Means with antihelicobacter activity. Helicobacter infection. What is used as part of a multicomponent treatment regimen

In Russia in the late 90s, about 3 million were under dispensary observation. patients with peptic ulcer, every tenth of whom was operated on.
Approximately 20 million people in the United States suffer from peptic ulcers, of whom 10,000 undergo surgery each year and 6,000 die from complications of the disease. Peptic ulcer is associated with a violation of the nervous, and then humoral mechanisms that regulate the secretory, motor functions of the stomach and duodenum, blood circulation in them. In the formation of ulcers in the stomach, the decrease in the resistance of the mucous membrane, the weakening of its resistance to the damaging effects of acidic gastric juice, is of the greatest importance. In the mechanism of development of ulcers in the outlet section of the stomach and especially in the duodenum, on the contrary, the decisive factor is the increased aggressiveness of the acid-peptic factor. The formation of ulcers is preceded by ultrastructural changes and disturbances in the tissue metabolism of the gastric mucosa. Once having arisen, the ulcer becomes a pathological focus that supports the development and deepening of the disease in general and dystrophic changes in the mucous membrane of the gastroduodenal zone in particular, contributes to the chronic course of the disease, involvement of other organs and body systems in the pathological process.
However, the etiology and pathogenesis of PU are far from being fully elucidated. Currently, a number of studies consider peptic ulcer as an infectious disease, in most cases associated with Helicobacter pylori. It is believed that Helicobacter pylori occupies a central place among the etiological and pathogenetic factors of diseases of the gastroduodenal zone.
Epidemiological data obtained in different countries indicate that more than 80% of gastric ulcers and 100% of duodenal ulcers are associated with the persistence of H. pylori.
It has been proven that after antiulcer therapy to eradicate H. pylori, relapses within 5 years are observed in 5-10% of patients as a result of reinfection.
In this regard, the choice of adequate treatment regimens for peptic ulcer disease, aimed at different aspects of the pathogenesis of ulcerative disease (reduction of gastric secretion, suppression of hydrochloric acid production, Helicobacter infection, stimulation of mucosal regeneration), is a very urgent task.
Antihelicobacter therapy is considered the standard of care for H. pylori-associated PU, which is reflected in the international (1 and 2 Maastricht agreements) and Russian guidelines for the treatment of gastroenterological patients.
According to these recommendations, therapy consisting of a basic drug (bismuth drug, proton pump inhibitor) and two antibacterial agents is considered the most effective.
The choice of antibiotics in antihelobacter therapy is of primary importance. It is these drugs that determine the effectiveness, tolerability and cost of treatment. WHO experts in the main list of drugs active against H. pylori include metronidazole, tinidazole, colloidal bismuth subcitrate, azithromycin, clarithromycin, amoxicillin and tetracycline.
There are several factors that significantly affect the outcome of antiulcer therapy. The main one is the dramatic increase in the proportion of H. pylori strains in the population that are resistant to antibiotics used in treatment regimens. The results of various clinical studies show that the effectiveness of therapy containing metronidazole is 30% lower if the H. pylori strain is resistant to this drug.
Another important issue is the cost of treatment. The higher it is, the greater the percentage of H. pylori eradication should be provided by the therapy regimen in order to be cost-effective. Standard treatment regimens were cost-effective at their relatively high cost if the H. pylori eradication rate was 80-90%. At present, when the prevalence of H. pylori strains resistant to metronidazole is quite high, and the effectiveness of standard treatment regimens is far from ideal, they are no longer economically viable.
In this regard, macrolides, mainly clarithromycin, have become widely used in anti-Helicobacter therapy regimens. However, despite the high efficiency, the drug is expensive and caused a number of adverse reactions (diarrhea), which worsened the tolerability of therapy, which served as the basis for the search for macrolides that would not be inferior to clarithromycin in terms of efficiency, but would be cheaper and give fewer side effects. One such drug is azithromycin.
Azithromycin-AKOS 0.25 No. 6 capsules (azithromycin produced by OAO Sintez, Kurgan) is the first representative of a new group of macrolide antibiotics - azalides. It has a wide spectrum of antimicrobial activity. By binding to the 50 S-subunit of the ribosome, azithromycin inhibits the biosynthesis of microorganism proteins. Azithromycin-AKOS is active against a number of gram-positive (S. pneumoniae, S. agalactiae, group C, F and G streptococci, Staphylococcus aureus and S. Epidermidis) and gram-negative microorganisms (Haemophilus influenzae, H. Parainfluenzae and H. ducreyi, Moraxella catarrhalis, Bordetella pertussis and B. parapertussis, Neisseria gonorrhoeae and N. meningitides, Brucella melitensis, Helicobacter pylori, Gardnerella vaginalis), as well as sensitive anaerobic microbes (Clostridium spp., Peptostreptococcus spp., and Peptococcus spp). In addition, the drug has activity against intracellular and other microorganisms, including Legionella pneumophila, Chlamydia trachomatis and C. pneumoniae, Mycoplasma pneumoniae, Ureaplasma urealyticum, Listeria monocitogenes, Treponema pallidum, Borrelia burgdorferi. The drug does not act on gram-positive bacteria resistant to erythromycin.
When administered orally, Azithromycin-AKOS is well absorbed, rapidly distributed in tissues, high concentrations of the antibiotic are achieved, it also has a long half-life and is slowly excreted from tissues. These properties allow you to use the drug once a day for 3 days with a good effect. Penetration of the drug into cells and accumulation in phagocytes, with the help of which azithromycin is transported to the site of infection, contribute, in turn, to an increase in its effectiveness. Azithromycin-AKOS is excreted mainly with bile in unchanged form (a small part - by the kidneys).
Azithromycin-AKOS is highly active against H. pylori: its MIC 90 is only 0.5 mg/l, and the percentage of H. pylori strains resistant to the drug in the population is very low - 3.7%.
The most important advantage of Azithromycin-AKOS over other macrolides is its distribution in blood plasma, gastric mucus, gastric juice and gastric tissue after a single dose. Data from a number of studies have convincingly proven that the drug is effective even at a dose of 250 mg / day, and the use of low doses of the drug reduces the risk of side effects and the cost of treatment.
It was noted that the frequency of adverse reactions when using short treatment regimens with Azithromycin-AKOS is approximately the same as when using standard anti-Helicobacter therapy regimens or even lower. Therefore, its most important advantage is to reduce the cost of treating the patient.
When comparing the cost of treatment regimens of equivalent duration using clarithromycin and Azithromycin-AKOS, the cost of Azithromycin-AKOS is about half as much, and in regimens with low doses and shortened periods of use, it is three times lower.
Thus, Azithromycin-AKOS is an effective modern antibiotic in the complex treatment of H. pylori.
Amosin® 0.25 No. 10-tab., 0.25 No. 20-caps., 0.5 No. 10-tab. (amoxicillin manufactured by Sintez JSC, Kurgan) is the only b-lactam used to treat H. pylori infection. Amoxicillin is an ampicillin derivative with significantly improved oral pharmacokinetics.
The bioavailability of Amosin® (amoxicillin) when taken orally reaches 90%. The highest activity of the drug was noted against S. pneumoniae and H. pylori.
Since 1996, the Russian Gastroenterological Association has been conducting dynamic monitoring of the level of H. pylori resistance to amoxicillin, metronidazole, and clarithromycin.
Thus, in Russia for the period from 1996 to 2001 the number of strains resistant to clarithromycin increased from 0 to 13.8%. The level of resistance to metronidazole in Russia by 2001 was 55.5%, which is almost 2 times higher than the European average (25.5%).
Amoxicillin-resistant strains of H. pylori have not been isolated since 1997.
In recent years, clinicians have faced the problem of choosing drugs, as their arsenal is constantly replenished with new pharmaceuticals. Relevant is the choice of adequate treatment regimens for H. pylori-associated peptic ulcer, taking into account the cost / effectiveness ratio of the recommended course of therapy. When using the basic drug, as well as Azithromycin-AKOS and Amosin® as two antibacterial drugs, the achieved treatment results (the degree of H. pylori eradication and the frequency of epithelialization of ulcerative defects) are quite high, while the cost of the course of therapy is reduced due to the lower cost of data drugs. Based on the analysis of a number of clinical studies, it follows that Azithromycin-AKOS and Amosin® are widely used in the treatment of peptic ulcer associated with H. pylori, and are effective modern antibiotics that optimize the treatment of patients with peptic ulcer.

Peptic ulcer is a chronic relapsing disease of the gastroduodenal region, the main manifestation of which is the formation of ulcers of the mucous membrane of the stomach or duodenum, in most cases developing against the background of chronic gastritis caused by an infection. Helicobacter pylori (H. pylori).

H. pylori is the main etiological factor in the development of peptic ulcer and the leading pathogenetic mechanism of this disease, causing damage to the mucosal epithelium, reducing its resistance to other factors of aggression, initiating an active inflammatory process in the mucosa and enhancing acid and pepsin formation in the gastric glands.

In our country, the infection rate of the adult population H. pylori is 80%. For people infected H. pylori, the risk of developing peptic ulcer is 10-20%, and oncological diseases of the stomach (adenocarcinoma and MALT-lymphoma) - 1-2%.

Anti-Helicobacter therapy is the main standard for the treatment of Helicobacter-associated diseases of the gastroduodenal zone, which is reflected in international agreements (Maastricht agreements 1-3, respectively, 1996, 2000 and 2005). After successful eradication therapy, recurrence of the disease occurs only in 10-15% of patients. At the same time, with the use of only antisecretory drugs, which also contribute to the relatively rapid healing of ulcers, during the first year after the end of therapy, relapses of the disease are observed in approximately 70-80% of patients.

Almost all modern schemes of anti-Helicobacter therapy are based on the use of antibacterial drugs and proton pump inhibitors (PPIs). The goal of treatment is the complete destruction of vegetative and coccal forms. H. pylori in the mucous membrane of the gastroduodenal zone (Table 1).

According to the Maastricht Consensus III, it is recommended when planning the treatment of an infection H. pylori from the very beginning to foresee the possibility of its inefficiency. This means that anti-Helicobacter therapy of the first and second line should be considered as a single block of the possible sequential prescription of eradication therapy schemes presented in Table. 2. When using reserve eradication schemes, the choice of drug is determined by the results of a bacteriological study to determine the sensitivity of H. pylori, including to first-line drugs that were previously used.

As an initial treatment for infection H. pylori several possible options are proposed (Table 2). Considering that in Russia in large cities resistance H. pylori to clarithromycin ranges from 19% to 40%, the preferred first-line anti-Helicobacter therapy regimen is the appointment of a standard dose of PPI (2 times a day) in combination with clarithromycin (500 mg × 2 times a day), amoxicillin (1000 mg × 2 times a day ) or metronidazole (500 mg x 2 times a day) while taking bismuth tripotassium dicitrate (120 mg x 2 times a day) for 14 days. The addition of bismuth allows clarithromycin to be retained as a first-line component of eradication therapy. When using this scheme of prescribing drugs, eradication is achieved in 93.7% of cases, and, even in the presence of strains resistant to clarithromycin H. pylori, treatment is successful in 84.6% of patients.

Currently one of the most promising treatment regimens H. pylori It is considered sequential therapy, which got its name because it consists of two consecutive stages. The course of sequential therapy takes 10 days. For the first 5 days (Stage 1) PPI at the standard dose 2 times a day in combination with amoxicillin 1000 mg × 2 times a day, then for another 5 days (Stage 2) PPI treatment at the same dosage in combination with clarithromycin 500 mg × 2 is continued. times and tinidazole 500 mg x 2 times. The use of a sequential therapy scheme makes it possible to overcome the antibiotic resistance of Helicobacter pylorus and increase the percentage of successful eradication to 82.2-97.5%.

In patients with severe atrophic gastritis and hypo- or achlorhydria, a 14-day regimen consisting of bismuth tripotassium dicitrate 120 mg x 4 times a day, amoxicillin 1000 mg x 2 times a day and clarithromycin 500 mg x 2 is recommended as first-line therapy. times a day. The eradication rate with this treatment regimen is 84%.

Thus, the following antibacterial drugs play a key role in various schemes of anti-Helicobacter therapy:

• amoxicillin;
• clarithromycin;
• bismuth tripotassium dicitrate.

Selection of drugs for combined eradication treatment H. pylori not accidental. The fact is that this microorganism, for a number of reasons, is a “difficult target” for antibacterial effects. Firstly, it inhabits a special habitat - it is located on the surface of the epithelial cells of the stomach under a layer of mucus in conditions of active acidic secretion. While many antibiotics do not have the ability to create high concentrations of the active substance in the gastric mucosa, mucus, gastric juice. In an acidic environment, the activity of antibiotics may decrease (for example, the values ​​​​of the minimum inhibitory concentration increase). Secondly, genetic and acquired resistance may be a problem. H. pylori to a wide range of antibacterial drugs.

Basic requirements for choosing an antimicrobial drug in eradication therapy regimens:

• selectively affect growth and survival H. pylori;
• maintain antimicrobial activity regardless of the pH of the environment of the stomach and duodenum (acidic, neutral, slightly alkaline);
• to penetrate through the mucous barrier from the lumen of the stomach and/or from the lamina propria of the mucous membrane without reducing the antimicrobial properties;
• do not cause side effects;
• do not suppress the normoflora.

One of the first antibiotics that was successfully used in anti-Helicobacter therapy regimens was amoxicillin. This drug has not lost its value at the present time. Amoxicillin is a broad-spectrum antibiotic of the group of semi-synthetic penicillins, characterized by a low level of resistance (single reports of the isolation of resistant strains have been published, and their prevalence in the population does not exceed 1%), good absorption, high bioavailability (93%) and acid resistance. The time to reach the maximum concentration after oral administration is 1-2 hours. Partially metabolizes with the formation of inactive metabolites. The half-life is 1-1.5 hours. It is excreted by 50-70% by the kidneys unchanged by tubular excretion (80%) and glomerular filtration (20%), by the liver - 10-20%. high activity against H. pylori associated with a violation of the synthesis of the cell membrane of the microbe. The bactericidal action of amoxicillin is based on the similarity of its structure with alanine-alanine or alanine-glutamine, which leads to the binding of the drug to transpeptidases and carboxypeptidases (penicillin-binding proteins), and damage to peptidoglycan (the reference protein of the cell membrane H. pylori) during the division and growth of the microbe, which leads to bacterial lysis (Fig. 1). Although amoxicillin is acid-resistant, an important condition for ensuring the anti-Helicobacter action of amoxicillin is the suppression of the secretion of hydrochloric acid in the stomach to a pH level of 4.5-5.0. This is possible only if sufficient doses of PPIs are administered simultaneously (Fig. 1).

The basic anti-Helicobacter drugs include clarithromycin. Clarithromycin is a modern representative of macrolides with lipophilic properties, which ensures the ease of penetration of the drug through histohematological barriers and the possibility of its accumulation in the mucous membrane of the stomach and duodenum. The concentration of clarithromycin in tissues is 10-100 times higher than that in plasma. When taken orally, clarithromycin is resistant to hydrochloric acid (100 times more resistant than erythromycin). It is rapidly absorbed in the gastrointestinal tract (the rate of reaching peak plasma concentration is 1.8-2.8 hours). The bioavailability of the drug is 52-55%, and the half-life when taking 500 mg 2 times a day is 7-8 hours. Clarithromycin is actively metabolized in the liver by cytochrome P450 with the formation of various metabolites (at least 8), one of which 14-hydroxyclarithromycin (14-GOCM) retains clinically significant antimicrobial activity. At the same time, in relation to sensitive pathogens, clarithromycin and its metabolite 14-GOCM have an additive or synergistic effect. In this regard, the effect of the antibiotic in vivo may be higher than in vitro. Eating immediately before the administration of the drug slightly slows down the onset of absorption of clarithromycin, but does not affect its bioavailability and the formation of the active metabolite 14-GOCM.

The action of clarithromycin is associated with the blockade of protein synthesis due to the reversible connection with the 50S subunit of the ribosome and is bacteriostatic. However, when a concentration in the focus of infection is 2-4 times higher than the minimum inhibitory concentration, it can also have a bactericidal effect. It acts on extra- and intracellularly located pathogens. Maintenance of pH ≥ 3 in the stomach with the help of antisecretory drugs sharply inhibits the degradation of clarithromycin, providing a high concentration of the drug in the stomach. Clarithromycin has a pronounced anti-inflammatory activity due to its ability to inhibit the production of pro-inflammatory and stimulate the synthesis of anti-inflammatory cytokines. New data on the anti-Helicobacter activity of clarithromycin were obtained after the discovery of the phenomenon of bacterial biofilms. 99% of microorganisms, which include H. pylori, exist not in the form of separately living microorganisms, but as part of complexly organized communities - biofilms. A biofilm is an organized dynamic community of microorganisms enclosed in a polymer matrix, synthesized by them and closely associated with the underlying surface. Due to cooperation and information exchange between bacteria united in a biofilm, their survival significantly increases. The polymer matrix protects bacterial cells from the effects of adverse environmental factors, reactions of the immune system of the macroorganism and the action of antibiotics. Clarithromycin has the ability to destroy the polysaccharide matrix of bacterial biofilms, thereby significantly increasing its permeability to other specific antibacterial agents (Fig. 2).

Clarithromycin shows synergy with PPIs in 91% of strains studied H. pylori. It provides the highest degree of eradication compared to any other antibiotic alone. And the combination of clarithromycin and bismuth preparations in anti-Helicobacter therapy makes it possible to effectively act even on strains H. pylori resistant to this antibiotic.

Bismuth preparations, due to the peculiarities of pharmacodynamics and pharmacokinetics, occupy a special place in the regimens of anti-Helicobacter pylori therapy. The features of bismuth preparations include: 1) a multicomponent mechanism of action in relation to H. pylori(the anti-helicobacter effect is associated with the suppression of the mobility and adhesion of bacteria to epitheliocytes, as well as with the precipitation of bismuth on the bacterial cell membrane, followed by a violation of its permeability and the death of the microorganism); 2) practically no resistance H. pylori; 3) the presence of "non-antibiotic effects" that have a potentiating effect in diseases of the stomach - enveloping, anti-inflammatory, cytoprotective; 4) the ability to potentiate the action of other antimicrobial drugs.

So, the main means of basic therapy H. pylori-associated diseases of the gastroduodenal zone are antisecretory and antibacterial drugs. But both PPIs and, especially, antibiotics during eradication therapy can lead to a violation of the dynamic balance of the symbiotic flora of the gastrointestinal tract.

Antisecretory drugs reduce the barrier function of acidic gastric contents for pathogenic flora. Against the background of long-term use of PPIs, there is an overgrowth of microorganisms in the small intestine (bacterial overgrowth syndrome).

Antibacterial drugs suppress the obligate microflora of the colon and induce the growth, reproduction, and then the dominance of opportunistic and pathogenic bacteria that turned out to be resistant to the action of the antibiotics used (dysbacteriosis). With the loss of the indigenous microflora of the colon with its protective properties and participation in metabolic, immunological and digestive processes, the body's resistance decreases, metabolic and trophic functions are disturbed.

A complex of pathological changes in the composition of the intestinal microflora with corresponding clinical manifestations associated with dysbacteriosis developed as a result of the use of antibiotics is referred to as antibiotic-associated diarrhea. It should be noted that anti-Helicobacter therapy is accompanied by the development of intestinal dysbiosis in most patients, which significantly worsens tolerance and adherence to therapy, and antibiotic-associated diarrhea (AAD) develops in 5-30% of patients.

AAD refers to three or more episodes of loose stools on two or more consecutive days following the use of antibacterial agents. In most cases, symptoms of AAD develop 4-10 days after the start of therapy, but a third of patients may appear 4 weeks after antibiotics are discontinued. The reason for this lies, apparently, in the fact that after the suppression of the eubiotic microflora of the colon by an antibiotic, a certain time is required for the growth and reproduction of the opportunistic flora responsible for the development of diarrhea.

A clear dependence of the incidence of AAD on the dose of the antibiotic taken and the duration of its administration (less than 3 days, more than 7 days) was noted. In 80-90% of cases, the development of AAD is not associated with a specific (specific) pathogen. Among the microbes of pathogens appear: Staphylococcus aureus, Clostridium perfringens, Clostridium difficile, enteropathogenic strains Escherichia coli, Salmonella, Klebsiella oxitoxa, and also, possibly, mushrooms of the genus Candida. In some patients (in about 1% of cases), antibiotics cause the development of the most severe clinical form of AAD - pseudomembranous colitis.

For this reason, a promising direction in the treatment of Helicobacter pylori infection is the use of ecoantibiotics.

Ecoantibiotic contains a standard dosage of an antibiotic and a prebiotic - lactulose in a special innovative form of anhydro. Preparations of this class are bioequivalent to the original antibiotic preparations, and significantly exceed them in terms of safety profile due to the inclusion of the most effective prebiotic, lactulose, in them. The pharmaceutical composition of an antibiotic with a prebiotic is aimed at preventing and/or leveling dysbiotic disorders of the intestine, mobilizing the metabolic potential of the normoflora during anti-Helicobacter therapy.

Ecoantibiotics are available in film-coated tablets. Tablets contain 250 mg or 500 mg of the antibiotic and prebiotic doses of lactulose - 300 mg or 600 mg, respectively. Each ecoantibiotic has a conclusion on bioequivalence to the original representative of the class of antibiotics in terms of antimicrobial activity (Table 3).

Lactulose in the form of anhydro is fundamentally different from conventional lactulose, which is part of other drugs, the highest degree of purification, its composition is 97-99% represented exclusively by the disaccharide lactulose. Conventional lactulose is used in pharmaceuticals in the form of 66% syrup and contains a significant (up to 30%) amount of residual sugars in the form of impurities: galactose, lactose, tagatose, epilactose, fructose. In addition, it should be noted that ecoantibiotics contain lactulose in prebiotic doses, which does not cause flatulence and does not accelerate intestinal motility.

Lactulose is a synthetic disaccharide in which each galactose molecule is linked by a β-1-4 bond to a fructose molecule. This connection is the reason why lactulose is not broken down by human digestive enzymes, passes through the gastrointestinal tract and reaches the colon unchanged. In the colon, lactulose is an ideal nutrient substrate for bifidobacteria and other lactate-producing microorganisms, therefore it selectively promotes the growth of these bacteria, while potentially pathogenic microorganisms such as E. coli, Clostridium, Candida, Salmonella metabolize this disaccharide with difficulty. The growth of saccharolytic intestinal microflora leads to competitive inhibition of the growth of proteolytic microflora, which reduces the production of entero- and cytotoxins. The latter are also destroyed by proteases synthesized by bifido- and latobacteria. In various studies, it has been proven that even low doses of lactulose significantly increase the level of bifidobacteria, lactobacilli and lower the level of bacteroids, clostridium, escherichia, eubacteria, and fungi candida albicans.

As a result of the hydrolysis of lactulose in the colon, organic short-chain fatty acids (SCFA) are formed - lactic, acetic, butyric and propionic, which inhibit the growth of pathogenic microorganisms and consequently reduce the production of nitrogen-containing toxic substances. SCFAs are utilized by the macroorganism, which is accompanied by the absorption of water from the intestinal lumen and a decrease in colonic contents.

The rate of bacterial fermentation of lactulose, that is, its digestibility by lactic acid bacteria, and the minimum energy consumption of this fermentation ensure the rapid growth of the normal intestinal flora (bifidogenic effect) and, therefore, high therapeutic and prophylactic efficacy of even minimal amounts of lactulose contained in ecoantibiotics. It is estimated that 1 g of lactulose provides the same bifidogenic effect as 7-10 g of other oligosaccharides (dietary fibers) that have a prebiotic effect.

Thus, lactulose in the ecoantibiotics Ecocitrin and Ecobol during anti-Helicobacter therapy, being a food substrate for the normal flora of the intestine, stimulates the entire population of beneficial bacteria, has a protective effect on bifidobacteria and lactobacilli, reduces the effects of intoxication and levels the risk of side effects associated with taking antibiotics. At the same time, daily doses of lactulose (from 1.2 to 3.6 g) are completely metabolized by obligate microflora and do not affect intestinal motility.

Due to their unique composition, ecoantibiotics are better tolerated than conventional antibiotics, which allows them to be recommended to patients for anti-Helicobacter therapy.

The purpose of this study was to study the effectiveness of eradication therapy with the inclusion of ecoantibiotics: Ecobol and Ecocitrin and to carry out a comparative analysis of the effect of ecoantibiotics and traditional antibiotic analogues included in the standard regimens of anti-Helicobacter pylori therapy on the state of intestinal microbiocenosis.

Under observation were 55 patients with peptic ulcer with localization of the ulcer in the duodenal bulb aged 18 to 68 years (mean age 37.3 years). The vast majority of patients had a typical clinical picture of peptic ulcer, in 5 patients (9.1%) only endoscopic signs of peptic ulcer were determined.

Depending on the received eradication therapy scheme, all patients were divided into two groups: in the 1st group (n = 27), ecoantibiotics were included in the therapy regimen: Ecobol 1000 mg × 2, Ecocitrin 500 mg × 2, Rabeprazole 20 mg × 2; patients of the 2nd group (n = 28) took Amoxicillin 1000 mg × 2 times, Clarithromycin 500 mg × 2, Rabeprazole 20 mg × 2. Helicobacter pylori therapy was carried out for 14 days.

All patients underwent general therapeutic and clinical and laboratory examinations (clinical blood count, general urinalysis, coprogram, biochemical blood test: levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (AP), bilirubin, creatinine, urea nitrogen). Fibrogastroduodenoscopy was performed in all patients with a biopsy taken from the mucous membrane of the edge of the ulcer. To identify H. pylori Giemsa staining method was used. Infection H. pylori studied using urease test and histological analysis. Feces taken from the last portion of the stool obtained in the morning on the day of the study served as the material for the study of intestinal dysbiosis. Analysis of the nature of the growth of microorganisms was carried out on elective nutrient media.

Results and discussion

Against the background of eradication therapy, regression of the main clinical manifestations of the disease (pain syndrome, heartburn) was observed in all examined patients. There were no changes in the levels of AST, ALT, creatinine, urea nitrogen, glucose, plasma amylase, erythrocytes and hemoglobin.

Side effects of eradication therapy (nausea, diarrhea) in patients treated with ecoantibiotics were observed much less frequently than in patients who were treated with traditional antibiotic analogues (29.6% and 60.7%, respectively). The severity of nausea in patients in both groups 1 and 2 did not require symptomatic correction. Two patients from the 2nd group due to severe diarrhea prematurely (on the 5th and 7th day) stopped taking amoxicillin and clarithromycin. The weakening of the stool had a negative impact on the quality of life of patients and required symptomatic correction: 9 of the patients from the 2nd group took Enterol probiotic 1 capsule three times a day. The majority of patients (25 people, 92.6%) noted good tolerance of ecoantibiotics (Fig. 3).

In the general scatological study against the background of anti-Helicobacter therapy with the inclusion of ecoantibiotics in patients of the 1st group, normalization of scatological parameters was noted. In patients of the 2nd group, an increase in the manifestations of the maldigestion syndrome, which is possibly due to a violation of absorption processes in the small intestine, accelerated evacuation from the large intestine due to aggravation of intestinal dysbiosis against the background of antibiotics (Fig. 4).

In 41 (74.5%) patients, already before the start of anti-Helicobacter therapy, there were already signs of intestinal dysbiosis and, first of all, a decrease in the number of bifidobacteria, and in 33 (60%) patients, a decrease in the number of lactobacilli. The data obtained indicate that the inclusion of ecoantibiotics in the eradication therapy regimen contributed to a significant improvement in the composition of the intestinal microflora. So, at the end of treatment in patients taking Ecobol and Ecocitrin, 13 (48%) showed a significant increase in the number of bifidobacteria and 9 (33%) normalized the level of lactobacilli. So, at the end of treatment, only 7 (25.9%) patients of the 1st group showed a decrease in bifidobacteria and in 9 (33.3%) - a decrease in the number of lactobacilli. In the 2nd group of patients taking traditional antibiotics, inhibition of the growth of normoflora representatives was noted in 26 (92.7%) patients. In the 2nd group, after the end of taking antibiotics, not only the number of patients with a reduced number of bifidobacteria and lactobacilli increased, but also in 29 (67.9%) patients, fungi of the genus Candida.

Thus, due to the presence of lactulose in the composition of antibiotics, normal intestinal microbiocenosis was maintained during antihelicobacter therapy with Ecozitrin and Ecobol, while the use of traditional antibiotics caused an imbalance in intestinal microbiocenosis and significantly increased the risk of developing candidiasis (Fig. 5).

Achieving eradication H. pylori was recorded in 22 (81.5%) patients of the 1st group and in 16 (57.1%) patients of the 2nd group, which may depend on better adherence to therapy by patients taking ecoantibiotics, due to their better portability.

Neutrophilic and lymphocytic infiltration of the mucous membrane of the edges of the ulcer before the start of eradication therapy was observed in all patients included in the study. Successful eradication in patients of both groups (group 1 - 22 and group 2 - 16 people) contributed to the restoration of the normal state of the inflamed mucosa, which was manifested by the disappearance of its infiltration by polymorphonuclear leukocytes. But the morphological signs of chronic inflammation with lymphocytic infiltration of the mucous membrane remained in 24 (43.6%) people: group 1 — 11 (40.7%), group 2 — 13 (46.4%) and after 4 weeks at the end of therapy (which is consistent with the literature data). However, it was noted that the inclusion of ecoantibiotics in eradication therapy leads to a significant decrease in the number of patients with immunoinflammatory changes in the mucosal epithelium after a course of therapy. Only 3 patients (11.1%) from group 1 had plasmacytic infiltration at the end of treatment compared with 15 (53.6%) patients from group 2 who received traditional antibiotic therapy (Fig. 6). The data obtained suggest that the preservation of normal intestinal microbiocenosis increases the body's immune status, which in turn contributes to an increase in the effectiveness of eradication therapy.

Thus, the results of the study show the undoubted advantage of ecoantibiotics in eradication therapy regimens compared to traditional antibiotic analogues. The inclusion of Ecobol and Ekozitrin in the anti-Helicobacter therapy regimens eliminates the undesirable effects characteristic of antibiotics associated with their adverse effect on the state of intestinal microbiocenosis. Ecoantibiotics prevent the development of antibiotic-associated diarrhea and do not cause candidiasis.

It is also very important that ecoantibiotics in the process of anti-Helicobacter pylori therapy provide an increase in the effectiveness of eradication therapy, due to the fact that they have a better therapeutic tolerance than traditional conventional antibiotics, increase patient adherence to treatment and achieve high compliance with drug regimens.

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L. I. Butorova*, Candidate of Medical Sciences
T. A. Plavnik**

* FGBU MUNCC im. P. V. Mandryka of the Ministry of Defense of the Russian Federation, ** GBUZ GP No. 195 DZM, Moscow

Therapy aimed at expelling a person infected with it from the stomach is not the easiest task that the doctor sets for himself.

This is due to the fact that pathogenic microorganisms are extremely reluctant to leave their favorite places of existence - epithelial cells of the inner lining of the stomach or submucosa, resistant strains to drugs are formed.

Therefore, the impact on the bacterium should be complex: medication, physiotherapy, nutrition, phytotherapy. The main point of application is drug therapy.

The expression "treat Helicobacter pylori infection" is not entirely true from a medical point of view. Doctors treat diseases caused by this microorganism, and the bacterium itself should be disposed of.

The main direction in drug therapy is eradication - a method of destroying an infectious agent with the help of drugs.

In addition to eradication therapy, it is important to correct the disturbed acidity of gastric juice, restore the motor and evacuation function of the gastrointestinal tract, stabilize enzymatic activity, and relieve inflammation.

All these functions are assigned to specific drugs, which, in combination with proper nutrition, give positive results. The main groups of drugs, medicines and tablets for Helicobacter pylori (helicobacter pylori):

• Antibacterial
• Bismuth salt preparations
• Proton pump blockers
• M-cholinolytics
• H2-histamine receptor blockers
• Antacids
• Spasmolytics
• Prokinetics

The most common dosage form of drugs is tablets, antacids can be used in the form of suspensions, powders that require dissolution in water.

What antibiotics kill Helicobacter pylori

Antibacterial drugs are the "heavy artillery" that causes the bacteria to desert and leave the patient's body.

The standards for the treatment of Helicobacter-associated gastric pathologies indicate at least two antibiotics. With significant seeding of the mucosa, pronounced clinical manifestations of the disease, it is impossible to do without them.

• Amoxicillin
• Clarithromycin
• Tetracycline
• Metronidazole
• Rifambutin
• Levofloxacin

Rifambutin and levofloxacin are “reserve” drugs, they are not included in the standard regimens of therapy, but can be used if pathogenic strains develop resistance to common drugs included in the protocols.

Antibacterial drugs have side effects: allergic reactions, dysbacteriosis, nausea. Often patients are afraid to drink antimicrobials for this very reason.

In case of infection with Helicobacter pylori and the presence of a clinic of gastric diseases, this should not be done. Taking antibiotics in this case is justified.

Without these medicines, the patient risks earning money for himself, and by refusing treatment, he exposes the body to the risk of developing oncopathology of the gastrointestinal tract. Gastric cancer is 3-6 times more likely to occur in patients infected with H. pylori who have not received proper therapy.

How to treat Helicobacter pylori with antibiotics - eradication therapy regimens

To date, 3- and 4-component treatment regimens aimed at destroying bacteria have been developed and are actively used.

If the patient has a microbe in the stomach, there are symptoms of gastrointestinal damage, the person has not previously received treatment, therapy is always started with a three-component scheme, including:

• Proton pump blocker (, lansoprazole, rabeprazole, pantoprazole 20 mg) 2 times a day
• Amoxicillin 1000 mg twice a day
• Clarithromycin 500 mg twice daily

A 3-component scheme is prescribed at the patient's initial treatment for treatment; elderly, debilitated patients can individually adjust the dose of drugs.

This therapy is prescribed from 7 (minimum) to 14 days. Clinical studies have shown that in some cases, weekly drug intake is not enough to ensure eradication, therapy is ineffective.

After two weeks of taking the drugs, on the contrary, the effect of the treatment was an order of magnitude higher: in a much larger number of patients, pathogen eradication reached 80% or more.

Four-component treatment regimen

In the case when the effect of the 3-component scheme is not achieved, the destruction of the infectious agent did not occur, the doctor will recommend after a month and a half to continue therapy, consisting of:

• Proton pump blocker (omeprazole, lansoprazole, rabeprazole, pantoprazole 20 mg) 2 times a day
• Bismuth salt preparations 120 mg 4 times a day
• Metronidachol 500 mg 3 times a day
• Tetracycline 500 mg 4 times a day

This is a 4-component eradication scheme. It is important to take into account that the antibacterial drugs used earlier are not repeated. If resistance to the above antibiotics is detected, “reserve” drugs can be prescribed: levofloxacin, rifambutin.

Despite the developed standards, the doctor, conducting eradication, should approach each case and disease individually, taking into account the patient's age, comorbidities, possible allergic reactions of the body and the resistance of specific bacterial strains to drugs.

How many days to take antibiotics for Helicobacter pylori

A 3-component scheme is prescribed by a doctor for a period of 7 to 14 days. It is not advisable to drink drugs for less than a week, there will be no effect from such treatment.

The bacterium is difficult to treat, develops resistance to drugs, so there is more and more evidence that even a week is not enough to achieve a positive result and get rid of the pathogen. More and more doctors are inclined to prolong antibiotic therapy up to 10-14 days.

The 4-component scheme is appointed for a period of two weeks.

The effectiveness of treatment should be assessed through diagnostic and laboratory methods no earlier than 1-1.5 months after the end of taking the drugs.

If eradication is 80% or more of the initial level, or bacteria are not found in the body at all, we can talk about success in the treatment of the disease associated with this pathogen.

More about drugs

Features of taking antibiotics for the treatment of Helicobacter pylori:

• Clarithromycin

This is an antibacterial drug from the group of macrolides. It is part of the first-line therapy for Helicobacter pylori infection. It is successfully used in gastroenterology, it is able to inhibit the synthesis of the helicobacter pylori cell wall, and therefore prevent its reproduction. Acid-resistant, effectively "works" with normal and high acidity, well absorbed.

Some bacterial strains are resistant to clarithromycin. In this case, the drug must be replaced with another one in order to achieve a better therapeutic effect.

• Amoxicillin and metronidazole

Metronidazole or Trichopolum is a drug that has a detrimental or bactericidal effect on H. pylori. Its activity does not depend on the pH level in the stomach, the drug can be used in both hyper- and hypoacid conditions.

To date, the resistance of many strains of Helicobacter pylori to metronidazole is very common. If the drug is prescribed together with de-nol, resistance to it develops more slowly.

Amoxicillin is an antibiotic of the penicillin series that blocks the synthesis of the cell wall of microbes, is well absorbed by the gastric mucosa. More active in a neutral environment than in an acidic one. Increasing the pH to 4 by 10 times enhances the pharmacological effect of this drug.

Metronidazole and amoxicillin are first-line drugs, but may also be given in a 4-component regimen.

• Tetracycline

Another antimicrobial agent actively used in the eradication therapy of helicobacter pylori. The mechanism of action of tetracycline is to inhibit protein synthesis of microbial cells.

The drug is well absorbed in the gastrointestinal tract. Dairy food slows down its absorption.

• Proton pump blockers

The most common representative of this group is. There are other very effective drugs: lansoprazole, pantoprazole, esomeprazole, rabeprazole).

Medicines suppress the production of hydrochloric acid. Thus, they affect the microbe indirectly: they do not destroy it, but create unfavorable conditions for existence, have a suppressive effect on the infection: they stop bacterial growth and development.

Omeprazole and other members of the group, by increasing the pH of gastric contents, contribute to the better functioning of antibacterial drugs, in particular amoxicillin.

There is evidence that proton pump inhibitors can block the bacterial enzyme urease.

Doctors recommend that after the end of the course of treatment with antibiotics, continue taking omeprazole for up to 4-8 weeks. Patients who continue to take proton pump blockers have better mucosal healing processes, a higher percentage of bacteria destruction relative to patients who stopped taking omeprazole after the end of the eradication regimen.

• Antacids and H2 receptor blockers

Most often, the acidity of gastric juice during infection with H. pylori is normal or increased.

In addition to omeprazole, which normalizes pH, antacids (almagel, phosphalugel, gefal, maalox, rennie) and H2-histamine receptor blockers (famotidine, ranitidine) also have this effect.

The mechanism of action of antacids is to neutralize the hydrochloric acid of the stomach. The active ingredients in these preparations are aluminum, magnesium hydroxides.

Means effectively eliminate the clinical manifestations of "acidism" - heartburn, belching sour. Take them 1-2 hours after eating and at night. Release form - suspensions, or powders, tablets.

It is not necessary to combine the intake of antacids with antibacterial drugs or bismuth salts, since aluminum and magnesium hydroxides interfere with the absorption of other substances in the gastrointestinal tract.

New generation H2-histamine receptor blockers (famotidine, ranitidine) have practically no side effects. Their mechanism of action: they inhibit the production of HCL and the production of pepsin, which reduces acidity. Assign tablets after breakfast and before bedtime.

• Bismuth preparations

This group of drugs in combination with antibiotics has a bactericidal effect - it destroys both coccal strains and vegetative forms.

Bismuth salts have many effects that have a positive effect in the complex treatment of diseases caused by Helicobacter pylori:

• Prevent pathogens from attaching to epithelial cells of the gastric mucosa
• interfere with microbial ATP synthesis
• block bacterial enzymes
• Contribute to the destruction of the cell wall of the infectious agent
• Increase the synthesis of protective immunoglobulins, gastric secretion prostaglandins
• Enhance the secretion of bicarbonates and protective mucus
• Reduce the absorption of antibiotics in the gastrointestinal tract, thereby increasing their concentration in the gastric contents
• Provide reparative, wound-healing effect of the internal gastric wall
• Improve local blood circulation

These pharmacological properties allowed the bismuth drug to occupy its niche in the treatment of helicobacteriosis in combination with two antibiotics. One of the most effective drugs in this group is de-nol.

De-nol kills helicobacter or not

Only in combination with antimicrobials, de-nol has a bactericidal effect. If you take this drug alone as monotherapy, this treatment will not have the desired effect.

But in the combined treatment regimen, de-nol fully reveals its therapeutic effects, while enhancing the properties of antibacterial drugs.

The combination "de-nol + 2 antibiotics" is extremely effective, and in case of sensitivity to Helicobacter pylori, it allows the microbe to disappear if the tablets are taken for 10-14 days.

How much to drink de-nol with helicobacter infection

The drug is prescribed 1 tab 4 times a day for 30 minutes. before meals and at night for a period of at least 21 days, you can take the medicine for up to 8 weeks on the recommendation of a doctor. You should be aware that when prescribing the drug, the stool turns black.

The tablets should be taken with a glass of boiled water, not with milk, since dairy products reduce the pharmacological effect of the drug. Do not combine tablets with juices.

Antacids slow down the absorption of de-nol, so you should not drink them together.

If side effects occur: diarrhea, nausea, allergic reactions, vomiting, the medication should be stopped and consult a doctor.

In 1985, in the Australian Journal of Medicine, scientists Barry Marshall and Robin Warren published the results of their experiments, which indicated that Helicobacter pylori infection causes gastritis. For the discovery of the role of this microorganism in the development of diseases of the digestive tract, scientists in 2005 were awarded the Nobel Prize in Physiology or Medicine. Many years have passed since then, and the role and influence of H. pylori on the gastrointestinal tract continues to be actively studied. The main questions of concern to scientists include the following: is it worth eradicating the bacteria, and also which antibiotic treatment regimen is most effective?

Is It Worth Treating Bacteria?

Although there are opponents of the theory that Helicobacter pylori is the main cause of gastritis and stomach ulcers, most doctors and researchers insist on the eradication (destruction) of this microorganism.

The prevalence of human infection with Helicobacter pylori reaches 50% worldwide.

Helicobacter pylori is the cause of most cases of gastritis, peptic ulcers of the stomach and duodenum

According to statistics, the bacterium Helicobacter pylori is the cause of more than 90% of duodenal ulcers and 70-80% of gastric ulcers, more than 90% of gastritis.

If you ask older doctors, you can find out that with the introduction of treatment based on the destruction of infection, the number of complications, sometimes requiring traumatic surgical interventions, has decreased several times.

Indications for eradication of Helicobacter pylori

Indications for bacterial eradication:

• stomach and / or duodenal ulcer (active or healed, complications of peptic ulcer);
• atrophic gastritis;
• MALT-lymphoma of the stomach;
• patients with stomach cancer relatives of the 1st degree;
• condition after partial or after endoscopic treatment due to neoplasm of the stomach (MALT-lymphoma, adenoma, cancer);
• severe inflammation affecting the entire stomach;
• inflammation limited mainly to the body of the stomach;
• intense atrophic changes;

Once every 5-6 years, a congress of scientists and doctors gathers, which publishes recommendations for the eradication of Helicobacter pylori. They are called the Maastricht Consensus. The last such consensus (fourth) was collected in 2010 in Florence, which, among other things, discussed how much one or another drug should be taken.

• long-term (more than 1 year) treatment that reduces the secretion of gastric acid;
• increased risk factor for development: smoking in large quantities, intense exposure to dust, coal, quartz, cement and / or work in a mine;
• the desire of a patient who is afraid of getting cancer;
• dyspepsia not associated with peptic ulcer (functional dyspepsia);
• undiagnosed dyspepsia (as part of the "examine and treat" strategy);
• gastroesophageal reflux disease;
• prevention of the development of ulcers and their complications before or during long-term treatment with non-steroidal anti-inflammatory drugs;
• unexplained iron deficiency anemia;
• primary immune thrombocytopenic purpura;
• vitamin B12 deficiency.

In the presence of these indications, the patient needs to be examined. If an infection is detected, treatment should be started.

What are the treatment regimens

The goal of eradication is to cure the disease, prevent peptic ulcer recurrence, and reduce the risk of developing stomach cancer. When prescribing a treatment regimen, the prevalence of clarithromycin-resistant Helicobacter pylori strains in the patient's area of ​​residence, drug prices, allergic and adverse reactions, and ease of taking medications are taken into account.

The optimal H. pylori eradication regimen should be ≥95% successful in patients infected with susceptible bacterial strains and ≥85% successful in patients with resistant strains of microorganisms. It is desirable that these drugs be easy to take, then the patient will be more inclined to treatment.H. pylori, like any other microorganism, has developed resistance to the action of antibacterial drugs, which led to the development of several methods of treatment.

The criteria for choosing a specific regimen are the presence of bacterial resistance to clarithromycin in the patient's region of residence. If in the country the resistance of Helicobacter pylori to this antibiotic exceeds 15–20%, it is not used in the course of treatment.

All H. pylori eradication regimens, in addition to antibacterial agents, include proton pump inhibitors (PPIs). They suppress the formation of gastric acid and increase the acidity in the stomach, creating unfavorable conditions for the life of this microorganism, thereby killing it. Proton pump inhibitors include omeprazole, pantoprazole, esomeprazole, lansoprazole.

Gallery of proton pump inhibitors (PPIs)

Pantoprazole Lansoprazole Omeprazole

Treatment in countries with low resistanceH.pylori to clarithromycin (<15–20% штаммов)

First line treatment (classic triple therapy)

The first line includes:

• traditional triple therapy: for 7 days PPI + clarithromycin + amoxicillin or metronidazole (if allergic to penicillins). To increase the effectiveness of treatment, doubling the PPI dose and/or increasing the duration of treatment to 10-14 days may be considered;
• bismuth-containing quadruple therapy (bismuth subcitrate (subsalicylate) + tetracycline hydrochloride + metronidazole or tinidazole + PPI for 10-14 days).

Second line

• bismuth-containing quadruple therapy (bismuth subcitrate (subsalicylate) + tetracycline hydrochloride + metronidazole or tinidazole + PPI for 10-14 days) - if traditional triple therapy was used as the first line;
• triple therapy based on levofloxacin (levofloxacin + amoxicillin + PPI for 10-14 days).

third line

If the first two lines of treatment fail, individualized therapy is prescribed based on determining the sensitivity of the H. pylori culture isolated after gastric biopsy to antibacterial agents (most often to clarithromycin and levofloxacin).

If H. pylori is sensitive to clarithromycin, triple therapy is recommended: amoxicillin + clarithromycin or tinidazole or metronidazole + PPI for 10–14 days

If she is sensitive to levofloxacin, the following list of drugs is prescribed: levofloxacin + PPI + amoxicillin for 14 days.

Countries with high bacterial resistanceto clarithromycin (>15–20% of strains)

First line therapy

• Bismuth-containing quadruple therapy (bismuth subcitrate (subsalicylate) + tetracycline hydrochloride + metronidazole or tinidazole + PPI for 10-14 days);
• sequential therapy (first five days - PPI + amoxicillin; next 5 days - PPI + clarithromycin + metronidazole or tinidazole); this regimen is not indicated for concurrent H. pylori resistance to clarithromycin and metronidazole;
• concomitant therapy (PPI + amoxicillin + clarithromycin + metronidazole or tinidazole for 10–14 days) - the so-called bismuth-free quadruple therapy.

Second line

If first-line treatment fails, levofloxacin-based triple therapy is recommended (levofloxacin + amoxicillin + PPI for 10–14 days).

third line

Treatment regimens are based on determining the sensitivity of Helicobacter pylori to antibiotics (most often to levofloxacin or clarithromycin).

It should be remembered that only a doctor can prescribe a specific treatment regimen, based on the individual characteristics of the patient's health, the results of the examination, and data on the prevalence of antibiotic-resistant strains of H. pylori in the region.

Contraindications and side effects

In 5–20% of patients, side effects are observed when taking drugs to eradicate the bacteria. They are usually mild and do not require discontinuation of treatment.

Discovery of antibiotic treatment (video)

Helicobacter pylori infection remains one of the main causes of gastritis and stomach ulcers. Timely treatment allows you to kill this bacterium and reduce the likelihood of recurrence of diseases, their complications and the development of stomach cancer.

In today's world, there are many different diseases. In this article, I would like to talk about how Helicobacter can be treated: a treatment regimen and getting rid of this problem.

What it is?

At the very beginning, you need to understand the concepts that will be used in this article. What is Helicobacter pylori? spiral-shaped, which lives either in the duodenum or in the stomach. The danger of Helicobacter is that it can cause various diseases, such as gastritis, polyps, hepatitis, ulcers and even cancer. It is also worth saying that the majority of the inhabitants of our planet, approximately 60%, are infected with this microorganism. Scientists say that it is in second place in terms of prevalence after herpes infection. It can be contracted through contaminated food or water, as well as during contact with a sick person through sputum or even saliva, which can be released during coughing or sneezing.

Requirements

It is very important to consider the schemes as well. So, it is worth saying that there are several simple but important requirements for therapy:

1. The main goal of therapy is to destroy (it is far from always possible to do this completely) these harmful bacteria.
2. You need to try to avoid side effects. In case of their occurrence, the drug can be changed.
3. It is very important that the treatment gives positive results within 7-14 days.

Important rules that involve the treatment of Helicobacter

The treatment regimen must meet very simple, but very important rules. What should be remembered not only by every doctor, but also by the patient:

1. If the treatment regimen does not produce the desired effect on the patient, it is not worth repeating it.
2. If the regimen is ineffective, this may mean that the bacterium has acquired immunity to one of the components that were used in therapy.
3. If no treatment regimen has a positive effect on a person, it is necessary to check the sensitivity of the disease strain to the entire spectrum of antibiotics.
4. If a year after recovery, a person becomes infected again, it should be considered as a relapse, but not as a reinfection.
5. If there was a relapse of the disease, you need to apply a more stringent treatment regimen.

Medications

What steps can be taken if Helicobacter treatment is foreseen? The treatment regimen may consist of the following medications:

1. Their main goal is to reduce the acidity of the stomach and envelop its walls.
2. You will also need substances that suppress the production of gastric juice. In this case, it is customary to talk about proton pump blockers and H2-histamine blockers.
3. Antibacterial agents - antibiotics. Their main goal is to destroy the harmful organism.

Scheme 1. Seven-day

How can Helicobacter pylori be treated with antibiotics? The scheme can be seven days (the so-called first line therapy). In this case, all medications are taken for a week twice a day. In this case, the doctor will most likely prescribe the following drugs to the patient:

1. proton pump inhibitors. This may be one of the following drugs: Omez, Lansoprazole, Esomeprazole.
2. Bactericidal agents, for example, a drug such as Klacid.
3. You can also use the antibiotic "Amoxiclav" (a group of penicillins).

Scheme 2. Ten- or fourteen-day treatment

For two weeks, Helicobacter pylori can be treated with antibiotics. The scheme in this case may be as follows:

1. Proton pump inhibitors are taken twice a day. These will again be drugs such as Omeprazole, Pariet, Nexium.
2. Four times a day, you will need to take a medication such as De-nol (bismuth subcitrate).
3. The drug "Metronidazole" is prescribed three times a day.
4. Four times a day, you will also need to take the drug "Tetracycline", which is a broad-spectrum antibiotic, for a complete cure.

Post-Treatment Actions

After the basic treatment regimen for Helicobacter pylori is completed, you should not relax. Next, you need to support your body with the help of medicines for a certain time:

1. Five weeks, if we are talking about the duodenal localization of the microorganism.
2. Seven weeks if its localization is gastric.

The subsequent antibiotic treatment regimen for Helicobacter pylori includes the use of one of the following drugs:

1. Proton pump inhibitors - drugs "Omez", "Rabeprazole". You need to take these funds 1-2 times a day.
2. Histamine H2 receptor blockers. These can be drugs such as Ranitidine, Famotidine. Taken twice a day.
3. Antibiotic "Amkosiklav" - 2 times a day.

Helicobacter pylori gastritis

Now the scheme of treatment of gastritis with Helicobacter will be considered. What drugs in this case can the doctor prescribe? These can be such drugs as "De-Nol", as well as "Metronidazole", "Clarithromycin", "Amoxicycline". To work more efficiently, the drug "Omeprazole" may be prescribed. To improve the recovery processes in the stomach, you can take medicines such as Solcoseryl, Gastrofarm.

Main Side Effects

If the Helicobacter pylori treatment regimen described above was used, it is worth saying that the drugs can also cause some side effects. I would like to talk about some of them separately:

1. If the patient took "Omeprazole", bismuth, "Tetracycline", flatulence, diarrhea, dizziness, dark stools, an increase in renal failure are possible.
2. If the patient was taking a medication such as Metronidazole, there may be the following side symptoms: vomiting, headache, fever.
3. During the reception of "Amoxicycline" pseudomembronous colitis may develop, there may be diarrhea, a rash.
4. When taking Clarithromycin, nausea, vomiting, diarrhea, headache, pseudomembranous colitis are possible.

Efficiency mark

What is important if Helicobacter treatment is supposed? The scheme of treatment, as well as an assessment of its effectiveness:

1. An important indicator is the disappearance of the pain syndrome.
2. The dyspeptic syndrome (unpleasant sensations in the upper abdomen) should disappear.
3. Well, the most important thing is the complete disappearance of the causative agent of the disease - Helicobacter pylori.

Small Conclusions

Separately, it should be said that doctors are still arguing about which treatment regimen is best to choose. After all, the complete extermination of the Helicobacter pylori bacterium is possible only with the use of a large number of various antibiotics (the microorganism can be resistant to most). And this is very harmful to the body. If the patient has previously taken a certain antibiotic, their treatment will already be completely ineffective. In addition, this can lead to the death of the intestinal microflora, which in itself is also very harmful to the patient's health.