Gouty arthritis x-ray. Rheumatology gout. Radiological features of gouty arthritis

The disease inevitably progresses, causes pathological changes in internal organs and threatens with disability. Proper examination helps to avoid a false diagnosis, slow down the progression of the disease.

Criteria for diagnosing gout

Joint diseases have similar symptoms, have a latent course and inevitably become chronic. This significantly complicates the differentiation of ailments, prevents timely treatment. In 1961, the global medical community defined general diagnostic criteria for gout:

• increased concentration of uric acid in the blood, urine, joint fluid;
• a history of sudden attacks of acute arthritis lasting up to 1-2 days;
• detection of uric acid crystals, urates in soft tissues, articular cavity;
• visual detection of salt deposits - .

The detection of two or more criteria from the above list is a strong basis for the diagnosis of gout. American scientists have expanded this list to 12 items:

• excess content of uric acid and salts;
• pathological absence of microflora in the synovial fluid;
• the presence of non-erosive subcortical cysts on x-rays;
• the presence in the history of the disease 2 or more attacks of gouty arthritis;
• the acute phase during attacks is observed on the first day;
• prolonged inflammation in the metatarsophalangeal joint on the legs;
• unilateral form of damage to the joints on the foot;
• asymmetric type of joint damage;
• signs of arthritis in one joint of the foot;
• hyperemia (redness) of the skin in the joint area;
• confirmed presence of tophi;
• damage to one metatarsophalangeal joint.

On a note!

The diagnosis of gout is made by the presence of six of these criteria or by the presence of uric acid and urate crystals in tophi (or synovial fluid).

Clinical picture and external examination

When making a diagnosis, the collection of data for anamnesis plays an important role. Studying the medical history, the doctor receives valuable information for identifying the disease. To diagnose gout, it is necessary to distinguish it from similar diseases (, rheumatism,). An external examination establishes the following facts:

• the time of onset and duration of the first symptoms;
• change in the appearance of the joint - swelling, redness, deformation;
• the presence of surgical operations, injuries, pathologies;
• burdened heredity and predisposition;
• the patient's lifestyle, habits.

On a note!

The clinical picture of a chronic, long-term disease often has a pronounced, clearly defined character. An experienced specialist is able to determine gout without analysis, guided by his own experience, skills and knowledge. However, most often a preliminary diagnosis is made, which requires confirmation and justification by an appropriate examination.

Features of differential diagnosis

At the first signs of damage to the joints on the legs, a rheumatologist, surgeon, traumatologist is required. After studying the clinical picture, the doctor decides what tests to take for gout. Differential diagnosis allows you to accurately determine the causes of the disease according to the results of laboratory tests of blood, urine, and instrumental examination.

Laboratory tests

The first stage in the diagnosis of any disease is a laboratory study of blood and urine. The results of the analysis indicate changes in the composition, rheological properties of liquids. These data allow us to suggest the cause, patterns of development of the disease. To identify gout you will need:

• results of a general blood test, urine;
• data of their biochemical research;
• the results of studying the composition of the joint fluid;
• study of the contents of tophi.

Results of a general blood test

A constant excess of uric acid and crystallization of urates is accompanied by metabolic disorders, inflammatory processes in the joints. These factors inevitably lead to a change in the chemical composition of fluids in the body. Indicators of a blood test for gout by general parameters:

• increase in the proportion of neutrophils;
• change in the leukocyte formula;
• decrease in the number of lymphocytes;
• an increase in the erythrocyte sedimentation rate (ESR).

On a note!

At the initial stage of gout in the general blood test, deviations from the norm may not be observed.

Features of a biochemical blood test

With a complete biochemical blood test, the value of various indicators is established. Their specific change, the ratio suggests the presence of gout and determine the degree of neglect.

Established and generally accepted norms of blood parameters:

The results of a general urine test

With hyperuricemia, there is an increase in the level of uric acid, urates in the urine, crystallization of salts in the urinary tract, kidneys, and bladder. General analysis is effective with concomitant. According to the results of a urine test for gout, it is established:

• increased concentration of uric acid;
• alkaline pH > 7 in advanced gout;
• deviation in color due to changes in the composition;
• the presence of urate crystals in the dry residue of urine;
• detection of protein molecules (albumin);
• small amounts of blood, epithelium.

The study of synovial fluid

An important step in the differential diagnosis of gout on the legs is the study of the articular (synovial) fluid. Its composition is close to blood plasma, it differs in the content of hyaluronic acid. The norm is the presence of cholesterol, cells (synovocytes, lymphocytes, monocytes, neutrophils). Synovial fluid is removed from the joint cavity by puncture for bacteriological, bacterioscopic examination. Changes in its indicators indicate gout:

• violation of color, density, viscosity;
• the appearance of turbidity, mucin clots;
• deviation from the norm pH=7.3 to 7.6;
• detection of erythrocytes, leukocytes;
• the appearance of phagocytes, destroyed cells;
• study of synoviocytogram;
• crystals of urates, phosphates.

X-ray examination

In chronic and advanced forms of gout, radiography is prescribed. The method is effective for diagnosing a disease on the legs, establishing the stage of the disease and detecting complications. X-ray reveals irreversible changes in the structure of the bones, cartilage of the affected joints. Typical x-ray signs of gout:

Other diagnostic methods

To establish the diagnosis of gout, modern diagnostic methods are used in medicine. They reveal additional signs of the disease used to confirm the diagnosis:

• Ultrasound, tomography (computer, magnetic resonance) - during the period of exacerbation, they are used to detect narrowing of the interarticular gap, inflammation, compaction of soft periarticular tissues, joint deformity, pathology in the kidneys and ureter;
• Biopsy - a detailed study of the intra-articular fluid to determine the excess uric acid in the synovial fluid in the problem joint.

How to prepare for analysis

There are cases of false indicators of a blood test for gout, biased results of a study of urine, joint fluid. Reliability, information content of laboratory research increases with proper preparation for the delivery of biological material:

• 3 days before the tests, follow a strict diet - exclude foods prohibited for gout;
• refuse to take vitamin C for 10 hours;
• do not drink diuretic drugs per day;
• do not engage in sports activities for 3 days;
• All tests are taken on an empty stomach, early in the morning.

Following these rules eliminates the possibility of distorting the results of analyzes and making an erroneous diagnosis.

Despite the characteristic clinical manifestations of gout, its diagnosis is often difficult. This is due not only to the similarity with the manifestations of arthritis, but also to the prevalence of the atypical form of the disease. Without differentiation, treatment can be prescribed incorrectly, which is fraught with the development of complications.

The disease debuts most often with an attack of gouty arthritis that occurs against the background of complete well-being. Clinically, it manifests itself as a pronounced pain syndrome in the I metatarsophalangeal joint against the background of its swelling and redness. In the future, all the symptoms of the inflammatory process quickly join. The duration of the attack is 5-6 days. In subsequent times, an increasing number of joints of the arms and legs (ankle, shoulder section) are affected.

For the first time, atypical localization is characteristic: the elbow and knee joints, small joints are affected. At the same time, the thumb is involved in the pathological process in 60% of patients. Forms of the disease:

• rheumatoid with specific involvement of the joints of the hands or one or two large ones (ankle);
• pseudophlegmonous type is expressed by monoarthritis of a large or medium joint;
• polyarthritis;
• subacute form;
• the asthenic appearance proceeds with the defeat of small joints without their swelling;
• the periarthritic form is localized in the tendons and synovial bags (most often in the heel).

Due to such a variety of forms, the diagnosis of gout is difficult at its initial manifestation.

A long course is characterized by the formation of tophi, secondary complications of the kidneys and articular syndrome. In most cases, if no more than 5 years have passed from the onset of development, during the remission period, all symptoms subside. In the future, the lower limbs are affected, sometimes even the spine. The hip joints are rarely affected. At the same time, the tendons become inflamed (more often the bursa of the olecranon).

The localization of the involved joints depends entirely on the course of the disease.

The first metatarsophalangeal joint is affected, then other small joints of the feet, then the hands, elbows and knees. In the future, signs of secondary osteoarthritis appear, contributing to increased joint deformity.

After 6 years from the onset of the disease, nodes of various sizes form under the skin. They can be located separately or merge and localized behind the ears, in the area of ​​​​the knees and elbows, on the feet and hands. Less commonly, tophi form on the face.

Radiography as a diagnostic method

X-ray diagnostics of the joints is indicative in the case of a chronic course of the disease. The characteristic signs of gout are the narrowing of the connective gap due to the destruction of cartilaginous tissue, the formation of "punches", erosion of surfaces as a result of the opening of tophi. In addition, the image reflects the thickening of the tissues around the joint.

The method is more often used as a diagnostic criterion not earlier than 5 years from the onset of the disease. In other cases, it is less informative.

Indications for research in gout

Based on the clinical symptoms, the doctor may suggest arthritis or arthrosis. Differential diagnosis is necessary to confirm the diagnosis of gout.

Laboratory determines the high content of urates in the body, including those found in the liquid. Fluoroscopy is especially effective at the stage of formed tophi. In the case of an atypical course of the pathology, attention is paid to the features of the course of the attack (rapid progression of symptoms and reversibility at an early stage). To confirm the diagnosis, it is sufficient to identify two criteria.

You should be aware that a jump in urate is possible as a side effect of taking salicylates in the treatment of arthritis. In the absence of tophi, a synovial fluid puncture or tissue biopsy is performed to microscopically confirm gout.

Indications for research:

• several bouts of arthritis;
• rapid development of the clinical picture;
• swelling and redness of the joint against the background of exacerbation;
• "bone" at the junction of the phalanx and metatarsus of the thumb;
• one-sided nature of complaints;
• hyperuricemia;
• asymmetric nature of the deformity of the joints on the radiograph.

According to statistics, in more than 84% of patients with gout, tophi and sodium salts are found in the joint fluid.

X-ray diagnostics

X-ray signs of gout are detected by exposure to rays on the affected area with a projection on a film or computer monitor. After developing the picture, the doctor can clarify the degree of destruction of the bone tissue.

At the initial stage, tissue edema, inflammation of the bone substance, and bone destruction are detected. Both inside and outside the connection, the process of destruction and erosion can take place. X-ray manifestations are localized along the edge of the joints.

Symptom of a "punch"

Its manifestations are the deformation of the thumb bone in the phalanx, from 5 mm in size. The symptom is found in the chronic stage of the course of the disease. After a considerable time, tophi are formed not only in the bone tissue, but also in the internal organs. Their surface may ulcerate with the release of white matter. "Punch" can be detected with the help of an X-ray machine.

X-ray changes in the joints at different stages of gout

To avoid obtaining false results, it is necessary to follow the recommendations of a specialist directly during the diagnosis. Do not overload the joint with excessive physical exertion the day before.

Depending on the degree of development of the pathology, not only the clinical picture changes, but also radiological signs. Description of the stages of gout by pictures:

• I - against the background of compaction of soft tissues, large cysts are found in the bone tissue;
• II - tophi are located near the joint with small erosions; fabrics are denser;
• II - lime is deposited in the tissue; erosion surface is significantly increased.

Depending on the stage of development, changes on the radiograph are characterized as moderate and significant.

Other methods of diagnosing the disease

An integrated approach in confirming gout is expressed in the appointment of the following laboratory and instrumental studies:

• general and biochemical blood tests;
• punctures of the periarticular fluid;
• biopsies;
• urinalysis.

At the discretion of the doctor, computed tomography and magnetic resonance imaging may be prescribed.

The emphasis on certain diagnostic methods is carried out by a rheumatologist, based on the symptoms of the disease.

Prediction of the consequences of gout

The severity of the pathological process is determined by the individual provocative factors of the patient (metabolic disorders, genetic predisposition, severe concomitant somatic diseases).

The development of secondary complications against the background of a long course of gout, in the absence of initial disorders, can be suspended in the case of timely treatment. Important importance is attached to the observance of the recommended lifestyle and nutritional correction. Otherwise, much depends on the general health of the patient.

Conclusion

The task of x-ray examination is to identify the exact foci of the inflammatory process. It helps to determine at a late stage of gout development how deformed the joint is. At the start of the disease, with the help of radiological signs of gout, differential diagnosis with other inflammatory processes is carried out. The diagnosis is established after a comprehensive examination and on the basis of patient complaints.

Gout is a systemic disease associated with impaired purine metabolism, which is manifested by the deposition of salts in the body. It affects men more often than women, and occurs in 1% of the world's population. In the diagnosis of the disease, laboratory tests and X-ray procedures of the affected areas play a very important role.

Signs of the disease

Gouty arthritis is difficult to diagnose in the early stages of the course of the disease, its symptoms are often similar to the characteristic signs of other diseases. The initial stage is asymptomatic, X-ray studies will be uninformative. When pain occurs in the joints, a series of tests is prescribed. To determine gout, the following examinations are used:

• general urine analysis;
• study of the concentration of uric acid;
• general and biochemical study of blood;
• puncture of the inflamed joint;
• study of the contents of tophi;
• Ultrasound of the joints;
• CT, MRI and scintigraphy with a blurred clinical picture.

X-ray examination of gout

The diagnostic method consists in the absorption of rays by the affected area and further projection on films or a PC monitor. Further, the doctor processes the information and makes recommendations. To clarify the degree of destruction of the skeleton in gouty arthritis, x-rays of the affected joints are prescribed. Such an x-ray phenomenon as a “punch” symptom, which is characteristic of the late stages of the disease, is very well known. This is a bone defect with a size of 5 mm, which is most often localized at the first metatarsophalangeal joint.

Early x-rays of gout can show transient osteoporosis.

X-ray signs of gout

A manifestation of the initial stages of gout can be diffuse compaction of soft tissues (swelling). Sometimes they find an inflammatory process of the bone substance - transient arthritis. During the disease, destruction of the patient's bone often occurs. Erosion and destruction can occur inside and outside the joint. X-ray manifestations first appear along the edge of the bones in the form of a shell or shell. There are several x-ray signs that are presented in the table:

According to statistics, radiological changes in the joints, characteristic of I-II stages of gout, occur within 9 years. Irreversible destruction is formed after 10-15 years. With adequate therapy and a decrease in the infiltration of the patient's joints with urates, “punches” and other signs of bone destruction on the radiograph can significantly decrease or even completely disappear. With timely recognition of gout, it is possible to avoid the transformation of the disease into a chronic one. To exclude complications, patients are advised to consult a rheumatologist and a urologist.

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Radiological manifestations of gout first described by G. Huber in 1896. Later, many studies were carried out that showed that at an early stage of the disease there are no characteristic changes. Then, radiographs show signs of bone and cartilage destruction due to the deposition of sodium urate crystals in the subchondral bone.

X-ray picture of gouty arthritis of the feet

X-ray picture of gouty arthritis of the right leg

• I - large cysts in the subchondral bone and in deeper layers. Sometimes soft tissue hardening;
• II - large cysts near the joint and small erosions on the articular surfaces, constant compaction of the periarticular soft tissues, sometimes with calcifications;
• III - large erosion, but less than 1/3 of the articular surface, osteolysis of the epiphysis, significant compaction of soft tissues with lime deposition.

More recent is the classification proposed by M. Cohen, V. Emmerson (1994), according to which the following are the main radiological signs in gout:

• in soft tissues - seals;
• eccentric darkening due to tophi;
• bones (joints) - the articular surface is clearly presented;
• juxta-articular osteoporosis is absent;
• erosion (punch, marginal sclerosis).

Thus, the presented classifications are significantly different and require the unification of a number of radiological signs in gout.

Instrumental and laboratory research.

In a clinical blood test during acute attacks of gout, patients reveal leukocytosis with a neutrophilic shift to the left and an increase in ESR.

In the blood serum, an increased content of uric acid is determined: in men, more than 7 mg% (0.42 mmol / l), in women - 6 mg% (0.36 mmol / l). Uric acid excretion testing should be done after a 3-day purine-free diet (meats, broths, fish, poultry, legumes, tea, coffee, cocoa, alcohol, beer). The volume of daily urine, pH, concentration of uric acid and creatinine in urine and blood serum are determined. Normally, 300-600 mg (1.8-3.6 mmol / l) of uric acid is excreted per day.

In the contents of tophi, crystals of uric acid are found. It should be borne in mind that during histological examination of tophi tissues, they should not be fixed with formalin in order to avoid dissolution of urate crystals.

Typical are intraosseous racemose formations of various sizes, caused by tophi. Chronic gouty arthritis may be accompanied by cartilage destruction (narrowing of the joint space) and the development of marginal bone erosions. A characteristic sign - "a symptom of a punch" - marginal bone or racemose formations of the correct form with clear, sometimes sclerotic contours, over time, a pronounced destruction is formed not only in the subchondral area of ​​​​the bone, but also in the epiphysis and even in the diaphysis, forming intra-articular osteolysis. Radiologically, the most pronounced pathology is observed in the joints of the feet (primarily in the joints of the thumb). Rarely, radiological changes in the shoulder, hip, sacroiliac joints and spine can occur. Bone changes in gout rarely decrease with specific therapy.

The study of synovial fluid.

The current literature on the composition of synovial fluid in patients with gout indicates the importance of its study for the diagnosis of joint diseases. According to many researchers, the detection of urate crystals in synovial fluid and especially in leukocytes is specific for gout. Of diagnostic importance is the detection of needle-shaped urate crystals located intracellularly and birefringent light when examined using a polarizing microscope. The threshold concentration of urate crystals in the synovial fluid, still available for identification, is about 10 µg/ml.

The sensitivity of this test ranges from 85-97%.

Another important indicator of synovial fluid for an acute attack of gout is its cellular composition, mainly the number of leukocytes, which reaches the following values: from 10. 10 9 to 60 10 9 /l, with a predominance of neutrophils.

Joint diseases
IN AND. Mazurov

Definition. Gout- a disease of heterogeneous origin, characterized by the deposition of urate crystals in various tissues in the form of sodium monourate or uric acid (Bunchuk N.V., 1997).

Historical information

The term gout comes from the Latin "gutta” (drop) and reflects the idea that the disease is the result of fasting malicious infusion (drop by drop). Another name for gout is also known - “the disease of kings”.

In the history of the study of gout, the following milestones can be distinguished ( M. coher, B . Emmerson, 1994):

5th century BC - description of gout by Hippocrates ("Gout is not bald and not a eunuch");

3rd century AD - Galen : describes tophi;

1679 - Van Leeuwenhoek identifies crystals in tophi;

1798 - Wallaston: revealed the presence of uric acid in tophi;

1814 - shows the effectiveness of colchicine in gout;

1913 - Folin, Denis offer a biochemical determination of the concentration of urate in the blood serum

1936 - Prophylactic efficacy of colchicine noted;

1963 Rundles proved the effectiveness of allopurinol for the prevention of gout attacks;

1967 - Kelly revealed etiopathogenetic deficit value hypoxanthylguanine phosphoribosyl transferase (GKGFT) for the development of gout.

Prevalence

Gout mostly affects men over 40 years of age. Women get gout about 20 times less often, but after 50 years this ratio decreases slightly. The rarer development of gout in women is due to the greater excretion of urate in the urine due to the effect of estrogens.

According to an epidemiological study conducted in the 1980s in the USSR, the frequency of gout among residents over the age of 15 was 0.1%, which is higher than in Japan (0.05%), but lower than in most European countries and USA (0.5-3.5%). In certain ethnic groups of residents of Polynesia, the Philippines and New Zealand, the incidence of gout reaches 10%. A study of the dynamics of incidence in the United States showed an increase in the frequency of gout - from 1967 to 1992. 7 times. An upward trend in incidence has also been noted in other developed countries.

Etiology

The determining factor in the development of gout are different in origin disorders of uric acid metabolism(synthesis and / or excretion), leading to a persistent increase in its level in the blood - hyperuricemia . Allocate primary and secondary gout (and hyperuricemia). Secondary gout is recognized when it is one of the syndromes of another disease, in which, for one reason or another (congenital or acquired), disturbances in the metabolism of uric acid occur. For example, secondary gout due to increased formation of uric acid develops in acute and chronic leukemia, multiple myeloma, lymphoma, kidney carcinoma and other malignant tumors, hyperparathyroidism, psoriasis, hemoglobinopathies, von Willebrand disease and some other diseases. Chronic renal failure is the most common cause of secondary gout due to slow excretion of uric acid by the kidneys. The development of secondary gout is also possible with sarcoidosis, hypothyroidism, salicylates, cyclosporine, and some other drugs.

In the case of primary gout, no diseases that could cause it are found. Among patients with primary gout, those who have increased urate synthesis make up only 10%. Specific enzymatic defects are detected in these patients only in isolated cases. In the vast majority of patients with primary gout, the cause of the disease is a violation of the excretion of uric acid by the kidneys. In these patients, both isolated defects in the various phases of uric acid excretion (decreased secretion, increased reabsorption) and combined disorders can be observed.

Persistent long-term hyperuricemia is a mandatory and main condition for the development of gout. In those who develop primary gout, hyperuricemia reaches its maximum severity by the age of 25, while the average age of patients with gout is approximately 47 years. The incidence of gout in individuals with hyperuricemia averages 2.7-12% and depends on the level of hyperuricemia. The development of primary gout requires a combination of hyperuricemia with such acquired factors in adult life as the consumption of large amounts of foods rich in purines, alcohol, overweight, which increase the already existing disorders of uric acid. There is a well-known aphorism: "Partners of hyperuricemia are friends of abundance."

Alcohol is one of the important factors contributing to the development of hyperuricemia. Mechanism hyperuricemic the effects of alcohol are presumably associated with an increase in the content of lactic acid, which makes it difficult for the kidneys to excrete urates ( J. Cameron et al ., 1981). In addition, alcohol contributes to the formation of urates, increasing the rate of ATP breakdown. Beer contains a significant amount guanosine-purine base, which becomes an additional load ( R. Janson, 1999).

It is widely believed that there is a direct relationship between a high level of uric acid in the blood and a person’s intelligence, about a special predisposition to the development of gout in men who have achieved success in life and have leadership qualities ( J. Wyngaarden, W Kelly , 1976). For example, Isaac Newton, Michelangelo, Benjamin Franklin, Charles Darwin suffered from gout.

The source of uric acid is purine bases (adenine and guanine) - components of nucleic acids (both endogenous and, to a much lesser extent, supplied with food), as well as purine nucleosides from which ATP is formed, and similar compounds. The metabolism of purine bases is regulated by several enzymes. Currently, the presence of two enzymatic defects has been proven, which are accompanied by a sharp increase in the synthesis of uric acid and the development of gout already in childhood: deficit hypoxanthine-guanine phosphoribosyl transferase (HCGFT) and increased activity of 5-phosphoribosyl-1-synthetase. These enzymes are controlled by genes associated with the X chromosome, so males are more likely to get sick.

It is well known that gout is often inherited: cases of this disease in relatives occur, according to various sources, in 6-81% of patients, and hyperuricemia is found in 25-27% of relatives of patients with primary gout. A six-generation family with gouty arthritis and progressive nephropathy has been described in Japan ( M. Yokota et al., 1991).

Information about the change in the main complex histocompatibility very little in patients with gout. A weak association of gout with HLA B 14 (B. Cassium et al., 1994).

Pathogenesis

If the content of uric acid in the blood or tissue fluid is more than 0.42 mmol / l (at a temperature of 37 0 C), there is a danger of urate crystallization. It remains unclear why some people with higher uremia do not develop either gouty arthritis or tophi. With a decrease in temperature, the crystallization of uric acid is facilitated, which explains the predominant deposition of urate crystals in avascular tissues (articular cartilage and cartilage of the auricles), in a relatively poor blood-supplied structures (tendons, ligaments) or relatively poorly blood-supplied anatomical areas (in particular, in the feet). The favorite onset of gout is from the metatarsophalangeal joints of the big toes, possibly due to the fact that it is in them that degenerative-dystrophic changes in the cartilage occur earlier and most often, which predisposes to the deposition of urates.

A gout attack is associated with the formation of sodium urate crystals ( M. Cohen et al ., 1994). The crystals are “coated” with a protein shell, as a result of which they have the ability to initiate inflammatory reactions.Ig G , adsorbed on crystals, reacts withFc-receptors of inflammatory cells, activating them, and apolipoprotein B, also included in the protein shell of urates, inhibits phagocytosis and cellular immune response. Thus, urates stimulate the production of chemotaxis factors, cytokines (interleukins 1,6,8 and tumor necrosis factor), prostaglandins, leukotrienes and oxygen radicals by neutrophils, monocytes and synovial cells. Cytokines cause an influx of neutrophils into the joint cavity, in addition, the complement system and the release of lysosomal enzymes by neutrophils are activated.

The very fact of the appearance of urate crystals in the joint cavity, apparently, is not enough for the onset of arthritis, since urate crystals are often found in the synovial fluid during the interictal period of gout (in about 52-58% - in the knee and first metatarsophalangeal joints).

self-passingthe nature of inflammation in the joint with gout is determined by the ability of phagocytes to digest crystals and the release of a number of anti-inflammatory factors, in particular platelet growth factor - beta. The predominant development of arthritis in gout at night is explained by the fact that tissue hydration decreases at rest and an increase in the concentration of uric acid in the joint fluid occurs.

Uric acid lithiasis approximately 40% of patients with gout precede articular manifestations. Hyperuricemia plays an important pathogenetic role in the development of urolithiasis, but plays an even greater role hyperuricosuria . With the release of less than 700 mg of uric acid per day, urolithiasis is observed in 21% of patients, and with the release of 1100 mg / day or more - in 50% of patients ( T.-F. Ju, A . b. Gutman, 1987). Other predisposing factors include impaired solubility of uric acid due to acidic urine. Stone formation is also facilitated by urinary stasis (congenital anomalies of the urinary tract, prostatic hypertrophy, etc.) and its infection.

Kidney damage in gout can be presented urate nephropathy, for which the deposition of monosodium urate crystals in the interstitial tissue is typical. Of primary importance in its origin is chronic hyperuricemia. The deposition of microtophi in the interstitium predisposes to arterial hypertension. Another type of kidney damage is characterized by the formation and deposition of uric acid crystals in the collecting ducts, calyces, pelvis, or ureter. Since both types of kidney damage in gout are often detected in one patient, this division is conditional.

Pathological picture

During acute gouty arthritis, urate crystals are found in the superficial layer of the synovial membrane. Synovitis is nonspecific. Histopathological changes include fibrin deposits, synovial cell proliferation, and marked neutrophilic leukocyte infiltration. Even in the early stages, infiltration by lymphocytes and plasma cells can be seen. Tophi in the synovial membrane are usually observed in patients with repeated attacks of gout. In tophi, there is a large accumulation of urate crystals, surrounded by granulomatous tissue containing giant multinucleated cells. In some cases, over time, tophi can calcify and even ossify. Joint damage in chronic gout is characterized by significant destruction of cartilage, and often subchondral bone, changes in tendons, ligaments and synovial bags.

Clinical picture

It is customary to count the onset of gout from the first attack of arthritis, although before that, on average 10 years earlier, 10-40% of patients develop one or more renal colic caused by urate lithiasis.

There is a classic description of a typical gout attack: “The victim goes to bed and falls asleep in good health. Around two in the morning she wakes up with pain in her big toe, less often in her heel or ankle. This pain is similar to that which occurs when a joint is dislocated, another part of the patients compares the pain with the feeling of cold water pouring on the joint. This is followed by chilliness and a feeling of trembling with low temperature. The pain, which is mild at first, gradually becomes intense. After a while, the attack peaks, bones, ligaments of the metatarsus and tarsus are involved. Now - this is an incredible tension of the ligaments and the feeling that the latter are torn to pieces - this is already a gnawing pain. So a refined and cheerful person, stricken with a disease, sleeps off his feet. He can't put on heavy night clothes, he can't walk around the room, everything gets on his nerves.

The night passes in torment, without sleep, the patient constantly changes position, which leads to constant pain in the joints and worsening of the attack. From this time on, all efforts aimed at relieving pain by changing the position of the trunk or limbs remain in vain ”( J. Wyngaarten et al.,1976).

With gout, acute and chronic arthritis is distinguished.

Acute arthritis. For the first "attack" of gout in men, monoarthritis and predominant damage to the joints of the foot are typical. Acute arthritis of the joints of the big toe during the entire period of the disease is observed in almost all patients, but during the first attack of gout it is observed only in 50%. Less typical for gout is inflammation of the elbow and wrist joints. Oligo- or polyarthritis at the onset of gout in men is not typical, but is typical for women. Another feature of gout in women is the more frequent involvement of the joints of the hands. In both men and women, the first to be affected with gout are those joints that were previously changed for some reason. It is known, for example, the involvement of the distal interphalangeal joints of bones altered due to osteoarthritis.

In classic cases, suddenly, often at night or early in the morning, a sharp pain develops in one joint, usually in the lower limb. The pain quickly, within a few hours, increases to intolerance, there is a pronounced swelling of the affected joint, usually accompanied by reddening of the skin over it. Movement in the inflamed joint becomes almost impossible, as well as support on the affected limb. The pain is significant even without movement, often its intensification is caused even by a light touch of the joint with a blanket. Pain, swelling of the joint and hyperemia of the skin over it can be so pronounced that they resemble phlegmon. During an attack of gout, moderate fever, leukocytosis, and an increase in ESR are often noted.

A characteristic feature of gouty arthritis is the spontaneous (without treatment) complete regression of symptoms in a few hours or more often in a few days.

The course of untreated gout is very variable. The most characteristic is the constant increase in the "attacks" of arthritis, a tendency to their more protracted nature. In rare cases, there is a clinical course of gout with an almost complete absence of light intervals between attacks of arthritis and the rapid development of tophi.

The development of acute gouty arthritis is facilitated by any abrupt changes in the content of uric acid in the blood, both upward and downward, and the latter, perhaps even to a greater extent. Acute gouty arthritis can be triggered by trauma, exercise, emotional stress, sudden changes in diet (both overeating and fasting), drinking alcohol, bleeding, infections, myocardial infarction, surgery (usually after 3-4 days), certain drugs (diuretic, mainly thiazide, vitamin B 12, allopurinol, chemotherapeutic anticancer drugs, intravenous heparin, cyclosporine, administration of protein drugs), as well as radiation therapy.

Allocate atypical forms of gout(V.A. Nasonova, M.G. Astapenko, 1989): rheumatoid-like, pseudophlegmonous, polyarthritic(migratory), subacute form, asthenic, periarthritic a form with localization of the process in the tendons and bursae (most often in the calcaneal tendon) with intact joints.

Chronic gout. It is characterized by the development of certain permanent manifestations of the disease: tophi(significant accumulations of urate crystals) of various localization, chronic arthritis, kidney damage or urolithiasis. From the first "attack" of the disease to the development of chronic gout, an average of 11.6 years passes (from 3 to 42 years). The rate of progression of the disease depends on the severity of hyperuricemia and kidney damage.

The most frequent localization of subcutaneous or intradermal located visible during direct examination tophi- in the area of ​​the fingers and toes, knee joints, protrusions on the ulnar surface of the forearms, as well as synovial bags (especially the elbows), tendons and auricles. Tophi are often concentrated around persistently altered joints. Sometimes the skin over the tophus can ulcerate, while their contents are spontaneously released, which have a pasty consistency and white color. It should be noted that intraosseous tophi, found only on radiographs, can often develop earlier than subcutaneous ones. There are known clinical descriptions of tofus lesions of the spine, compression of the spinal cord, changes in the myocardium, heart valves, conduction system, various structures of the eye and larynx. In very rare cases, tophi are determined before the development of gouty arthritis.

Joint damage . Chronic arthritis and gout can involve a variable number of joints. The small joints of the hands and feet are often affected. Articular syndrome may include destructive signs, deformity and stiffness joints. Infiltration of articular tissues with urates is accompanied by an inflammatory reaction of the tissues surrounding the joint.

An X-ray examination helps to assess changes in the joints in detail. Gout is characterized by intraosseous cystic formations of various sizes, caused by tophi. Chronic gouty arthritis may be accompanied by cartilage destruction (narrowing of the joint gap) and the development of marginal bone erosions. Over time, pronounced destruction is noted not only subchondral part of the bone, but also the entire epiphysis and even part of the diaphysis ( intra-articular osteolysis). At the same time, there is a significant expansion of the “corroded” articular sections of the bones and sharpening of their edges. The so-called “punch” symptom is marginal bone erosion or cystic formations of the correct form with clear, sometimes sclerosed contours - observed in gout infrequently and nonspecific. Bone ankylosis in gout is extremely rare. X-ray changes are most pronounced in the joints of the feet (primarily in the joints of the thumbs) and hands. More rare localization of radiographic changes in gout are the shoulder, hip, sacroiliac joints and spine. Bone changes in gout rarely improve with specific therapy. Tophi located in soft tissues can also be detected by X-ray, especially if they are calcified.

Main x-ray signs of gout summarized in Table 1.

Table 1.

X-ray signs of gout
( M. Cohen and B. Emmerson , 1994)

Kidney damage. Factors favoring the development of nephropathy in gout are uricosuria over 700 mg/day. diuresis and decrease Ph urine (X. Kappen, 1990). Massive "excretion" of uric "acid" can lead to damage to the tubular apparatus of the kidneys and, secondarily, to the interstitium of the kidneys. Later, damage to the glomeruli may occur with the development immunocomplex jade. Gout is characterized by a predominance of disorders of tubular functions (especially a violation of the concentration function) over a decrease in glomerular. The most common sign of renal dysfunction in gout is mild proteinuria, which occurs in 20-40% of patients with gout and may be intermittent. The more pronounced the clinic of articular gout, the more significant the damage to the kidneys. With tofus gout, proteinuria, slight disturbances in the concentration function and a decrease in glomerular filtration are observed. Over time, changes in the kidneys gradually increase. Among the clinical manifestations of gout, it is nephropathy that most often determines the prognosis of the disease. Approximately 10% of patients with gout die of kidney failure. With the development of severe renal failure, there is a tendency to infrequent development of acute arthritis. Hemodialysis also leads to a decrease in articular "attacks".

According to Shukurova S.M. (1997), echolocation of the kidneys revealed changes in 75.4% of cases. Stones were determined with the greatest frequency (in 1/3 nephrolithiasis was bilateral). In 23% of cases, changes in the pelvicalyceal segments and calculi were simultaneously detected, which, in combination with leukocyturia, made it possible to discuss the diagnosis of concomitant pyelonephritis. Kidney cysts were determined in only 13% of patients.

Accompanying illnesses. Common diseases associated with gout include obesity, arterial hypertension, hyperlipidemia, impaired glucose tolerance (metabolic syndrome), and coronary heart disease.

According to epidemiological studies, approximately 78% of gout patients are over 10% overweight, and 57% are over 30% (Brochner-K. Morteus, 1984). Reduced glucose tolerance is found in 7-74% of patients with gout, although diabetes mellitus develops infrequently.

Hypertriglyceridemiaobserved in 50-75% of patients with gout, and hyperuricemia in 82% of patients with hypertriglyceridemia. Especially often this type of hyperlipidemia in gout is observed in patients who abuse alcohol. Although a number of patients with gout also have hypercholesterolemia, several studies have shown no correlation between uricemia and cholesterol levels.

Arterial hypertension is noted in ¼-½ of patients with gout. This may be due to decreased renal blood flow. Obesity may be an important link between arterial hypertension and hyperuricemia. In turn, hyperuricemia is detected in 22-38% of patients with arterial hypertension. It is assumed that an increase in the level of uric acid in the blood may be an indicator of damage to the vessels of the kidneys (or renal tubules) in arterial hypertension.

It is noted that young patients with coronary heart disease often have hyperuricemia. More than half of the causes of death in patients with gout are cardiovascular diseases.

Diagnostics. The most common criteria for the diagnosis of gout, adopted at the international symposium in Rome (1961):

Hyperuricemia- uric acid in the blood more than 0.42 mlmol/l in men and more than 0.36 mlmol/l in women

Presence of gouty nodules (tophi)

Detection of urate crystals in synovial fluid or tissues

A history of acute arthritis accompanied by severe pain that began suddenly and subsided in 1-2 days

/ The diagnosis of gout is considered reliable if any two signs

Later, S. Wallace et al. (1974), also proposed to take into account the peculiarities of the course of gouty arthritis - unilateral lesion I metatarsophalangeal joint, accompanied by redness and pain, the maximum development of symptoms on the first day, asymmetric changes in the joints on the x-ray, the absence of flora when sowing the joint fluid.

In an acute attack of gout, an increase in the level of uric acid in the blood is usually noted, but the normal value of this indicator is no exception. Of greatest value in the diagnosis of gout is polarizing microscopy of synovial fluid and other tissues (for example, tophi), in which it is possible to detect characteristic urate crystals that have a needle-like shape, and most importantly, peculiar distinctive light-optical properties - negative birefringence and a number of others. The main diagnostic value is the detection of intracellular crystals, and their extracellular location may be accompanied by asymptomatic hyperuricemia (5%) or chronic renal failure (approximately 20%). The sensitivity of this study is 69%, the specificity is about 97% ( C. Gordon et al ., 1989). The threshold concentration of urate crystals in the synovial fluid, still available for identification, is about 10 µg/ml. There are cases of acute arthritis in gout, when using polarizing microscopy, urate crystals were not detected due to their small size, but were detected by electron microscopy. Errors are possible in the presence of other crystals in the synovial fluid, in particular lipid ones. It is especially easy to identify urate crystals in superficially located tophi using polarizing microscopy.

It is important to determine the daily excretion of uric acid in the urine. Normally, after a 3-day restriction of purines in the diet, 300-600 mg (1.8-3.6 ml mol) of urates are excreted, and with normal nutrition - 600-900 mg. It is advisable to conduct this study before dieting and 7 days after it (meat, meat soups and sauces, poultry, fish, legumes, oatmeal, tea, coffee, cocoa, alcohol are excluded). Initially and in dynamics simultaneously determine the volume of urine, Ph urine, uric acid and creatinine levels in the blood. It has been established that with an increase in the daily excretion of urate in the urine of more than 1100 mg, the risk of kidney damage is 50%.

The therapeutic effect of colchicine is of particular importance in the diagnosis of acute gouty arthritis. However, it should be borne in mind that a striking effect with gout is not always observed and, conversely, with pyrophosphate arthropathy and calcifying tendonitis colchicine can be very effective.

Treatment

Treatment of gout involves a differentiated strategy depending on the stage of the disease - an acute attack or an interictal period, a tofus form.

Allocate main goals in the treatment of goutPanrotsky J., 1996):

End an acute attack as soon as possible;

- Prevent relapse.

Prevent or reduce the manifestations of chronic gout, primarily the formation of kidney stones and tophi.

In a number of gout patients with relatively low hyperuricemia and infrequently recurrent arthritis, measures such as dietary restrictions, weight loss, refusal to drink beer and strong alcoholic beverages can bring a significant therapeutic effect and should be tried before prescribing drugs, but even very strict a low-purine diet can reduce uricemia by no more than 0.06 mlmol / l, and daily uricosuria - by no more than 200-400 mg, which is clearly not enough in most patients. Dietary recommendations include the exclusion of broths and sauces, the restriction of meat and fish products, legumes, strong coffee and tea, and alcohol. The amount of proteins is reduced to 1 g / kg, fat - less than 1 g / kg, the need for calories is satisfied mainly due to carbohydrates. A slight increase in the amount of fluid you drink (up to 2-3 liters per day), regular visits to the bath or sauna are useful, which contributes to the extrarenal excretion of uric acid. It is also important to control the maintenance of normal body weight and blood pressure, glucose and blood lipids. An important place in the treatment of gout is occupied by the education of the patient, the purpose of which is to understand the role of various factors that positively and negatively affect his disease.

Before choosing a therapy, each patient with gout should be properly examined. The magnitude and persistence of hyperuricemia and daily uricosuria, kidney function and the state of the urinary tract should be analyzed, the stage of the disease and concomitant diseases should be determined.

Treatment of asymptomatic hyperuricemia . To address the issue of treatment tactics, the results of determining the daily excretion of uric acid in the urine are of primary importance. When a persistent hyperuricosuria more than 900 mg per day, which is not eliminated by a low-purine diet, the question of the constant use of allopurinol should be considered. If the daily excretion of uric acid in the urine is not increased, then anti-gouty drugs are not indicated and a low-purine diet, weight loss and other preventive measures are of primary importance in the treatment.

Management of acute gouty arthritis usually administered with colchicine or non-steroidal anti-inflammatory drugs (NSAIDs). It is believed that colchicine is able to eliminate the symptoms of acute gouty arthritis in about 80% of patients within 48 hours after the start of therapy. In the case of using the drug in the first few hours after the onset of an attack, the effectiveness increases to 90%. The physician prescribing colchicine must be aware of the patient's comorbidities. Colchicine (Colchicum - Dispert,Solvay Pharma) is administered orally, at an initial dose of 0.5 mg (in accordance with the recommendations of other authors - 1 mg). Then, every hour, an additional 0.5 mg of the drug is prescribed (or 1 mg of the drug every 2 hours) until the arthritis is completely relieved or until diarrhea (vomiting) appears, but not less than 6-8 mg per day. The dose of the drug should be reduced with a decrease in creatinine clearance below 50-60 ml / min. In most patients, the effect is already noted from 0.5 mg of colchicine and becomes distinct by 12 hours of treatment. For more than one day, colchicine is usually not used to treat a gout attack. Perhaps parallel use in acute gouty arthritis of colchicine in small doses (0.5 mg 2 times a day) and NSAIDs. Sometimes, when oral colchicine cannot be administered, for example, after surgery, the drug is used intravenously.

Among NSAIDs, preference is given to drugs with a rapid onset of action and the most active in anti-inflammatory respect: diclofenac sodium and phenylbutazone, but not acetylsalicylic acid. Diclofenac sodium at the first appointment, it is prescribed orally at a dose of 50-100 mg or intramuscularly at a dose of 75 mg. Phenylbutazone (butadione) - at a dose of 0.3 g. Then, if necessary, every 2-3 hours, NSAIDs are repeated: diclofenac sodium at a dose of 25-50 mg up to 200 and even 400 mg per day, and phenylbutazone - up to 0.6 g in 3-4 doses. Due to frequent adverse reactions (edema, arterial hypertension, gastrointestinal disorders, hematological disorders), phenylbutazone is almost never used. For the relief of acute gouty arthritis, ibuprofen at a dose of 2,000-3,200 mg / day can also be used, taking into account the good tolerability of the drug. For all NSAIDs, the same principle remains as for colchicine - the earliest possible appointment at a sufficiently high initial dosage.

An acute attack of gout can be stopped by injecting into the inflamed joint glucocorticosteroids, having previously evacuated the synovial fluid, as well as prescribing these drugs orally (prednisolone 20-40 mg for 3-4 days) or intramuscularly. This method of treatment should be resorted to if colchicine or NSAIDs are ineffective or poorly tolerated.

Treatment anti-gouty means ( allopurinol, benzbromarone) is carried out only after the relief of gouty arthritis, usually not earlier than after 3 weeks.

Treatment of frequently recurrent gouty arthritis. With absence hyperuricosuria, signs of kidney damage and urolithiasis There are two possible approaches to treatment.

The issue of starting specific therapy is resolved positively with a significant severity of uricemia (more than 0.6 mlmol / l) and the presence of tophi. In this situation, it is possible to use both allopurinol and uricosuric funds.

The dose of allopurinol is selected individually. Most often, it is recommended to start treatment with the appointment of 0.3-0.4 g of the drug per day, once. Sometimes a smaller dose is enough. The effectiveness of treatment is monitored by repeated determination of the level of uric acid in the blood. The desired level of this indicator is less than 0.36 mlmol / l (in men), and the ideal level is within the range of 0.24-0.3 mlmol / l. It must be borne in mind that the dissolution of urates in the extracellular fluid and tissues occurs only if the uricemia is less than 0.42 mlmol / l. Usually, under the influence of allopurinol, the level of uric acid decreases after 24-48 hours and normalizes when an adequate dose is selected after 4-14 days. The selection of a maintenance dose of allopurinol is carried out so as to ensure not only a stable normal level of uricemia, but also to prevent recurrence of arthritis and kidney damage. Resorption of subcutaneous tophi is observed no earlier than after 6-12 months of continuous allopurinol therapy. In this situation, the choice between allopurinol and uricosuric drugs are administered empirically.

probenecidappoint an initial dose of 0.25 g 2 times a day. Uricosuric The effect of the drug develops after 30 minutes. After 3-4 days, with insufficient reduction in uricemia, every 1-2 weeks increase the dose of the drug by 0.5 g. The disadvantage of the drug is often developing resistance to treatment.

Treatment sulfinpyrazone start with a dose of 0.05 g, appointing it 2 times a day. The first dose of the drug is recommended to be taken as early as possible in the morning, and the last - as late as possible in the evening. After 3-4 days, in the absence of a sufficient decrease in the level of uric acid in the blood, the daily dose sulfinpyrazone gradually, every week, increase by 0.1 g. But not more than 0.8 g / day, increasing the number of doses during the day to 3-4. Usually the maintenance dose of the drug is 0.3-0.4 g / day.

Benzbromarone (hipurik, dezurik, normurat) compares favorably with others uricosuric means of prolonged action, can be administered 1 time per day. The usual dose is 0.08-0.1 g per day, the maximum is 0.6 g.

In the treatment of gout, it is possible to use a combination of allopurinol with uricosuric means (usually sulfinpyrazone or with benzobromarone, but not with probenecid), as well as a combination of individual uricosuric funds among themselves. However, a significant “benefit” from combination therapy for gout is usually not achieved.

In primary gout, drugs are usually prescribed for lifelong daily intake, their cancellation or interruptions in treatment lead to a rapid (within 1-3 weeks) increase in the level of uric acid in the blood and the resumption of the clinical manifestations of the disease. In the first days and weeks of treatment, any antigout drugs can provoke the development of gouty arthritis. Therefore, at first, either colchicine (1.5 mg per day) or NSAIDs in average daily doses are additionally prescribed. While taking anti-inflammatory drugs, the amount of fluid you drink should be increased to 3 liters / day, so that the daily amount of urine would be at least 2 liters. It is important that diuresis is sufficient at night.

If uricemia does not reach 0.6 mlmol / l, no hyperuricosuria and tophi , for continuous use, colchicine is prescribed at a dose of 0.5-1.5 mg / day or NSAIDs in medium doses, and a low-purine diet is also recommended. The advantage of this non-specific therapy lies in the good tolerability of the drugs. placebo controlled The study showed that prophylactic administration of colchicine at a dose of 0.5 mg 2 times a day prevented arthritis relapses in 74% of patients and reduced their severity in 20%. Colchicine is generally well tolerated when taken long-term at the indicated dose.

With increased excretion of uric acid in the urine and / or in the presence of kidney damage due to urolithiasis preference is certainly given to allopurinol. Uricosuric funds are contraindicated. When choosing the dose of allopurinol in patients with reduced kidney function, it is conditionally considered that every 30 ml / min of filtered urine corresponds to a daily dose of the drug, which is 0.1 g. Allopurinol can lead to the gradual dissolution of existing urate stones, reduce the severity of gouty kidney damage, and also prevent the formation of both uric acid and oxalate stones. In the first weeks of allopurinol therapy in such patients, especially with a significant severity of kidney damage or urolithiasis, the appointment of agents that increase the solubility of uric acid in the urine is indicated. More often they use a mixture of citrate salts (magurlite, uralit- U etc.), which increases Ph -urine to alkaline values, optimum Ph is 6-7. These drugs are taken before meals, 3-4 times a day, 2-3 hours before the maximum value. Ph urine. The daily dose of citrates is usually from 6 to 18 g. Contraindications are acute and chronic renal failure and urinary tract infection. These drugs also reduce the saturation of urine with calcium oxalate, nucleation and crystal growth of this composition. The dose is selected individually, under control Ph urine. It is possible to use sodium bicarbonate for the same purpose at a dose of about 2 g per day, until alkaline values ​​\u200b\u200bare reached. Ph urine. Rapid and effective alkalinization of urine can also be achieved with the help of the diuretic drug acetazolamide (diacarb, etc.). It is administered orally at a dose of 125-250 mg every 6-8 hours. Due to the rather sharp and rapidly advancing increase Ph urine carbonic anhydrase inhibitors (acetazolamide) are usually prescribed to patients with severe urolithiasis, when it is especially important to achieve alkalization of urine at night, as well as in acute renal failure in patients with "gouty kidney". Acetazolamide is used short-term, usually within 3-5 days. If necessary, the drug is repeated after a break of 2-3 days.

Allopurinolis the drug of choice in patients with secondary gout that develops in hematological diseases or malignant tumors of any localization during the period of active cytotoxic or radiation therapy, when the risk of developing acute gouty nephropathy sharply increases.

Treatment of "acute gouty kidney". Treatment of acute renal failure due to blockade intrarenal urine outflow with urate crystals is classified as critical and requires immediate intensive care. The patient must be urgently hospitalized. Measures are being taken to stimulate forced diuresis - intravenous administration of a large amount of fluid and the simultaneous use of saluretics in large doses (furosemide up to 2 g per day). Allopurinol is prescribed orally at a daily dose of 8 mg / kg and urine alkalizing agents (sodium bicarbonate intravenously, acetazolamide orally). The ongoing therapy is considered effective if diuresis of at least 100 ml per hour is achieved within 1-2 days. In the absence of the desired effect, hemodialysis is used.

The prognosis of gout in most cases is favorable, especially with timely recognition and rational therapy. Most predictively unfavorable factors are considered: early development of the disease (up to 30 years), persistent hyperuricemia exceeding 0.6 mlmol / l, persistent hyperuricosuria exceeding 1.100 mg / day, the presence of urolithiasis in combination with urinary tract infection, progressive nephropathy, especially in combination with diabetes mellitus and arterial hypertension.

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