerbation. reactive pancreatitis. Photo 11 shows the CG of the blood serum of patient III, there are subparallel lamellae.
Technology: drops of the patient Sh.'s SC were applied to a glass slide (5 drops), each with a volume of 0.01 ml. Each drop was covered with a cover slip and dried in a thermostat for 2 hours at a temperature of +38 o C, the sample was kept in the open air for 1.5 hours and microscoped. Subparallel lamellas were found. At the same time, the level of amylase was determined in the SC, which turned out to be elevated and amounted to 48 mmol/l.h. (norm - 18.5 mmol / l.h.). The suspected hyperenzymemia (hyperamylasemia) was confirmed.
The implementation method allows:
1. Simplify the definition of hyperenzymemia.
2 Eliminate the use of complex chemicals and instruments.
3. Reduce the cost of diagnostics.
4. Creates the possibility of express diagnostics of disorders of the exocrine function of the pancreas.
5. Provides high information content.
6. Increases the reliability of obtaining results.
A method for diagnosing a violation of the external secretory function of the pancreas, including the study of the patient's blood serum, applied to a glass slide, covered with a coverslip, dried with o C for 1.5-2 hours, followed by the study of crystals, characterized in that model composites are preliminarily created by enriching the blood serum of a healthy person with enzymes, with the crystals of which the crystals of the patient's blood serum are compared, and diagnosing hyperenzymemia: in the presence of crystals in the form of a cellular or dendritic mesh, hypertrypsinemia is diagnosed, in the presence of subparallel lamellae - hyperamylasemia, in the presence of bubble chambers with processes - hyperlipasemia.
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Hyperfermentemia (with a predominant increase in ALT activity by 30-50 times) is recorded during the entire icteric period, then there is a gradual decrease in its level. The protein-synthetic function of the liver in HBV is impaired in the severe course of the disease, which is manifested by a decrease in the sublimate test, albumin content, prothrombin index, activity (3-lipoproteins. The thymol test usually does not increase.
There are no significant abnormalities in the peripheral blood. the number of leukocytes is normal or low.
The recovery period can last up to six months. Clinical and biochemical changes disappear slowly. The content of bilirubin in the blood serum normalizes relatively quickly (within 2-4 weeks), and the increased activity of enzymes persists from 1 to 3 months. In a number of patients, a wave-like nature of hyperenzymemia can be observed during the period of convalescence. It should be taken into account that the recurrence of the disease with enzymatic exacerbation and hyperbilirubinemia requires the exclusion of HDV infection.
Clinical variants of HBV can be very diverse: icteric, anicteric, erased, inapparent (subclinical). It is difficult to judge the frequency of each of them, since usually only the icteric variant is diagnosed and, accordingly, recorded. Meanwhile. according to epidemiological studies, the anicteric variant is found 20-40 times more often than the icteric one.
One of the features of the icteric variant of HBV is the severity of the cholestatic syndrome in some cases. At the same time, intoxication is insignificant, the main complaint of patients is itching of the skin; jaundice is intense, with a greenish or gray-green tint of the skin, persists for a long time. The liver is significantly enlarged, dense. Acholic feces, dark urine for a long time. In the blood serum - high bilirubinemia. elevated cholesterol and alkaline phosphatase activity. and the level of hyieralatemim is relatively low (5-10 norms). The icteric period can be delayed up to 2-4 months, the full normalization of biochemical changes occurs even later.
HBV can be mild, moderate, or severe.
The most informative for assessing the severity of viral hepatitis is the syndrome of hepatic intoxication, which is manifested by weakness, adynamia, loss of appetite, vegetovascular disorders, and in some cases, impaired consciousness. It is the severity of intoxication (in combination with the results of laboratory tests, primarily prothrombin activity) that characterizes the severity of hepatitis.
59. Breslau N., Lipton R.B., Stewart W.F. et al. Comorbidity of migraine and depression: Investigating potential etiology and prognosis. Neurology. 2003; 60:1308-12.
60. Lake A.E., Saper J.R., Hamel R.L. Comprehensive inpatient treatment of refractory chronic daily headache. headache. 2009; 49:555-62.
61. Saper J.R., Lake A.E. Inpatient strategies for refractory migraine. In: Shulman E.A., Levin M., Lake A.E. et al. Refractory migraine. Mechanisms and management. New York: Oxford University Press; 2010: 314-41.
62. Franzini A., Messina G., Leone M. et al. Occipital nerve stimulation (ONS). Surgical technique and prevention of late electrode migration. Acta Neurochir. (Wien). 2009; 151:861-5.
63. Silberstein S.D., Dodick D.W., Saper J. et al. Safety and efficacy of peripheral nerve stimulation of the occipital nerves for the management of chronic migraine: results from a randomized, multicenter, double-blinded, controlled study. Cephalalgia. 2012; 32:1165-79.
Received 04/12/14 Received 04/12/14
UDC 616.153.1-008.61-02:616.37]-036.1
Krasnovsky A.L.1, Grigoriev S.P.1, Zolkina I.V.1, Loshkareva E.O.1, Brutskaya L.A.2, Bykova E.A.1 ASYMPTOMIC PANCREATIC HYPERFERMENTEMIA
‘Department of Internal Medicine, State Budgetary Educational Establishment of Higher Professional Education Russian National Research Medical University. N.I. Pirogov. 117997, Moscow; 2FGBUZ "Central Clinical Hospital of the Russian Academy of Sciences". 117593, Moscow, Russia
For correspondence: Krasnovsky Alexander Leonidovich, Ph.D. honey. in Medicine, Assistant of the Department of Internal Diseases, Faculty of Medicine and Biology. Email:
Correspondence to: Aleksandr Krasnovskiy - MD, PhD, assistant of department of internal diseases of medicobiologic faculty. Email:
♦ Asymptomatic elevations in pancreatic enzymes often lead to a misdiagnosis of chronic pancreatitis and unnecessary treatment. Meanwhile, in many such cases, hyperenzymemia is benign. The article describes the possible causes of pancreatic hyperenzymemia in apparently healthy people and proposes a diagnostic search algorithm in this clinical situation.
Key words: asymptomatic pancreatic hyperenzymemia; Gullo syndrome; pancreas;
hyperamylasemia; macroamylasemia; amylase; lipase; trypsin; chronic pancreatitis
Krasnovskiy A.L.1, GrigoriyevS.P.1, Zolkina I.V.1, Loshkareva E.O.1, Brutskaya E.O.2, Bykova E.A.1
THE ASYMPTOMATIC PANCREATIC HYPERFERMENTATION
‘The N.I. Pirogov Russian national research medical university Minzdrav of Russia, 117997 Moscow, Russia
2The central clinical hospital of the Russian academy of sciences, 117593 Moscow, Russia
♦ The asymptomatic increase of the level of enzymes of pancreas often results in such incorrect diagnosis as chronic pancreatitis and in prescription of unnecessary treatment. Meanwhile, in many similar cases hyperenzymemia has a benevolent nature. The article discusses possible causes of pancreatic hyperenzymemia in healthy persons. The algorithm of diagnostic search in this clinical situation is proposed.
Keywords: asymptomatic pancreatic hyperenzymemia; Gullo's Syndrome; pancreas; hyperamylasemia; macroamylasemia; amylase; lipase; trypsin; Chronic pancreatitis
Raise serum level pancreatic enzymes is usually regarded as a manifestation of diseases of the pancreas, primarily of an inflammatory or tumor nature, less often as a manifestation of the pathology of other organs (see table).
In recent years, the study of the level of pancreatic enzymes has been included in the screening panel of biochemical analyzes, in connection with this, asymptomatic pancreatic hyperenzymemia is increasingly accidentally detected, and standard diagnostic methods (history taking, physical examination, transabdominal ultrasound of the abdominal organs) do not reveal any pathology, explaining laboratory abnormalities. There is currently no generally accepted algorithm for diagnostic search in such cases. At the same time, the results of a number of studies, which formed the basis of the recommendations of leading experts in the field of pancreatology, can help the clinician in making tactical decisions.
In 1978, A. Warshaw and K. Lee described 17 cases with chronic hyperamylasemia without clinical manifestations and other signs of pancreatic disease. In 1988, the same group of authors already described 117 similar cases, suggesting that laboratory abnormalities in these patients are not associated with pancreatic pathology.
In 1996, L. Gullo (Lucio Gullo) described a series of 18 cases of increased activity of pancreatic enzymes (isolated or combined 2-15-fold increase in total amylase, pancreatic amylase, lipase or trypsin) in apparently healthy people. Accidentally detected hyperfermentemia was the reason for an in-depth examination, however, with a detailed history taking, a thorough physical and laboratory-instrumental examination, including ultrasound and computed tomography, of the abdominal organs, as well as
performing endoscopic retrograde cholangiopancreatography (ERCP), the pathology explaining the increased activity of pancreatic enzymes could not be identified. Prof. Gullo continued to follow most of these patients from 1987 to 2006 and stated that persistent hyperenzymemia persisted during this period in the absence of overt pancreatic disease or other known causes. The author came to the conclusion that the increase in the activity of pancreatic enzymes in these patients is benign, in connection with which he called the described anomaly chronic non-pathological pancreatic hyperenzymemia, or benign pancreatic hyperenzymemia, or Gullo's syndrome. In most cases, with this syndrome, the level of at least two pancreatic enzymes is increased, in other cases there is an isolated increase in the activity of amylase or lipase, often small (1.5-4 times). After stimulation with secretin, there is a further increase in the initially increased levels of pancreatic enzymes, while the Wirsung duct expands to the same extent as in healthy volunteers without hyperenzymemia. Therefore, it is impossible to associate benign hyperenzymemia with stenosis of the pancreatic ducts.
In 2000 prof. Gullo described several families in which at least two blood relatives, including children, had an asymptomatic increase in the activity of pancreatic enzymes. He designated this condition as "familial pancreatic hyperenzymemia". He later described 15 more cases of benign pancreatic hyperenzymemia in children. In this context, the results of the study by E. Tsianos et al. . They measured the level of total amylase, as well as isoenzymes (B- and P-isoamylase) in 92 volunteers in England, divided into 3 ethnic subgroups.
Causes of pancreatic hyperenzymemia with clinical manifestations
State group
Diseases and provoking factors
Pathology of the pancreas and other abdominal organs
Malignant neoplasms
Multisystem diseases
Diseases of other organs and other conditions
Taking medications
Acute pancreatitis or exacerbation of chronic pancreatitis, obstruction of the pancreatic duct (stones, tumors), acute cholecystitis, consequences of endoscopic retrograde cholangiopancreatography, abdominal surgery, cardiac surgery, liver transplantation, secondary pancreatitis in diseases of the abdominal cavity and small pelvis ( gastric ulcer perforation, intestinal obstruction, mesenteric thrombosis, peritonitis, small bowel afferent loop obstruction after gastrectomy, periampullary diverticula, inflammatory bowel disease, gastroenteritis, salpingitis, ectopic pregnancy, endometriosis), dissecting descending aortic aneurysm, abdominal trauma, liver disease (viral hepatitis) , cirrhosis of the liver)
Cancer of the lungs, ovaries, thyroid, colon, prostate, kidneys, mammary glands, hemoblastosis
AIDS, critical conditions in intensive care patients (including various types of shock, acidosis, intracranial hemorrhage), acute porphyria, SLE and other rheumatic diseases, toxic epidermal necrolysis, leptospirosis, sarcoidosis
Diseases of the salivary glands (mumps, duct stones and tumors of the salivary glands, Sjögren's disease), macro-amylasemia and macrolipasemia, renal failure (decreased clearance of pancreatic enzymes), alcoholism (acute alcohol intoxication), pheochromocytoma, thrombosis
Paracetamol, corticosteroids, azathioprine, ephedrine, ritodrine, cytostatics, roxithromycin, cyclosporine, clozapine, pentamidine, didanosine, opiates
Note. SLE - systemic lupus erythematosus.
Native English, Asian, and West Indian subjects. Serum amylase activity has been found to be higher in immigrants than in native English. The authors concluded that these differences in serum amylase activity may be genetically determined and named this condition ethnic hyperamylasemia. They also emphasized the need to develop ethnic standards in order to avoid diagnostic and tactical errors.
In a specially designed study, the activity of pancreatic enzymes (lipase, total amylase, pancreatic amylase, trypsin) was determined daily for five consecutive days in 42 patients diagnosed with Gullo's syndrome. All patients showed pronounced fluctuations in the content of enzymes, and in 33 (78.6%) of them it normalized within a few days, then increased again. Gullo proposed to consider such variability as a diagnostic criterion for benign pancreatic hyperenzymemia, and to include the determination of the level of the corresponding enzymes daily for five days in the examination plan for such patients.
A report on the study by E. Gaia881 et al. is currently being prepared for publication. . They summarized the results of a 5-year follow-up of 183 patients with benign pancreatic hyperenzymemia. In 74.9% of them, the levels of lipase and both isoenzymes of amylase were increased, in 7.2% - only lipase, in 6.3% - only amylase, and the level of lipase increased to a greater extent. They also stated a significant variability in the activity of enzymes up to their temporary normalization.
At the same time, Gullo drew attention to the fact that in several cases an asymptomatic increase in the activity of pancreatic enzymes was combined with Gilbert's syndrome, with an asymptomatic increase in the level of CPK or transaminases in the absence of obvious liver disease. He also observed a patient with benign hyperamylasemia, in whom clinically, as well as according to ultrasound and CT of the abdominal organs, no pathology of the pancreas was detected. Eight years later, at age 56, this patient developed jaundice and was diagnosed with pancreatic cancer. Discussing such cases, Prof. Gullo pointed out that it is not possible to confirm or refute the presence or absence of causal relationships between the detected pathology and pancreatic hyperenzymemia. In this regard, he proposed to make it a rule to follow up patients with presumably benign pancreatic hyperenzymemia for at least 1-2 years before the diagnosis, in the absence of clinical and laboratory and instrumental data confirming another disease, can be finally established.
Ya. Re77DN et al. showed that chronic asymptomatic pancreatic hyperenzymemia only in half of the cases is truly benign, i.e. does not have a detectable morphological substrate. They examined in detail 75 patients aged 19 to 78 years who had an asymptomatic increase in the activity of one or more pancreatic organs for at least six months.
enzymes (exclusion criteria were the presence of renal failure and celiac disease). The examination plan included (one or more studies): MSCT of the abdominal organs with contrast enhancement (44 patients), magnetic resonance cholangiopancreatography (MRCP - 50 patients), endoscopic ultrasound (16 patients). Laboratory examination included a clinical blood test, determination of the level of trans-aminases, gamma-glutamyl transpeptidase (GGTP), total bilirubin, alkaline phosphatase (AP), total protein, albumin, globulins, cholesterol, triglycerides, calcium, CA 19-9, as well as a study for macroamylasemia by selective precipitation. Chronic pancreatitis was diagnosed in 20 (26.7%) patients, 5 (5.7%) patients had intraductal papillary mucinous tumors, 3 - pancreatic ductal adenocarcinoma, 2 - Crohn's disease, 4 - chronic viral hepatitis , 3 - macroamylasemia, 1 case each - autoimmune pancreatitis and benign pancreatic cyst, 2 cases - serous cystadenoma. Only 4 cases revealed familial hyperenzymemia and 31 (41.3%) - chronic non-pathological hyperenzymemia. The authors concluded that the "watch and wait" tactics in chronic asymptomatic pancreatic hyperenzymemia is unacceptable, a thorough diagnostic search is needed to identify the cause, which can be found in most of these patients.
In the study by A. Amodio et al. included 160 patients (age 49.6±13.6 years) who had a long-term (more than six months) increase in the activity of pancreatic enzymes in the absence of clinical manifestations. Exclusion criteria were based on known causes of pancreatic hyperenzymemia: previously diagnosed pancreatic disease, liver cirrhosis, celiac disease, renal failure, endometriosis, symptomatic cholelithiasis, diabetes mellitus, previous endoscopic procedures involving the papilla of Vater, surgical interventions on the stomach, duodenum or biliary tract in history, as well as alcohol consumption> 40 g per day. All patients included in the final analysis underwent MRI of the abdominal organs, MRCP with secretin stimulation. Laboratory examination included determination of the level of total amylase, pancreatic amylase and lipase (first-degree relatives were also examined), basic renal and hepatic parameters, tests for viral hepatitis B and C, serological tests for celiac disease, determination of cholesterol and triglycerides. An isolated increase in amylase activity was detected in 59 patients, lipase - in one, a combined increase in the activity of both enzymes - in 100 patients. Normal data on the results of MRCP before administration of secretin were determined in 117 (73%) patients, while after stimulation with secretin - only in 80 (50%). Pathological changes detected after stimulation with secretin: cysts (4 patients; 2.5%), diffuse dilation of the Wirsung duct (31; 19.4%), segmental dilatation of the Wirsung duct (11; 6.9%), diffuse dilatation of small ducts ( 41; 25.6%), focal dilation of small ducts (17; 10.6%), Santorini-
cele (5; 3.1%), tumors (5; 3.1%). In 14.4% of cases, the identified changes were regarded as clinically significant, as they influenced the management of these patients. Thus, 5 patients were operated on for identified endocrine tumors (3 patients), pancreatic cancer (1) and intraductal papillary mucinous tumor (1), another 18 patients remained under observation due to identified intraductal tumors (17) or an endocrine tumor (1). In 20% of cases, changes in the pancreatic ducts are regarded as early manifestations of chronic pancreatitis. In 26 (19.5%) cases, familial asymptomatic pancreatic hyperenzymemia was detected, however, the frequency of anomalies of the ductal system according to the results of MRCP with secretin stimulation in this subgroup of patients did not differ from that in other patients. In 11 (6.9%) patients, viral hepatitis, renal failure or celiac disease were diagnosed for the first time, which could cause pancreatic hyperenzymemia. Thus, only in half of the patients with asymptomatic pancreatic hyperenzymemia, after a thorough examination, Gullo's syndrome was established, in the remaining cases specific reasons. According to the authors, the results of their study suggest that in cases of asymptomatic pancreatic hyperenzymemia, it is necessary to perform MRCP with secretin stimulation, as well as an examination to rule out extrapancreatic causes of hyperenzymemia. The same conclusions were reached by the authors of other studies evaluating the informativeness of MRCP with secretin stimulation in asymptomatic pancreatic hyperenzymemia. The tactics of observation with the performance of repeated ultrasound of the abdominal organs after 3-6 months does not justify itself: although in most cases there will be no clinically significant complications of possible diseases during this time, diagnostic value Ultrasound after 3-6 months will be minimal.
F. Gallucd et al. compared baseline and final diagnoses in 51 patients with asymptomatic hyperamylasemia (alone or in combination with hyperlipasemia). Initially, chronic pancreatitis was diagnosed in 31 patients, recurrent - in 13, and in 7 patients the diagnosis remained unclear. All patients were examined at least three times with an interval of at least six months. In addition to collecting complaints and anamnesis, all patients underwent laboratory tests (total amylase, salivary and pancreatic isoamylase, pancreatic lipase, daily amylase, lipid profile, creatinine clearance, CA level 19-9) and instrumental examination (ultrasound of the abdominal organs, an average of 3 studies during the observation period; CT of the abdominal organs with contrast enhancement, repeated in 34 cases). In addition, ERCP was performed in 21 cases, MRCP was performed in 25, and endoscopic ultrasound was performed in 11 cases. In all patients, these instrumental studies did not reveal any clinically significant pathology. The final diagnoses were distributed as follows: salivary hyperamylazemia - 13 (25.4%) cases, macroamylasemia - 18 (35.2%), benign pancreatic hyperamylasemia - 20 (39.2%) cases. The criteria for diagnosing benign pancreatic hyperamylasemia corresponded to those previously described by Gullo. The diagnosis of salivary hyperamylasemia was made in the case of an increase in the activity of total serum amylase, mainly due to salivary isoamylase (60%). In this case, the authors recommend referring the patient for a consultation with a dentist, ultrasound and/or scintigraphy of the salivary glands to look for the cause (sialolithiasis, salivary gland tumors, mumps, Sjögren's syndrome). Macroamylasemia was noted with an increase general level amylase with a normal level of lipase and normal or reduced amylasuria (normal 400-600 U / l) in combination with a decrease in the ratio of amylase clearance / creatinine clearance of less than 1%.
Macroamylasemia is a condition in which complexes of normal serum amylase with proteins or carbohydrates circulate in the blood (the presence of polymeric forms of enzymes or abnormal amylase is also possible, but the existence of such forms has not been proven). It should also be said that there are references to macrolipasemia in the literature. Clinical manifestations may be absent, sometimes abdominal pain is possible. In 1964, P. Wilding et al. described the clinical picture in a patient with long-term asymptomatic hyperamylasemia, which was explained by the binding of amylase to serum globulins. Then J. Berk et al. published data obtained from the observation of three patients with the same phenomenon, and proposed the term "macroamylasemia". This pathology is described in detail in the review by N.B. Gubergritsa et al. . This condition arises due to the appearance in blood
a stream of enzyme-active macromolecular complexes of proteins or carbohydrates with amylase (mainly salivary, S-amylase). Most often, macroamylase is a complex of amylase with a high molecular weight protein, usually IgA, less often IgG. Due to their large size, these complexes are poorly filtered by the kidneys and are retained in the bloodstream. The frequency of macroamylasemia, according to different authors, ranges from 0.4% in healthy people to 8.4% in patients with hyperamylasemia. There are three types of macroamylasemia. Type 1 - persistent hyper-amylasemia, high serum macroamylase complex and decreased urinary amylase; type 2 - also hyperamylasemia, a slight decrease in the level of amylase in the urine, the ratio of macroamylase and normal amylase in serum is much less than in type 1 macroamylasemia; type 3 - normal activity of amylase in serum, urine, as well as a low ratio of macroamylase and normal amylase in serum. A simple and affordable method for diagnosing macroamylasemia is to determine the ratio of clearances of amylase (Ka) and creatinine (Kk). For this, the concentration of creatinine and amylase in the daily urine, as well as creatinine and amylase in the blood, is determined (the analysis is taken in the morning on an empty stomach).
The indicator is calculated according to the following formula:
Ka / Kk \u003d A urine / A blood K blood / K urine 100%,
where And urine - the level of amylase in the urine; And blood - the level of amylase in the blood; To urine - the level of creatinine in the urine; To the blood - the level of creatinine in the blood. It is necessary to pay special attention to ensuring that the units of measurement of each indicator in urine and blood are brought into line. A decrease in the ratio of amylase and creatinine clearances of less than 1% with intact kidney function confirms the diagnosis of macroamylasemia with a high probability; other forms of hyperamylasemia are characterized by an increase in this ratio of more than 1% (within the normal range, 1-4% or above normal).
In order to demonstrate the possibilities of verifying the cause of pancreatic hyperenzymemia, we present our observation of a 28-year-old patient in whom isolated hyperamylasemia was accidentally detected during examination before surgery for nasal septum deviation, as a result of which the patient was refused surgery until the reasons for the increase in amylase activity were clarified. Good health, absence of concomitant diseases or habitual intoxications, abnormalities in physical examination, normal results of laboratory tests, except for amylase, as well as the absence of pathology according to ultrasound of the abdominal cavity did not clarify the situation. Upon re-examination, the level of alpha-amylase in the blood is 360 U / l, in the urine - 200 U / l, the concentration of creatinine in the blood is 80 μmol / l, in the urine - 17.7 mmol / l (which is equal to 17,700 μmol / l - translation in the same units of measurement as blood creatinine). The Ka/Kk ratio in our patient was:
Ka / Kk \u003d (200/360) (80/17700) 100% \u003d 0.26%.
Based on the above data, a diagnosis of type 1 macroamylasemia was made, which, in the absence of other abnormalities and diseases, is not a contraindication for elective surgery.
A case of long-term (12 years) follow-up of a patient suffering from macroamylasemia is described by D.I. Abdulganieva et al. . The diagnosis was established on the 5th year of a stable increase in amylase activity, however, even after that, the patient continued to periodically undergo examination and treatment for chronic pancreatitis, which led to the development of anaphylactic shock against the background of the administration of an unnecessary drug (contric feces). Thus, the timely and correct diagnosis of patients with asymptomatic laboratory abnormalities can actually have a significant impact on their further evaluation, treatment, and well-being.
Unfortunately, a decrease in the ratio of amylase and creatinine clearances occurs not only in macroamylasemia, similar changes are also observed in S-type hyperamylasemia. In addition, macroamylasemia types 2 and 3 may not be accompanied by a change in amylase clearance and its content in the urine. Therefore, for reliable diagnosis macroamylasemia requires additional examinations. For the diagnosis of macroamylasemia, chromatography is used - column, accelerated liquid, thin-layer, ultracentrifugation, electrophoresis, isoelectric focusing, precipitation with polyethylene glycol, assessment of the thermal sensitivity of amylase, immunological methods (reaction with monoclonal antibodies, the use of antiserum to immunoglobulins - components of the macroamylase complex). Most-
Diagnostic algorithm for asymptomatic pancreatic hyperenzymemia.
The simplest and fastest methods for diagnosing macroamylemia are electrophoresis and the polyethylene glycol test. Unfortunately, none of the tests listed above are performed in the laboratories available to us. Apparently, both domestic and foreign clinicians face a similar problem, so macroamylasemia is often stated only on the basis of the absence of clinical manifestations in combination with a decrease in the ratio of amylase and creatinine clearances. At the same time, it must be remembered that macroamylasemia can sometimes coexist with diseases of the pancreas. Therefore, the suspicion of macroamylasemia does not negate the need for further examination of the patient to rule out pancreatic pathology and to look for other possible causes of macroamylasemia (celiac disease, Crohn's disease, UC, rheumatoid arthritis, SLE, liver disease, HIV, lymphoma, thyroid cancer, renal cellular cancer; in addition, macroamylasemia is often associated with Gilbert's syndrome).
Finally, we must not forget that asymptomatic hyperamylasemia may be a manifestation of paraneoplastic syndrome or ectopic amylase production (usually S-type) by malignant tumors. Thus, the production of amylase by lung tumors, with multiple myeloma, pheochromocytoma and other tumors is described (see table). In this regard, in diagnostically unclear cases of pancreatic hyperenzymemia, it is necessary to consider the issue of conducting a detailed oncological search.
Based on the literature data, we propose a diagnostic algorithm for asymptomatic increases in the level of pancreatic enzymes (see figure). At the first stage, it is necessary to perform screening laboratory tests to exclude hepatitis, celiac disease, and renal failure as the causes of an increase in the level of pancreatic enzymes. An increase in the content of CA 19-9 increases the alertness of possible pancreatic cancer; to exclude pronounced structural changes in the pancreas, ultrasound of the abdominal organs is performed. At the same time, the level of total amylase, S- and P-isoamylase, lipase and trypsin is determined, as well as the daily excretion of amylase in the urine with the calculation of the ratio of amylase clearance and creatinine clearance. In the case of isolated hyperamylasemia due to the salivary fraction, it is necessary to exclude the pathology of the salivary glands. Due to the fact that an isolated increase in S-amylase activity may not be accompanied by an increase in amylasuria and a decrease in the ratio of amylase and creatinine clearances, after exclusion of the pathology of the salivary glands, an examination is necessary to diagnose possible macroamylasemia, as well as a detailed oncological search, since hyperamylasemia is often within the framework of paraneoplastic syndrome is represented by S-amylase.
A decrease in daily amylasuria, combined with a decrease in the ratio of amylase and creatinine clearances in the absence of complaints and other abnormalities during the examination, makes it possible to diagnose macroamylasemia. Further diagnostic search in this case depends on the possibilities of laboratory examination to confirm macroamylasemia and identify diseases associated with the development of macroamylasemia. In addition, the presence of macroamylasemia does not exclude concomitant pancreatic disease, therefore, regardless of whether macroamylasemia is confirmed or not, continued instrumental examination is indicated.
With increased amylazuria in combination with a normal ratio of amylase and creatinine clearance in patients with pancreatic hyperenzymemia, a detailed examination of the pancreas is necessary. The most sensitive method is secretin-stimulated MRCP; if this method is not possible, endoscopic ultrasound or contrast-enhanced CT can be used. Investigation of pancreatic enzyme levels in first-degree relatives to detect familial pancreatic hyperenzymemia is recommended, as well as daily determination of the patient's pancreatic enzyme levels for five consecutive days. In the absence of structural pathology of the pancreas, according to the results of instrumental studies, in combination with pronounced fluctuations in the activity of pancreatic enzymes from day to day, the most likely diagnosis is benign pancreatic hyperenzymemia (Gullo's syndrome). If no other pathology is detected during the 2-year follow-up period during repeated laboratory and instrumental examinations, the diagnosis of Gullo's syndrome becomes final.
LITERATURE (PP. 1-2 1, 24, 25 SEE IN REFERENCES)
22. Gubergrits N.B., Lukashevich G.M., Zagoreko Yu.A. Macroamylasemia - harmless delusion or dangerous ignorance? Su-chasna gastroenterology. 2006; 32(6): 93-9.
23. Abdulganieva D.I., Odintsova A.Kh., Cheremina N.A., Khafizova A.Kh. etc. Is hyperamylasemia always associated with chronic pancreatitis? Practical medicine. 2011; 55(7): 157-9.
1. Siegenthaler W., ed. Differential Diagnosis in Internal Medicine: From Symptom to Diagnosis. 1st English Ed. Stuttgart; New York: Thieme; 2007.
2. Frulloni L., Patrizi F., Bernardoni L., Cavallini G. Pancreatic hyperenzymemia: clinical significance and diagnostic approach. JOP. 2005; 6(6): 536-51.
3. Warshaw A.L., Lee K.H. Macroamylasemia and other chronic nonspecific hyperamylasemias: chemical oddities or clinical entities? Am. J. Surg. 1978; 135(4): 488-93.
4. Warshaw A.L., Hawboldt M.M. Puzzling persistent hyperamylasemia, probably neither pancreatic nor pathologic. Am. J. Surg. 1988; 155(3): 453-6.
5. Gullo L. Chronic nonpathologicalhyperamylasemia of pancreatic origin. gastroenterology. 1996; 110(6): 1905-8.
6. Gullo L. Benign pancreatic hyperenzymemia. Dig. LiverDis. 2007; 39(7): 698-702.
7. Gullo L., Ventrucci M., Barakat B., Migliori M., Tomassetti P., Pezzilli R. Effect of secretin on serum pancreatic enzymes and on the Wirsung duct in chronic nonpathological pancreatic hyperenzyme-mia. pancreatology. 2003; 3(3): 191-4.
8. Gullo L. Familial pancreatic hyperenzymemia. pancreas. 2000; 20(2): 158-60.
9. Gullo L., Migliori M. Benign pancreatic hyperenzymemia in children. Eur. J. Pediatr. 2007; 166(2): 125-9.
10. Tsianos E.B., Jalali M.T., Gowenlock A.H., Braganza J.M. Ethnic ‘hyperamylasaemia’: clarification by isoamylase analysis. Clin. Chim. acta. 1982; 124(1): 13-21.
11. Gullo L. Day-to-day variations of serum pancreatic enzymes in benign pancreatic hyperenzymemia. Clin. Gastroenterol. Hepatol. 2007; 5(1): 70-4.
12. Galassi E., Birtolo C., Migliori M., Bastagli L. et al. A 5-year experience of benign pancreatic hyperenzymemia. pancreas. 2014 Apr 16. .
13. Pezzilli R., Morselli-Labate A.M., Casadei R., Campana D. et al. Chronic asymptomatic pancreatic hyperenzymemia is a benign condition in only half of the cases: a prospective study. Scand. J. Gastro-enterol. 2009; 44(7): 888-93.
14. Amodio A., Manfredi R., Katsotourchi A.M., Gabbrielli A. et al. Prospective evaluation of subjects with chronic asymptomatic pancreatic hyperenzymemia. Am. J. Gastroenterol. 2012; 107(7): 1089-95.
15. Testoni P.A., Mariani A., Curioni S., Giussani A. et al. Pancreatic ductal abnormalities documented by secretin-enhanced MRCP in asymptomatic subjects with chronic pancreatic hyperenzymemia. Am. J. Gastroenterol. 2009; 104(7): 1780-6.
16. Donati F., Boraschi P., Gigoni R., Salemi S. et al. Secretin-stimulated MR cholangio-pancreatography in the evaluation of asymptomatic patients with non-specific pancreatic hyperenzymemia. Eur. J. Radiol. 2010; 75(2): e38-44.
17. Gallucci F., Buono R., Ferrara L., Madrid E. et al. Chronic asymptomatic hyperamylasemia unrelated to pancreatic diseases. Adv. Med. sci. 2010; 55(2): 143-5.
18. Bode C., Riederer J., Brauner B., Bode J. C. Macrolipasemia: a rare cause of persistently elevated serum lipase. Am. J. Gastroenterol. 1990; 85(4): 412-6.
19. Oita T., Yamashiro A., Mizutani F., Tamura A. et al. Simultaneous presence of macroamylase and macrolipase in a patient with celiac disease. RinshoByori. 2003; 51(10): 974-7.
20. Wilding P., Cooke W.T., Nicholson G.I. Globulin-bound amylase: a cause of persistently elevated levels in serum. Ann. Intern. Med. 1964; 60(6): 1053-9.
21. Berk J.E., Kizu H., Wilding P., Searcy R.L. Macroamylasemia: a newly recognized cause for elevated serum amylase activity. N. Engl. J. Med. 1967; 277(18): 941-6.
22. Gubergrits N.B., Lukashevich G.M., Zagoreko Yu.A. Macroamy-lasemia: is it harmless delusion or dangerous ignorance? Contemporary gastroenterology. 2006; 32(6): 93-9. (in Ukrainian)
23. Abdulganieva D.I., Odintsova A.Kh., Cheremina N.A., Khafizova A.Kh. et al. Whether always the hyperamylasemia is a consequence of chronic pancreatitis? Prakticheskaya Meditsina. 2011; 55(7): 157-9. (in English)
24. Crook M.A. Hyperamylasaemia: don'tforgetundiagnosedcarcino ma. Ann. Clin. Biochem. Published online before print November 5, 2013, doi: 10.1177/0004563213510490
25. Mariani A. Chronic asymptomatic pancreatic hyperenzymemia: is it a benign anomaly or a disease? JOP. 2010; 11(2): 95-8.
Received 05/25/14 Received 05/25/14
Increasing the rate of enzyme synthesis in cells.
An increase in the number of cells that synthesize the enzyme.
Increasing the permeability of cell membranes.
Necrosis (death) of cells.
The use of enzymes in medicine
For screening diagnostics- selective tests.
For diagnosing diseases(aspartic transaminase - for the diagnosis of myocardial infarction, alanine transaminase - for the diagnosis of liver diseases).
For differential diagnosis(acid phosphatase - prostate cancer, alkaline phosphatases - bone tissue, cancer metastases).
For the treatment of diseases:
a) replacement therapy (for diseases of the gastrointestinal tract, pepsin, pancreatin, festal, panzinorm, mezim-forte are used - these are hydrolytic enzymes; enzyme inhibitors can be used for pancreatitis);
b) to treat diseases and eliminate pathological processes, enzymes are used to:
destruction of dead tissue (in the treatment of burns, ulcers, abscesses - trypsin, chymotrypsin, nuclease);
liquefaction of viscous secrets in the treatment of bronchitis (trypsin, chymotrypsin, broncholithin);
for smoothing postoperative scars (protease, lidase, nuclease);
for the destruction of blood clots (streptokinase, fibrinolysin).
The use of enzymes in dentistry: for the treatment of caries, pulpitis, periodontitis, gingivitis, aphthous stomatitis, oral ulcers.
Enzymes can be used both independently (tablets, powders, aerosols, solutions) and on a carrier, i.e. in an immobilized form (gels, ointments, pastes). Immobilized enzymes have a prolonged effect.
INTRODUCTION TO METABOLISM. CENTRAL METABOLIC WAYS.
Metabolism - a set of chemical reactions occurring in the cells of the body from the moment of receipt nutrients into the body before the formation of end products of metabolism.
Metabolic functions:
supply of cells with chemical energy;
turning food molecules into building blocks;
the assembly of these blocks of cell components (proteins, lipids, nucleic acids);
synthesis and destruction of specialized biological molecules (heme, choline).
metabolic pathway - the sequence of chemical transformations of a substance. Metabolic pathways are multi-stage, interconnected, regulated, coordinated in space. They are linear (disintegration and synthesis of glycogen, glycolysis, etc.) and cyclic (tricarboxylic acid cycle, ornithine cycle):
P is an example of a linear metabolic pathway, where S is the initial substrate, P is the final product, A, B, C, D are metabolites (intermediate products).
Enzymes (enzyme), which determine the speed of the entire process as a whole, are calledkey , catalyze irreversible reactions, have a quaternary structure and are easily regulated.
2 sides of metabolism
catabolism - the process of splitting complex molecules into simpler ones, going with the release of energy.
With active forms, a persistent, albeit insignificant, rise in aminotransferase activity occurs in 74-77% of cases [Khazanov A.I., 1988].
Bilirubin aminotransferase dissociation deserves attention, i.e. cases of severe hyperbilirubinemia (mainly due to direct bilirubin) and low activity of aminotransferases. Dissociation is observed in subhepatic jaundice with stable biliary hypertension, acute liver failure.
An increase in the activity of ALT and ACT can also be detected in practically healthy carriers of the hepatitis B surface antigen, which indicates the presence of apparently asymptomatic active processes in the liver.
Serum total lactate dehydrogenase (LDH)
The level of activity of total LDH is normally 240-480 IU / l.
LDH is a glycolytic zinc-containing enzyme that reversibly catalyzes the oxidation of L-lactate to pyruvic acid and is widely distributed in the human body. The highest activity of LDH is found in the kidneys, cardiac muscle, skeletal muscles and liver. LDH is contained not only in serum, but also in a significant amount in erythrocytes, so the serum for the study should be without traces of hemolysis. Most human organs and tissues contain five LDH isoenzymes. The nature of the LDH isoenzyme spectrum and the type of metabolism in the tissue correlate with each other. In tissues with a predominantly aerobic metabolism (heart, brain, kidneys), LDP and LDH2 isoenzymes have the highest LDH activity. In tissues with a pronounced anaerobic metabolism (liver, skeletal muscles), LDH4 and LDH5 isoenzymes predominate. In the blood serum of a healthy person, all five LDH isoenzymes are constantly detected. There is a pattern in relation to the activity of LDH isoenzymes: the activity of LDH2H1DP>LDHZ>LDH4>LDH5 [Komarov F.I. et al., 1981]. Damage to one or another organ changes the isoenzyme spectrum of blood serum, and these changes are due to the specifics of the isoenzyme composition of the damaged organ.
What indicators of ALT and AST in hepatitis C are the norm?
Hepatitis C is a dangerous infectious disease leading to irreversible liver damage and severe life-threatening consequences. The indicators of ALT and AST in hepatitis C reflect the state of the enzymatic function of the liver and the degree of its damage and make it possible to detect adverse changes. This allows you to start timely treatment, which will slow the progression of the disease and help prevent serious complications.
What are ALT and AST?
Infection with viral hepatitis C is possible only through contact with blood, that is, by the parenteral route. Often, infection occurs during medical procedures (injections, blood transfusions), if the rules of sterility are violated and the virus enters the body along with infected blood.
In the diagnosis of hepatitis C, the study of aminotransferases, liver enzymes that are present in the liver and muscle tissue of other organs, plays a key role. Two of them are of clinical importance - alanine (ALT) and aspartic (AST). They are determined during a biochemical blood test. Tracking such indicators in dynamics allows assessing the effectiveness of treatment and, in the absence of positive dynamics, taking measures to correct it.
Indicators in normal and pathological conditions
ALT and AST are found in the liver and muscle tissue of the skeletal muscles and heart. It is there that they perform their function, and only a small part of them enters the blood, where they are determined during biochemical analysis. When these organs are damaged, the content of enzymes in the blood increases. Since ALT is more often elevated in liver disease, it is called "hepatic aminotransferase", and AST, respectively, "cardiac".
In fact, this division is very arbitrary, since both enzymes increase during pathological processes. Sometimes an increase in their concentration in the blood can provoke the use of certain medications (for example, oral contraceptives, anticoagulants, or medicines from the NSAID group).
The doctor receives more detailed information by comparing data on changes in the concentration of other enzymes, as well as the results of other tests. Normally, the content of these enzymes has the following meaning:
An increase in the amount of one or another enzyme in the blood is called hyperenzymemia. It is classified according to severity:
- mild (increased concentration up to 5 times);
- medium (6-10 times);
- severe (enzyme concentration exceeded by more than 10 times).
In hepatitis C, moderate hyperenzymemia is most often observed, which can decrease to mild or increase to severe. If hepatitis is complicated by cirrhosis, then hyperfermentemia gradually increases, moving from moderate to high severity. Often, laboratory blood changes in hepatitis are asymptomatic and imperceptible to the patient. Therefore, you will have to donate blood for analysis regularly in order to track the dynamics of the development of the disease.
What diseases cause hyperfermentemia?
An increase in the content of aminotransferases in the blood occurs with liver diseases (hepatitis, cirrhosis), myocardial infarction and muscle injuries. In the case of injuries, biochemical parameters are not of great diagnostic value, since other symptoms come to the fore.
In the case of myocardial infarction, the increase in the content of enzymes in the blood varies significantly with time and can accurately indicate how many hours have passed since the onset of the disease. In this case, AST is higher than ALT, which is why AST is called "cardiac aminotransferase". The determination of blood biochemical parameters in myocardial infarction is used to establish the possibility of thrombolysis in the first hours from the onset of an attack, as well as to assess the dynamics of the patient's condition and the effectiveness of the treatment. A decrease in aminotransferases to the norm or values close to it is a sign of the effectiveness of the therapy provided.
As a rule, in liver diseases, ALT is higher than AST, which is why the alanine enzyme is called "hepatic aminotransferase." The degree of enhancement can range from mild to high. In hepatitis C, the increase in the concentration of ALT and AST occurs in waves. The first increase occurs about two weeks after infection and often goes unnoticed. This is a slight increase, most often kept within the framework of mild hyperfermentemia, less often - medium. Then, for several years, biochemical parameters return to normal, sometimes the content of enzymes, more often ALT, is slightly higher than normal.
The next big wave of increase in fermentemia occurs 5-8 years after infection. ALT rises to figures corresponding to moderate hyperfermentemia, AST - mild or moderate. Indicators can vary, sometimes dropping almost to the norm, or, on the contrary, increasing. If the disease is complicated by cirrhosis, then hyperfermentemia becomes persistent and high. In the future, in the course of therapy, a biochemical blood test is done regularly. An indicator of the effectiveness of treatment will be the absence of fluctuations and a stable decrease in the level of ALT and AST in the blood. After treatment, biochemical parameters depend on what changes have occurred in the liver at the time of detection of the disease and the start of intensive therapy.
What to do with an increased concentration of enzymes?
An increase in the concentration of enzymes in the blood does not have pronounced symptoms that the patient might notice. Therefore, a person may not suspect for a long time that he has hepatitis C. Violations indicating infection are detected only in the laboratory, and all other symptoms of liver damage are caused by other causes.
However, patients are concerned about what to do if ALT and AST are elevated? In fact, nothing needs to be done to reduce the actual concentration of enzymes - it will decrease by itself if the treatment is effective. In hepatitis C, the change in these indicators is used only as one of the methods for assessing the patient's condition.
This is one of the fastest and most affordable ways to track changes in the patient's condition and adjust the treatment regimen in time. Given the high cost of drugs and examinations for hepatitis C, the method of biochemical blood analysis remains relevant and retains high clinical significance.
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hyperenzymemia
Universal Russian-English Dictionary. Akademik.ru. 2011 .
See what "hyperfermentemia" is in other dictionaries:
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what is hyperfermentemia during pregnancy
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Encyclopedia of ultrasound and MRI
Doppler ultrasound diagnostics during pregnancy: what is it?
Nowadays, ultrasound is an important part of the mandatory examinations of a pregnant woman. Such an examination is carried out at least three times during the entire pregnancy. And in almost every study during ultrasound, the doctor, in addition to the usual gray scale mode, also uses a special technique that registers and evaluates the fetal blood flow, called Doppler.
Doppler during pregnancy - what is the essence of the study?
Dopplerography is such a method of ultrasound, with the help of which the doctor registers and evaluates the parameters of blood flow in the large vessels of the fetus and uterus: in the arteries of the uterus, in the umbilical cord, in the middle artery of the fetal brain, in the venous duct and others according to indications. This technique is based on the Doppler effect, which consists in the reflection of ultrasonic waves emitted by the sensor from moving particles (erythrocytes) and their registration by the device.
The device displays on the screen a graph of the movement of blood or a color display of the blood flow. Based on the data obtained, a conclusion is made about how the fetus feels in this moment and further tactics of pregnancy management are decided.
Indications for Doppler ultrasound during pregnancy
In the third trimester of pregnancy, Doppler is performed for all pregnant women during the 3rd ultrasound screening in addition to the results of cardiotocography (CTG) to fully assess the condition of the fetus in the womb. For some women, such a study is indicated already in the second trimester of pregnancy, since during this period it is still impossible to assess the well-being of the fetus by any other methods other than Doppler.
How is Doppler ultrasound performed during pregnancy?
Doppler of the fetus is carried out in exactly the same way and on the same device as the usual gray scale 2-D ultrasound. Most often, these two types of research
Screening during pregnancy
The waiting period for a baby is a magical time for every woman. And nothing can overshadow him, even all kinds of examinations and tests that every pregnant woman has to do. However, some laboratory tests are somewhat frightening for expectant mothers, for example, screening.
What is this procedure? Why and how is it done to pregnant women? Is she sick or not? At what time and is it necessary to do screening during pregnancy? We will answer all these and many other questions in our today's publication.
Biochemical, genetic, prenatal screening during pregnancy: what is it?
A pregnant woman learns about what screening is already in the first weeks of gestation. The local doctor is obliged to explain in detail the purpose of this study. However, if after visiting the doctor the expectant mother still has some questions, then here she will be able to find the necessary answers.
Biochemical screening during pregnancy has been practiced for more than a decade. The purpose of this examination is to detect the likelihood of deviations in the genetic development of the fetus. The most common diseases associated with such disorders are Down syndrome, neural tube pathologies, Edwards syndrome. Biochemical and genetic screening are a series of blood tests, during which the level of marker compounds is determined - chorionic gonadotropin, alpha-fetoprotein, free estriol and others. The concentration of these substances in the mother's blood, depending on the condition of the fetus and the duration of pregnancy, varies, which in fact makes it possible to identify possible deviations.
Ultrasound screening of pregnant women is the first, but this procedure is repeated in each trimester. The main task of ultrasound is to identify possible numerous anomalies and anatomical defects in the development of
what are hemorrhoids during pregnancy signs
What is hemorrhoids?
The word "hemorrhoids" in Latin means "bleeding". With hemorrhoids, the venous plexuses located in the anus overflow with blood, expand and change. This is how bleeding hemorrhoids are formed, causing a lot of suffering to the patient.
The congestion of the veins in the anus is primarily caused by in a sedentary manner life, due to which there is stagnation of blood in this area. Added to this is improper and irregular nutrition, which leads to obesity and chronic constipation. In addition, hereditary is involved in the development of hemorrhoids. congenital deficiency structures of the veins in the anus. Contribute to the development of this disease and some drugs, oral contraceptives, abuse of laxatives and alcohol, as well as certain sports (car, motorcycle, cycling, rowing, equestrianism and weightlifting). For women, the factor provoking hemorrhoids is constant wear heavy bags.
Hemorrhoids in expectant mothers usually occur in the second half of pregnancy, and may worsen after childbirth. Hemorrhoids during pregnancy may appear due to the fact that the enlarged uterus strongly presses on the pelvic floor, and especially on the hemorrhoidal venous plexus. If constipation characteristic of pregnant women is added to this, then hemorrhoids may develop.
The degree of risk of developing this disease increases in direct proportion to the number of births and the age of the woman during pregnancy. For example, twenty-year-old primiparous women suffer from hemorrhoids three times less often than thirty-year-old women who also give birth for the first time.
Since at first hemorrhoids may not cause much discomfort, women usually do not rush to the doctor with such complaints, thinking that they
Haemorrhoids
OAA during pregnancy: what is it, how to decipher?
Pregnancy is a difficult period for many women, associated with difficult bearing, anxiety and unrest, unstable emotional state. In addition, doctors often scare the expectant mother with her diagnoses. In exchange cards, you can sometimes find such an abbreviation as OAA during pregnancy. What is it and how scary is it? You will find answers to these questions in the article.
OAA during pregnancy: transcript
The abbreviation "OAA" means "burdened obstetric history." Let's break it down piece by piece. Anamnesis is the history of the disease from its onset to the visit to the doctor. But pregnancy is not a disease, but a condition. Therefore, in this area, an obstetric history is everything that is interconnected with other pregnancies and their course. What does the word "burdened" mean? Previously, there could be some risk factors that affect the bearing of the unborn baby and successful delivery.
What is OAA?
We got a little acquainted with the concept of OAA during pregnancy. The decoding is known to us, but the essence is not yet entirely clear. This term includes:
These factors have a huge impact on the course of subsequent pregnancies and their outcome, so they must be taken into account by the doctor in order to reduce possible risks to the maximum.
There is a concept similar to OAA - OGA, which means "burdened gynecological history." It includes everything related to the health of a woman in terms of gynecology: the course of menstrual cycles, failures in them, sexual diseases. The concept of OGA is closely interconnected with OAA, therefore they are often called by the general words "burdened obstetric and gynecological history".
Pregnancy of every woman is accompanied by certain physiological, psychological and emotional changes. Therefore, the question of whether it is possible to have sex during pregnancy is very relevant.
It should be noted that the diagnosis of OAA during pregnancy (what it is, we explained above) is made by very many women. So
Changes in ALT and AST in hepatitis C
Hepatitis C is an infectious disease caused by the hepatitis C virus that affects the liver. Infection occurs parenterally, i.e. through contact with infected blood, which can occur during its transfusion, medical manipulations, the introduction narcotic substances etc.
Studies of the function of liver enzymes - alanine aminotransferase (ALT) and aspartate aminotransferase (AST) - play a key role in the diagnosis of viral hepatitis C, and allow us to evaluate the effectiveness of the treatment and the need for its correction.
Enzyme levels are normal
Alanine aminotransferase and aspartate aminotransferase are enzymes associated with the conversion of a number of amino acids. Their synthesis occurs only inside the cells of the body, most often in the cells of the liver.
That is why when a doctor sees an increase in AST and ALT during a biochemical blood test, he, first of all, thinks about the development of damage to the liver tissue. It is important to note that these enzymes are also found in other organs of the body: the kidneys, muscles and heart. In men, their activity is higher than in women, which is associated with differences in hormonal levels.
The liver cells are dominated by the alanine aminotransferase enzyme, which is one of the most studied molecules in modern medicine. Its changes in the peripheral blood, determined during the analysis, indicate the functional state of the liver tissue and can signal the development of pathological processes in it (inflammatory diseases, necrosis, the development of benign and malignant tumors).
Ciprolet is not allowed to be used during pregnancy, even though it is sufficient safe drug, which rarely gives side effects. The reason for this ban is that pregnant women were not carried out
In childhood, enzyme indicators are very dependent on the functional maturity of the liver and differ in different periods of the child's growth. For newborns, the indicators are quite high, which is associated with the restructuring of the work of the organ and amount to ALT - up to 50
Uterine tone during pregnancy: what is behind one of the most common diagnoses?
Pregnancy is an almost magical state, well, at least it’s definitely miraculous. Naturally, at this time, a woman simply has to be attentive to herself and very careful. During pregnancy, a woman faces a huge number of dangers and unpleasant diagnoses. One of the most common diagnoses is the so-called uterine tone during pregnancy, or uterine hypertonicity. What does "Mother in tone" mean?
What is uterine tone?
The uterus is a hollow muscular organ consisting of three layers: the outer mucosa is the perimetrium, the middle muscular layer is the myometrium and the inner mucosa is the endometrium. Myometrium is smooth muscle capable of contraction, for example, it contracts during childbirth. However, in its natural state, this muscle should be relaxed, and this state is usually called the normal tone of the uterus.
If during pregnancy, but before the onset of labor, the uterus begins to contract, they say that the tone of the uterus during pregnancy is increased. It is worth mentioning here: since the process of muscle contraction is natural, it is not always that the uterus in good shape is a problem.
In Western medicine, this condition is considered a normal physiological process. Of course, in the event that this diagnosis is not associated with other symptoms that cause discomfort, as well as indicative of serious violations. There is some common sense in this reasoning, because even in the process of sneezing or laughing, almost all muscles contract, including the uterus. The same applies to the ordinary orgasm. Affects the condition of the uterus and psychological condition pregnant. Very often, tension in the muscles of the uterus is observed during a gynecological examination.
Causes of hyperfermentemia
Increasing the rate of enzyme synthesis in cells.
An increase in the number of cells that synthesize the enzyme.
Increasing the permeability of cell membranes.
Necrosis (death) of cells.
The use of enzymes in medicine
For screening diagnostics- selective tests.
For diagnosing diseases(aspartic transaminase - for the diagnosis of myocardial infarction, alanine transaminase - for the diagnosis of liver diseases).
For differential diagnosis(acid phosphatase - prostate cancer, alkaline phosphatases - bone tissue, cancer metastases).
For the treatment of diseases:
a) replacement therapy (for diseases of the gastrointestinal tract, pepsin, pancreatin, festal, panzinorm, mezim-forte are used - these are hydrolytic enzymes; enzyme inhibitors can be used for pancreatitis);
b) to treat diseases and eliminate pathological processes, enzymes are used to:
destruction of dead tissue (in the treatment of burns, ulcers, abscesses - trypsin, chymotrypsin, nuclease);
liquefaction of viscous secrets in the treatment of bronchitis (trypsin, chymotrypsin, broncholithin);
for smoothing postoperative scars (protease, lidase, nuclease);
for the destruction of blood clots (streptokinase, fibrinolysin).
The use of enzymes in dentistry: for the treatment of caries, pulpitis, periodontitis, gingivitis, aphthous stomatitis, oral ulcers.
Enzymes can be used both independently (tablets, powders, aerosols, solutions) and on a carrier, i.e. in an immobilized form (gels, ointments, pastes). Immobilized enzymes have a prolonged effect.
INTRODUCTION TO METABOLISM. CENTRAL METABOLIC WAYS.
Metabolism- a set of chemical reactions occurring in the cells of the body from the moment nutrients enter the body to the formation of end products of metabolism.
supply of cells with chemical energy;
turning food molecules into building blocks;
the assembly of these blocks of cell components (proteins, lipids, nucleic acids);
synthesis and destruction of specialized biological molecules (heme, choline).
Metabolic pathway- the sequence of chemical transformations of a substance. Metabolic pathways are multi-stage, interconnected, regulated, coordinated in space. They are linear (decomposition and synthesis of glycogen, glycolysis, etc.) and cyclic (tricarboxylic acid cycle, ornithine cycle):
S A B C D P is an example of a linear metabolic pathway, where S is the initial substrate, P is the final product, A, B, C, D are metabolites (intermediate products).
Enzymes (enzyme), which determine the speed of the entire process as a whole, are called key, catalyze irreversible reactions, have a quaternary structure and are easily regulated.
2 sides of metabolism
catabolism- the process of splitting complex molecules into simpler ones, going with the release of energy.
Anabolism- the process of synthesis of complex substances from simpler ones, going with the expenditure of energy in the form of ATP.
Anabolism and catabolism are closely related:
at the level substrates (sources of carbon);
catabolism ATP anabolism.
Direct conversion of the chemical energy of substrates into the energy of high-energy bonds of ATP is impossible. This process is divided into two stages:
S chemical energy ATP
Consider stage 1 - energy release For example general scheme catabolism.
End products of exchange:
CO 2 - is formed by decarboxylation;
H 2 O - is formed by the oxidation of hydrogen with oxygen in the respiratory chain (tissue respiration).
stage of catabolism occurs in the gastrointestinal tract and is reduced to the reactions of hydrolysis of nutrients. Chemical energy is dissipated as heat.
stage (intracellular catabolism) occurs in the cytoplasm and mitochondria. Chemical energy is partly dissipated in the form of heat, partly accumulated in the form of reduced coenzyme forms, and partly stored in macroergic ATP bonds (substrate phosphorylation).
the final stage of catabolism takes place in mitochondria and is reduced to the formation of end products of CO 2 and H 2 O metabolism. Chemical energy is partially dissipated in the form of heat, 40–45% of it is stored in the form of ATP (oxidative phosphorylation).
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hyperenzymemia
It started when I was treated in a day hospital, there was a tone (chimes + papaverine + hofitol).
Then another course of hofitol (already based on the results of this analysis) and chimes.
Just treated ureaplasma (Vilprofen, Terzhinan, Genferon)
Since the beginning of the 2nd trimester, I have been taking vitamins Vitrum prenatal forte + magne v6 forte 2r / day.
The gynecologist sent me to an infectious disease specialist, in the direction - hyperfermentemia, I will go on Monday.
Such tests happen with hepatitis, but I don’t have jaundice
never had a problem with the liver.
In general, I have no complaints. only heartburn - tolerable.
Could this be from drugs?
Mobile application "Happy Mama" 4.7 Communicating in the application is much more convenient!
Have appointed or nominated analyzes - once again control on enzymes,
as well as viral hepatitis.
They said to stop taking vitamins (but curantyl is possible.)
and temporarily not eat fruit!
An ultrasound of the liver was ordered.
liver, kidneys on ultrasound are normal,
viral hepatitis was not detected.
ALT levels returned to normal.
what it was - the doctors did not clearly explain.
The gastroenterologist advised to peel the apples from the peel before eating))))))))
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Liver hyperfermentemia
Hyperfermentemia (with a predominant increase in ALT activity at once) is recorded during the entire icteric period, then there is a gradual decrease in its level. The protein-synthetic function of the liver in HBV is impaired in the severe course of the disease, which is manifested by a decrease in the sublimate test, albumin content, prothrombin index, activity (3-lipoproteins. The thymol test usually does not increase.
There are no significant abnormalities in the peripheral blood. the number of leukocytes is normal or low.
The recovery period can last up to six months. Clinical and biochemical changes disappear slowly. The content of bilirubin in the blood serum normalizes relatively quickly (within 2-4 weeks), and the increased activity of enzymes persists from 1 to 3 months. In a number of patients, a wave-like nature of hyperenzymemia can be observed during the period of convalescence. It should be taken into account that the recurrence of the disease with enzymatic exacerbation and hyperbilirubinemia requires the exclusion of HDV infection.
Clinical variants of HBV can be very diverse: icteric, anicteric, erased, inapparent (subclinical). It is difficult to judge the frequency of each of them, since usually only the icteric variant is diagnosed and, accordingly, recorded. Meanwhile. according to epidemiological studies, the anicteric variant is found much more often than the icteric one.
One of the features of the icteric variant of HBV is the severity of the cholestatic syndrome in some cases. At the same time, intoxication is insignificant, the main complaint of patients is itching of the skin; jaundice is intense, with a greenish or gray-green tint of the skin, persists for a long time. The liver is significantly enlarged, dense. Acholic feces, dark urine for a long time. In the blood serum - high bilirubinemia. elevated cholesterol and alkaline phosphatase activity. and the level of hyieralatemim is relatively low (5-10 norms). The icteric period can be delayed up to 2-4 months, the full normalization of biochemical changes occurs even later.
HBV can be mild, moderate, or severe.
The most informative for assessing the severity of viral hepatitis is the syndrome of hepatic intoxication, which is manifested by weakness, adynamia, loss of appetite, vegetovascular disorders, and in some cases, impaired consciousness. It is the severity of intoxication (in combination with the results of laboratory tests, primarily prothrombin activity) that characterizes the severity of hepatitis.
Hepatic transaminases in the blood material are ALT and AST. They contribute to the movement of amino groups, which will later be converted into amino acids. Most of their action takes place in the liver. Quantitative indicators of tests may differ depending on the patient's gender, body weight and age.
01 Value of transaminases and reasons for fluctuations
The blood of a healthy person does not show the activity of transaminases, an increase in their number is referred to as alarm bells. As a rule, a deviation from the norm in a big direction is not always provoked by liver diseases. Often, AST is used as a marker that shows problems with the heart muscle in myocardial infarction. In addition, an increase in concentration is provoked by a severe attack of angina pectoris.
There is an increase in transaminases with burns, sepsis, shock, a strong inflammatory process in the pancreas or gallbladder, and skeletal injuries.
The indicator of enzyme activity in this case does not differ in the specifics of the tests. However, fluctuations in AST and ALT are considered reliable indicators with high sensitivity. They determine liver damage, subject to the manifestation of clinical symptoms. When is a jump in the activity of hepatic transaminases observed in liver defects? This happens in the following cases:
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02 How are the symptoms of deviations expressed?
A very low percentage of the population constantly monitors their health by regularly undergoing a series of procedures. AST and ALT look at the blood material, which means that you will have to go to the doctor for a referral. Particular attention should be paid to patients who have a history of symptoms of liver disease.
The incredible value of such tests for the study of enzyme activity lies in the anticipation of an increase in transaminases. That is, in the presence of viral hepatitis A, a jump in ALT and AST is observed in a patient even in the preicteric stage. The patient still has a few weeks before the onset of symptoms of the disease, and the blood has already shown changes.
A patient with a history of hepatitis B is characterized by hyperfermentemia already 3 weeks before the visual manifestation of the disease. Early diagnosis of a serious illness suggests the absence of complications. If you do not take into account the abundance of causes, almost all liver diseases are characterized by similar symptoms:
1. Nausea and vomiting. Urges are noted without relationship with meals. 2. Aversion to certain food groups, refusal to eat, almost no appetite. 3. Sluggish state of health, weakness. The sensations may pass or be permanent. 4. The abdomen increases significantly in size, the saphenous veins are visualized in the form of a grid. 5. Mucous membranes bleed. There are discharges from the nose, mouth and intestines. 6. Skin itching is debilitating, worse at night. 7. Natural discharge changes normal color, feces are discolored, and urine is unnecessarily dark. 8. Pain on the right side, in the epigastric zone. There is tingling in the intercostal space.
It is quite easy to determine that the norm of transaminases is exceeded by these symptoms. It is important not to self-medicate, but immediately seek medical help.
03 Significance in diagnosing various diseases
Peak values of enzyme activity in the presence of acute viral hepatitis are observed during the 3rd week of the disease. A month later, experts note a decrease in ALT and AST to a normal amount.
If a patient has a 1.5-fold increase in transaminases, then we are talking about a moderate degree of hyperenzymemia. When fluctuating from 6 to 10 times, an average degree is assumed. The most severe option, when the degree becomes high, is fluctuations in values more than 10 times higher than the norm.
If the disease has a chronic course, then outside the exacerbation phase, there is no sharp fluctuation of enzymes in the blood material. Sometimes there is a moderate change in the big side. An interesting fact, but the latent phase of cirrhosis proceeds with normal ALT and AST.
Most often, experts look not only at the level of hepatic transaminases, but also at the state of other indicators. Changes in bilirubin, alkaline phosphatase and a number of other biochemical values will narrow the search for pathology.
Acute liver failure and obstructive jaundice suggest the identification of high levels of bilirubin. During this period, the concentration of ALT and AST will be below the mark. This pathology is called bilirubin aminotransferase dissociation.
Jumps in indicators in children are due to the presence of the hepatitis virus or damage to the organ due to drug exposure. Doctors are always afraid of Reye's syndrome, a pathology that can take the life of the patient. It usually occurs when acute hepatic encephalopathy develops after the use of Aspirin.
For a deeper study of the analyzes, the ALT and AST values are compared, deriving the de Retis coefficient. Usually it fluctuates around the mark of 1.33, but when the figure drops, it is worth talking about possible inflammation in the liver or its infection. With necrosis of the heart muscle or possible hepatitis due to alcohol, the coefficient exceeds 2 units. But acute hepatitis of the viral type is diagnosed with a result of 0.55.
04 How important are liver transaminases?
Regardless of the patient's condition, an excess of transaminases indicates destructive processes in the liver. Hyperfermentemia can give a relapse after stabilization of the condition and the normal values of ALT and AST in the blood. Often this is due to the emergence of a new pathological process or exacerbation of an existing defect.
A decrease in transaminases can only be achieved if the real cause of their growth is identified. Normal indicators return subject to high-quality diagnostics and the appointment of adequate therapy. Usually, specialists allow patients to undergo treatment at home or at a day hospital. However, if too high rates are detected, hospitalization and a more detailed examination are suggested.
For a thorough diagnosis, the results of electrocardiography, ultrasound or CT of the abdominal organs, and a detailed biochemical blood test will be required. Sometimes experts suggest the appointment of an ELISA to find antibodies to the hepatitis virus. As an alternative, PCR is carried out, DNA and RNA of the existing virus are already removed here.
It is noted that the cost of these tests is quite high, so they are carried out only when necessary. Usually the reason is reliable data from previous studies. Since the tests are sensitive to various changes in the liver, using a laboratory analysis, you can determine the effect of therapy on the patient's body, adding to it a few more instrumental techniques.
05 Treatments to lower ALT and AST
First of all, doctors prescribe a drug from the group of hepatoprotectors to the patient. This measure contributes to the correction of processes in the affected liver. Medicines from this area include all products containing ursodeoxycholic acid. The most popular names are Ursodez, Ursosan or Ursofalk.
There are more gentle drugs containing phospholipids, Rezalut or Essentiale Forte. Sometimes they are replaced by Karsil, especially often it is prescribed to elderly people. Heptral or Heptor have proven themselves well, the drug contains ademetionine. When using it, patients showed a rapid improvement in their condition. The results of control studies were always positive.
The appointment of funds occurs according to an individual method, the specialist is repelled by the patient's indicators. Some may be allergic to components or not respond to therapy. In such cases, the treatment is adjusted with a subsequent examination. Repeated therapy suggests early control of hepatic transaminases.
And some secrets...
A healthy liver is the key to your longevity. This body performs a huge number of vital functions. If the first symptoms of a disease of the gastrointestinal tract or liver were noticed, namely: yellowing of the sclera of the eyes, nausea, rare or frequent stools, you simply must take action.
Liver dysfunction can go unnoticed for a long time. Symptoms of diseases often appear in the later stages, which makes treatment difficult and obviously reduces its effectiveness. Determination of liver transaminase activity is one of the most accurate laboratory tests performed to assess the condition of the liver.
What are transaminases
Transaminases, or transferases, are enzymes that catalyze the chemical reactions of nitrogen metabolism, the main task of which is the transport of amino groups to form new amino acids. Biochemical processes requiring their participation are carried out mainly in the liver.
The transit movement of transaminases in the blood normally does not affect the result of the tests; in quantitative terms, their concentration for women and men, respectively, is up to 31 and 37 U/l for ALT and 31 and 47 U/l for AST.
Hepatic transferases determined during standard laboratory tests:
alanine aminotransferase, or alanine transaminase (ALT); aspartate aminotransferase, or aspartic transaminase (AST).
The level of enzymes in a healthy liver is influenced by such characteristics as age (increased value in newborns), gender (the norm of transaminases in the blood in women is lower than in men), overweight (there is a slight increase in transaminases).
Causes of fluctuations in AST, ALT
Transaminases in the blood of a healthy person do not show activity; a sharp increase in their level is an alarm signal. It is worth knowing that the growth of indicators is not always provoked by liver disease. AST is used as a marker of cardiac muscle damage in myocardial infarction; increases concentration and with a severe attack of angina pectoris.
Transaminases are elevated in skeletal injuries, burns, acute inflammation of the pancreas or gallbladder, sepsis, and shock conditions.
Therefore, the determination of the enzymatic activity of transaminases cannot be attributed to specific tests. But at the same time, AST and ALT are reliable and sensitive indicators of liver damage in the presence of clinical symptoms or history of the disease.
An increase in the activity of hepatic transaminases applicable to liver pathology is observed in the following cases:
1. Necrosis of hepatocytes (liver cells).
Necrosis is an irreversible process during which a cell ceases to exist as a structural and functional unit of tissue. The integrity of the cell membrane is violated and the cellular components come out, which leads to an increase in the concentration of biologically active intracellular substances in the blood.
Massive necrosis of hepatocytes provokes a rapid and multiple increase in hepatic transaminases. For the same reason, significant cirrhosis of the liver is not accompanied by enzymatic hyperactivity: there are too few functioning hepatocytes for their destruction to cause an increase in AST and ALT.
The transaminase values correspond to the norm, although the process is already in the stage of decompensation. ALT is considered a more sensitive indicator in liver diseases, therefore, with appropriate symptoms, first of all, attention is paid to its level.
Necrotic changes in the liver tissue are observed in acute and chronic hepatitis of various etiologies: viral, toxic (in particular, alcoholic and medicinal), acute hypoxia, which occurs as a result of a sharp drop in blood pressure during shock.
The release of enzymes directly depends on the number of affected cells, therefore, the severity of the process before conducting specific studies is estimated by the quantitative level of AST and ALT transaminases and an increase compared to the norm.
However, to determine further tactics, an additional examination is necessary along with a biochemical blood test in dynamics.
2. Cholestasis (stagnation of bile).
Despite the fact that a violation of the outflow of bile can occur for various reasons, its prolonged stagnation in conditions of preserved secretion by hepatocytes leads to overstretching, metabolic disorders, and, at the end of the pathological chain, to necrosis.
3. Dystrophic changes.
Dystrophy is a violation of tissue metabolism. It somehow accompanies inflammation; as its variety, one can consider the replacement of necrotic areas with connective tissue, which is the pathogenetic basis of liver cirrhosis.
Among the reasons for the increase in transaminases, fatty degeneration of the liver (alcoholic fatty hepatosis) is indicated.
Genetic diseases are also important, for example, Wilson-Konovalov disease (hepatolenticular degeneration), characterized by excessive accumulation of copper.
Liver tumors, both benign and malignant, in the process of growth destroy the surrounding tissues, which causes inflammation. This is reflected in a persistent increase in liver transaminases.
A similar effect is exerted by metastases - tumor cells brought with the blood or lymphatic fluid, forming secondary tumor foci in the liver tissue.
6. Medicinal effect.
To date, science has the data of numerous studies that have proven that drugs cause elevated transaminases. These include:
antibacterial agents (tetracycline, erythromycin, gentamicin, ampicillin); anabolic steroids (decanabol, eubolin); non-steroidal anti-inflammatory drugs (acetylsalicylic acid, indomethacin, paracetamol); monoamine oxidase inhibitors (selegiline, imipramine); testosterone, progesterone, oral contraceptives; sulfa drugs (biseptol, berlotsid); barbiturates (secobarbital, reposal); cytostatics, immunosuppressants (azathioprine, cyclosporine); preparations containing copper, iron.
The increase in transaminases does not depend on the form of the drug; tablets, as well as intravenous infusions, can adversely affect the liver or cause false activity of AST and ALT, which is due to the specifics of their determination in blood serum.
Symptoms
Despite the variety of causes, liver diseases have a number of similar symptoms, accompanied by an increase in liver transaminases:
weakness, lethargy, which appeared suddenly or persisted for a long time; nausea, vomiting, regardless of whether there is a connection with food intake; loss of appetite or its complete absence, aversion to certain types of food; pain in the abdomen, especially when localized in the right hypochondrium, epigastrium; an increase in the abdomen, the appearance of an extensive network of saphenous veins; icteric coloration of the skin, sclera of the eyes, visible mucous membranes of any degree of intensity; painful obsessive skin itching, aggravated at night; discoloration of discharge: darkening of urine, acholic (discolored) feces; bleeding of mucous membranes, nasal, gastrointestinal bleeding.
The value of the study of enzymatic activity explains the proactive clinical symptoms of an increase in AST and ALT transaminases in viral hepatitis A - already in the preicteric period, 10-14 days before the onset of icteric syndrome.
In hepatitis B, predominantly alanine transaminase is increased, hyperenzymemia is observed several weeks before the onset of signs of the disease.
Significance in diagnosis
To determine the characteristics of liver pathology according to the level of hyperenzymemia, a special scale is used. The degree of increase in hepatic transaminases is divided as:
Moderate (up to 1–1.5 norms or 1–1.5 times). Average (from 6 to 10 norms or 6-10 times). High (more than 10-20 norms or more than 10 times).
The peak of transaminase activity in acute viral hepatitis is observed in the second or third week of the disease, after which it decreases to normal ALT and AST values within 30–35 days.
In a chronic course without exacerbation, hyperfermentemia is not characterized by sharp fluctuations, and remains within a moderate or slight increase. In the latent (asymptomatic) phase of liver cirrhosis, transaminases are most often within the normal range.
It is important to pay attention to whether hepatic transaminases are elevated in isolation or in combination with other indicators of the biochemical spectrum: bilirubin, gamma-glutamyl transpeptidase, alkaline phosphatase, since the combination of an increase in indicators indicates a specific pathology or narrows the range of probable causes.
So, elevated transaminases are detected in carriers of hepatitis B, despite the absence of symptoms.
Subhepatic (mechanical) jaundice, acute liver failure may be accompanied by an increase in the level of bilirubin with a simultaneous normal or low concentration of AST and ALT. This phenomenon is called bilirubin aminotransferase dissociation.
An increase in transaminases in children is often due to infection with the hepatitis virus, drug-induced liver injury. A dangerous pathology that occurs in childhood is Reye's syndrome. Acute hepatic encephalopathy, a life-threatening condition, develops as a result of the use of acetylsalicylic acid (aspirin).
For the purpose of in-depth diagnostics, the de Ritis coefficient is used, which is the ratio of the AST and ALT transaminases. Normally, it is 1.33. If the de Ritis coefficient is less than 1, this is regarded as a sign of an infectious-inflammatory lesion of the liver.
For acute viral hepatitis, for example, it is 0.55-0.83. Achieving a level equal to 2 or higher suggests presumptive alcoholic hepatitis or necrosis of the heart muscle.
Significance in therapy
An increased content of transaminases in the blood is in most cases an unfavorable sign, evidence that liver cells are being destroyed.
Hyperenzymemia can be detected again some time after the normalization of indicators. As a rule, this indicates the beginning of a new or recurrence of an existing pathological process and renewed necrosis of hepatocytes.
How to lower transaminases? The level of AST and ALT is only a reflection of the presence of the disease; therefore, it is possible to achieve a return to normal values only with adequate diagnosis and treatment of the detected pathology. High and extremely high levels of enzymes necessitate hospitalization and immediate additional examination.
It includes general clinical blood tests, a detailed biochemical blood test with the determination of electrolytes, glucose, as well as instrumental methods - electrocardiography, ultrasound and / or computed tomography of the abdominal organs.
If necessary, ELISA (enzyme-linked immunosorbent assay) is performed to search for antibodies to hepatitis viruses or PCR (polymerase chain reaction) to determine the DNA or RNA of viruses.
Given the high cost, it is not economically feasible to perform them without proper clinical justification or reliable anamnestic data.
The test for the determination of transaminases is sensitive to changes in the liver, so it can be used to assess the effectiveness of therapy in combination with other laboratory and instrumental methods.
