Peptic ulcer of the stomach and duodenum is a chronic disease characterized by the formation of ulcers in the stomach and duodenum. Peptic ulcer disease is characterized by seasonal exacerbations (spring and autumn).

According to statistics, every 10 resident of Russia suffers from this disease, and men predominate among patients (80%).

Peptic ulcer disease is dangerous due to its complications, which pose a serious threat to health. Thus, gastrointestinal bleeding often occurs, perforation of the stomach wall and penetration of the ulcer into neighboring organs, malignancy of the ulcer with the development of stomach cancer.

Peptic ulcer of the stomach and duodenum: causes.

2. An imbalance between the production of substances that aggressively affect the wall of the stomach and duodenum and protective factors.

Factors of aggression include hydrochloric acid and pepsin produced in the stomach, as well as pancreatic enzymes, bile acids, lysolecithin, which enter the lumen of the duodenum from the pancreas and liver.

The protective factors in this case are the production of mucus by the stomach cells, which envelops the mucous membrane, preventing direct contact of hydrochloric acid and enzymes with epithelial cells, timely renewal of the epithelium of the stomach and duodenum and its full blood supply. The production of bicarbonates in the stomach (its antrum) and duodenum and the complete closure of the pyloric sphincter ensures the protection of the duodenum from the acidic contents of the stomach.

An imbalance of aggressive and protective factors can occur under the influence of psycho-emotional stress, as a result of alcohol abuse, unhealthy diet, uncontrolled use of certain medications (aspirin and other non-steroidal anti-inflammatory drugs, glucocorticosteroid hormones (prednisolone, dexamethasone, metipred), cytostatics (methotrexate, etc.) and others).

Poor nutrition includes eating too cold or hot, spicy, fried, smoked food, dry food, and drinking coffee.

Symptoms of peptic ulcer of the stomach and duodenum.

Gastric ulcer: clinical picture. Symptoms of a stomach ulcer.

In more than half of patients, an ulcer forms in the body of the stomach along its lesser curvature, so pain, which is the most common symptom of an ulcer, occurs in the majority of patients in the epigastric region, often slightly to the left of the midline of the abdomen. With this localization of the ulcer, pain occurs 60-90 minutes after eating, moderate, aching.

When an ulcer is localized in the upper part of the stomach, inflammation is often transmitted to the sphincter (sphincter), which separates the stomach cavity from the esophagus. As a result, sphincter insufficiency occurs, and the contents rise during peristalsis of the stomach through the esophagus, causing nausea and even vomiting. Pain with this location of the ulcer occurs half an hour after eating, is often localized behind the sternum and can radiate to the heart, to the left arm or shoulder blade, simulating an attack of angina. A distinctive feature of the pain syndrome in peptic ulcer disease is the connection between the occurrence of pain and food intake and the lack of connection with physical activity.

With an ulcer located in the pyloric region, pain occurs in the epigastric region on an “empty stomach” and at night. “Hungry” and “night” pains are classic symptoms of gastric ulcers, and almost never occur with gastritis. The intensity of pain is usually pronounced. The pain can occur in attacks repeatedly during the day. Often, patients do not find any connection between a painful attack and food intake.

In addition to pain, patients may be bothered by sour belching, heartburn, nausea, vomiting, excessive salivation, and a feeling of fullness in the stomach after eating a small portion of food. It is not uncommon for patients with ulcers to lose weight.

Duodenal ulcer: symptoms. Clinical picture of duodenal ulcer.

With a duodenal ulcer, pain occurs 1.5-4 hours after eating and is more often found in the right half of the abdomen, in its upper part. The pain is usually intense, paroxysmal, and can radiate to the right side of the chest. Eating brings relief: the pain subsides within 5-20 minutes after eating.

Diagnosis of peptic ulcer of the stomach and duodenum.

Until now, the “gold standard” for diagnosis is endoscopic examination of the stomach and duodenum with targeted biopsy (FGDS - fibrogastroduodenoscopy).

In addition, to detect Helicobacter pylori infection, a urease breath test can be performed and blood taken to detect antibodies to this pathogen.

Treatment of peptic ulcer of the stomach and duodenum.

Approaches to the treatment of gastric ulcers, duodenal ulcers and those caused by Helicobacter are the same: treatment is carried out with antibiotics, enveloping (gastroprotective) and hydrochloric acid neutralizing drugs for a course of 10-14 days.

At the end of treatment, a control endoscopic examination of the stomach and duodenum is performed. If the ulcerative defect persists, proton pump inhibitors or bismuth preparations (De-nol) are added to treatment for the next 2-3 weeks. 1-1.5 months after the end of treatment, a repeat endoscopic examination of the stomach and duodenum is required, during which the effectiveness of treatment is assessed: whether the ulcer has healed and whether Helicobacter pylori has been destroyed.

If cure does not occur, treatment is carried out with second-line drugs.

IMPORTANT! It is imperative to complete the course of treatment in full and strictly follow the doctor’s instructions. Otherwise, the effectiveness of treatment sharply decreases, and bacteria (Helicobacter), if they are not completely destroyed, very quickly become resistant to the antibiotics used during therapy.

It has been proven that most failures in the treatment of peptic ulcers are caused by the patient’s unscrupulous compliance with medical instructions.

It is important for the doctor to remember that if the patient has ever taken nitrofurantoin drugs (metronidazole, tinidazole, etc.) to treat any disease, they should not use treatment regimens in which they are used, since Helicobacter is already immune to their action.

Correctly administered treatment can lead to a complete cure of the patient. But even if there is no cure, long-term remission is achieved in 2/3 of patients, the frequency of exacerbations and the risk of complications of peptic ulcer disease, such as gastrointestinal bleeding, perforation and penetration of the ulcer, are sharply reduced.

Treatment of gastric and duodenal ulcers caused by Helicobacter pylori.

Three-component scheme

Treatment is carried out for 10-14 days simultaneously with three drugs:

• Proton pump inhibitors (Omeprazole 20 mg 1-2 times a day, rabeprazole (Pariet) 20 mg 1 time a day, pantoprazole (Nolpaza) 40 mg 2 times a day, lansoprozole 30 mg 2 times a day, esomeprazole 20 mg 2 slot per day);

Four-component scheme

Treatment is also carried out for 10-14 days.

• Amoxicillin (Flemoxin Solutab®) 500 mg 4 times a day, or 1000 mg twice a day;
• Clarithromycin (Klacid) 500 mg twice a day, or josamycin (Vilprafen®) 1000 mg twice a day, or nifuratel (MacMirror) 400 mg twice a day;
• Proton pump inhibitors (Omeprazole 20 mg 1-2 times a day, rabeprazole (Pariet) 20 mg 1 time a day, pantoprazole (Nolpaza) 40 mg 2 times a day);

A three-component regimen for the treatment of patients with chronic gastritis and gastric ulcer, if the patient has atrophy of the gastric mucosa with a decrease in acid-forming function (low acidity)

The course of treatment is 10-14 days.

• Amoxicillin (Flemoxin Solutab®) 500 mg 4 times a day, or 1000 mg twice a day;
• Clarithromycin (Klacid) 500 mg twice a day, or josamycin (Vilprafen®) 1000 mg twice a day, or nifuratel (MacMirror) 400 mg twice a day;
• Bismuth tripotassium dicitrate (De-Nol®, Ventrisol) 120 mg 4 times a day, or 240 mg twice a day.

In 20% of patients with gastric ulcer, Helicobacter pylori is not detected. To treat such patients, regimens without an antibacterial component are used, which are prescribed in a course of 14-21 days. For example:

1. Drugs that suppress the secretion of hydrochloric acid:

Proton pump inhibitors:

• Omeprazole (Omez) 30 mg 1 - 2 times a day, or pantoprazole 40 mg 1 - 2 times a day, or esomeprazole 20 - 40 mg 1 - 2 times a day, or rabeprazole 20 mg 1 - 2 times a day.

or H2-histamine receptor blockers:

• Famotidine 20 mg twice a day for 2-3 weeks.

2. Gastroprotectors:

• Tripotassium bismuth dicitrate (De-nol, Ventrisol) 120 mg 4 times a day 30 minutes before meals;
• Sucralfate (Venter, Alsukral) 500-1000 mg 4 times a day 30-60 minutes before meals for 14-28 days.

Upon completion of the course of treatment, patients with peptic ulcer disease are often (especially with a history of complicated ulcers and gastric ulcers) prescribed drugs that reduce the secretion of hydrochloric acid for daily use. In such cases, as a rule, the drug is used in a minimum dosage once a day.

If complications of a peptic ulcer occur, such as bleeding from an ulcer with massive blood loss, perforation of an ulcer or degeneration of an ulcer into stomach cancer, impaired evacuation of food from the stomach as a result of narrowing of the outlet (pyloric) section of the stomach, and for a number of other indications, the patient may be offered surgical treatment.

“Second-line” regimens for the treatment of gastric and duodenal ulcers.

These regimens are also prescribed in a course of 10-14 days.

Four-component “second line” scheme with nitrofurans

1. Proton pump inhibitors;
2. Amoxicycline (500 mg 4 times a day or 1000 mg 2 times a day);
3. Nitrofuran drug: nifuratel (400 mg 2 times a day) or furazolidone (100 mg 4 times a day)
4. Bismuth tripotassium dicitrate (120 mg 4 times a day or 240 mg 2 times a day).

Quadruple second-line regimen with rifamixin

1. Proton pump inhibitor.
2. Amoxicillin (500 mg 4 times a day or 1000 mg 2 times a day).
3. Rifaximin (Alpha Normix) 400 mg 2 times a day.
4. Bismuth tripotassium dicitrate (120 mg 4 times a day) for 14 days.

For quotation: Lapina T.L., Ivashkin V.T. Modern approaches to the treatment of gastric and duodenal ulcers // RMZh. 2001. No. 1. P. 10

The historical stages of treatment of gastric and duodenal ulcers reflect not only the social significance of the disease, but also the development of scientific progress, which has armed modern doctors with powerful antiulcer drugs (Table 1). It is important to note that nowadays some therapeutic approaches have lost their significance, others have found a certain “niche” among various treatment methods, and still others, in fact, determine the current level of treatment for peptic ulcer disease.

Control of gastric acid production is the cornerstone of peptic ulcer treatment. The classic formula of the early 20th century “no acid - no ulcer” has not lost its relevance; the most effective groups of drugs, according to their mechanism of action, are aimed at combating acidity.
Antacids
Antacid drugs have been known since ancient times. This is a group of drugs that reduce the acidity of gastric contents through chemical interaction with acid in the stomach cavity. Currently, preference is given to non-absorbable antacids, which are relatively insoluble salts of weak bases. Non-absorbable antacids usually contain a mixture of aluminum hydroxide and magnesium hydroxide (Almagel, Maalox) or are aluminum phosphate (Phosphalugel). Unlike absorbable antacids (soda), they have much fewer side effects. They interact with hydrochloric acid, forming non-absorbable or poorly absorbed salts, thereby increasing the pH inside the stomach. At a pH greater than 4, pepsin activity decreases and it can be adsorbed by some antacids. Acid production in duodenal ulcers ranges between 60 and 600 mEq/day, in two thirds of patients - between 150 and 400 mEq/day. The total daily dose of antacids should be in the range of 200-400 mEq for neutralizing ability, for gastric ulcers - 60-300 mEq.
Deciphering the mechanism of parietal cells and the regulation of acid secretion has made it possible to create new classes of drugs. The secretion of hydrochloric acid is under the stimulatory control of three classes of parietal cell receptors: acetylcholine (M), histamine (H2), gastrin (G) receptors. The path of pharmacological action on muscarinic receptors turned out to be historically the earliest. Non-selective M-anticholinergic blockers (atropine) and selective M1-antagonists (pirenzepine) have lost their importance in the treatment of peptic ulcers with the progress of drugs of other classes that act at the molecular level, interfere with intimate intracellular processes and provide a more powerful antisecretory effect.
Histamine H2 receptor blockers
Thanks to clinical studies, it has been established that there is a direct relationship between ulcer healing and the ability of drugs to suppress acidity. Ulcer healing is determined not only by the duration of administration of antisecretory agents, but also by their ability to “hold” intragastric pH above 3 for a given time. The meta-analysis made it possible to establish that a duodenal ulcer will heal within 4 weeks in 100% (!) of cases if the intragastric pH is maintained above 3 for 18-20 hours during the day.
Despite the fact that patients with gastric ulcer have moderate levels of gastric secretion, antisecretory therapy is mandatory for them as well. Gastric ulcers are characterized by slower healing than duodenal ulcers. Therefore, the duration of prescription of antisecretory drugs should be longer (up to 8 weeks). It is assumed that we can expect scarring of gastric ulcers in 100% of cases if intragastric pH is maintained above 3 for 18 hours a day for about 8 weeks.
Such control of acid secretion was achieved thanks to blockers of histamine H2 receptors in parietal cells. These drugs significantly influenced the course of peptic ulcer disease: the duration of ulcer scarring was reduced, the frequency of ulcer healing increased, and the number of complications of the disease decreased.
Ranitidine for exacerbation of peptic ulcer is prescribed at a dose of 300 mg per day (once in the evening or 2 times a day, 150 mg), for duodenal ulcers, usually for 4 weeks, for gastric ulcers for 6-8 weeks. To prevent early relapses of the disease, it is advisable to continue taking a maintenance dose of ranitidine 150 mg/day.
Famotidine (Quamatel) is used in a lower daily dose than ranitidine (40 and 300 mg, respectively). The antisecretory activity of the drug is more than 12 hours with a single dose. Famotidine is prescribed at a dose of 40 mg for the same duration as ranitidine. To prevent relapses of gastric ulcer - 20 mg/day.
Histamine H2 receptor blockers are of particular importance in the treatment of bleeding from the upper gastrointestinal tract. Their effect is due to inhibition of hydrochloric acid production and an indirect decrease in fibrinolysis. In case of massive bleeding, drugs with parenteral forms of administration (Kvamatel) have an advantage.
The effectiveness of histamine H2 receptor antagonists is due primarily to their inhibitory effect on acid secretion. The antisecretory effect of cimetidine lasts up to 5 hours after taking the drug, ranitidine - up to 10 hours, famotidine, nizatidine and roxatidine - 12 hours.
Proton pump inhibitors
A new step in the creation of antisecretory drugs was the inhibitors of H+,K+-ATPase of parietal cells - the enzyme that actually ensures the transfer of hydrogen ions from the parietal cell into the lumen of the stomach. These benzimidazole derivatives form strong covalent bonds with the sulfhydryl groups of the proton pump and permanently disable it. Acid secretion is restored only when new H+,K+-ATPase molecules are synthesized. The most powerful drug inhibition of gastric secretion today is provided by this group of drugs. This group includes drugs: omeprazole (Gastrozole), pantoprazole, lansoprazole and rabeprazole.
Benzimidazole derivatives maintain pH values ​​in a range favorable for the healing of gastric or duodenal ulcers for a long period of time in 1 day. After a single dose of a standard dose of a proton pump inhibitor, the pH above 4 is maintained for 7-12 hours. The consequence of such an active reduction in acid production is the amazing clinical effectiveness of these drugs. Data from numerous clinical trials regarding omeprazole therapy are summarized in Table 2.
Anti-helicobacter therapy
In parallel with the development of the latest generation of antisecretory drugs, there was an accumulation of scientific data and clinical experience, which indicated the decisive importance of the Helicobacter pylori organism in the pathogenesis of peptic ulcer disease. Treatment that kills H. pylori is effective not only in healing the ulcer, but also in preventing recurrence of the disease. Thus, the strategy for treating peptic ulcer disease by eradicating H. pylori infection has an undeniable advantage over all groups of antiulcer drugs: this strategy provides long-term remission of the disease, and possible complete cure.
Anti-Helicobacter therapy has been well studied in accordance with the standards of evidence-based medicine. A large number of controlled clinical trials provide grounds for confident use of certain eradication regimens. The clinical material is extensive and makes it possible to conduct meta-analysis. I will cite the results of just one of the meta-analyses conducted under the auspices of the US Food and Drug Administration: R.J. Hopkins et al. (1996) concluded that in case of duodenal ulcer after successful eradication of H. pylori, relapses during long-term observation occur in 6% of cases (compared to 67% in the group of patients with persistent bacteria), and in case of gastric ulcer - in 4 % of cases versus 59%.
Modern approaches to the diagnosis and treatment of H. pylori infection, meeting the requirements of evidence-based medicine, are reflected in the final document of the conference, which took place in Maastricht on September 21-22, 2000. For the second time, the European Helicobacter pylori Study Group organized an authoritative meeting to adopt modern guidelines on the problem of H. pylori. The first Maastricht Agreement (1996) played a significant role in regulating the diagnosis and treatment of H. pylori in the European Union. Over the past 4 years, significant progress has been made in this area of ​​knowledge, which has forced the updating of previous recommendations.
The Second Maastricht Agreement puts gastric ulcer and duodenal ulcer in first place among the indications for anti-helicobacter therapy, regardless of the phase of the disease (exacerbation or remission), including their complicated forms. It is especially noted that eradication therapy for peptic ulcer disease is a necessary therapeutic measure, and the validity of its use in this disease is based on obvious scientific facts.
Indeed, eradication of H. pylori infection radically changes the course of the disease, preventing its relapse. Anti-helicobacter therapy is accompanied by successful healing of the ulcer. Moreover, the ulcer-healing effect is due not only to the active antiulcer components of eradication regimens (for example, proton pump inhibitors or ranitidine bismuth citrate), but also to the actual elimination of H. pylori infection, which is accompanied by the normalization of the processes of proliferation and apoptosis in the gastroduodenal mucosa. The Second Maastricht Agreement emphasizes that in uncomplicated duodenal ulcers there is no need to continue antisecretory therapy after a course of eradication therapy. A number of clinical studies have shown that after a successful eradication course, ulcer healing actually does not require further medication. It is also recommended to diagnose H. pylori infection in patients with peptic ulcer disease who are receiving maintenance or course therapy with antisecretory drugs, with the prescription of antibacterial treatment. Carrying out eradication in these patients provides a significant economic effect due to the cessation of long-term use of antisecretory drugs.
The outcome document of the 2000 Maastricht conference suggested for the first time that treatment for H. pylori infection should be planned without excluding the possibility of failure. Therefore, it is proposed to consider it as a single block, providing not only first-line eradication therapy, but also in case of persistence of H. pylori - second line at the same time (Table 3).
It is important to note that the number of possible anti-helicobacter therapy regimens has been reduced. For triple therapy, only two pairs of antibiotics are offered; for quadruple therapy, only tetracycline and metronidazole are provided as antibacterial agents.
First-line therapy: Proton pump inhibitor (or ranitidine bismuth citrate) at a standard dose 2 times a day + clarithromycin 500 mg 2 times a day + amoxicillin 1000 mg 2 times a day or metronidazole 500 mg 2 times a day. Triple therapy is prescribed for at least 7 days.
The combination of clarithromycin with amoxicillin is preferable to clarithromycin with metronadzole, as it can help achieve a better result when prescribing second-line treatment - quadruple therapy.
If treatment is unsuccessful, second-line therapy is prescribed: Proton pump inhibitor at a standard dose 2 times a day + bismuth subsalicylate/subcitrate 120 mg 4 times a day + metronidazole 500 mg 3 times a day + tetracycline 500 mg 4 times a day. Quad therapy is prescribed for at least 7 days.
If bismuth preparations cannot be used, triple treatment regimens based on proton pump inhibitors are proposed as a second course of treatment. If the second course of treatment fails, further tactics are determined on a case-by-case basis.
The treatment regimen of proton pump blocker + amoxicillin + nitroimidazole derivative (metronidazole) was excluded from the recommendations of the Second Maastricht Agreement. This combination is common in Russia, where metronidazole, due to its low cost and “traditional” use as a “reparant” for peptic ulcer disease, is an almost unchanged anti-Helicobacter agent. Unfortunately, in the presence of a H. pylori strain resistant to nitroimidazole derivatives, the effectiveness of this treatment regimen is significantly reduced, which has been proven not only in European studies, but also in Russia. Based on the results of a randomized controlled multicenter study, the purpose of which was to evaluate and compare the effectiveness of two triple therapy regimens: 1) metronidazole, amoxicillin and 2) omeprazole and azithromycin, amoxicillin and omeprazole in the eradication of H. pylori infection during exacerbation of duodenal ulcer. Eradication of infection in the group receiving metronidazole 1000 mg, amoxicillin 2000 mg and omeprazole 40 mg per day for 7 days was achieved in 30% of cases (confidence interval for the 95% probability was 17%-43%). We can only join the opinion of our European colleagues who excluded this scheme from the recommendations.
Unfortunately, eradication therapy for H. pylori infection is not 100% effective. Not all provisions of the Second Maastricht Agreement can be unequivocally agreed with and without thoughtful analysis they can be transferred to our country.
Bismuth-based eradication therapy regimens are currently not very widely used in Europe. However, the frequency of use of bismuth preparations in H. pylori eradication regimens varies across countries and continents. In particular, in the United States, triple therapy regimens containing bismuth are used to treat about 10% of patients. In China, regimens with a bismuth preparation and two antibiotics are in first place in terms of frequency of prescription. In his editorial in the European Journal of Gastroenterology and Hepatology, Wink de Boer (1999) rightly noted that “bismuth-based triple therapy is perhaps the most widely used in the world, as it is the only anti-Helicobacter therapy that is effective and economically accessible in developing countries.” countries of the world in which the majority of the world's population is concentrated.” Bismuth is also recommended for widespread use in the treatment of H. pylori infection in children.
In Russia, the most widely used bismuth preparation is colloidal bismuth subcitrate (De-nol); Research is being conducted to determine the effectiveness and safety of eradication regimens using it. In 2000, the results of a study conducted by the Russian group studying H. pylori were published. In this study, eradication therapy included colloidal bismuth subcitrate (240 mg 2 times a day) + clarithromycin (250 mg 2 times a day) + amoxicillin (1000 mg 2 times a day). The duration of therapy was 1 week, eradication of H. pylori was achieved in 93% of patients. A list of other possible regimens based on data from various clinical trials is given in Table 4.
Anti-Helicobacter therapy must be improved, and these recommendations are essential for its optimization.
Antibiotics specifically directed against H. pylori, probiotics and vaccines may be included in the arsenal of anti-Helicobacter therapy in the future, but at present these drugs and treatment approaches are under development, and practical recommendations do not exist.
Some new antibacterial drugs are of great interest, which have every chance of soon taking their rightful place in generally accepted eradication therapy regimens. A good example to illustrate the possibilities of optimizing a triple therapy regimen is azithromycin, a new drug from the macrolide group. Macrolide antibiotics, presented in triple eradication regimens mainly with clarithromycin, are perhaps the most effective. Therefore, azithromycin has been tried for a number of years as one of the possible components of therapy, but in early studies a relatively low dose of the drug was used. Increasing the course dose to 3 g led to an increase in the effectiveness of the standard seven-day triple regimen based on a proton pump inhibitor to the required level of more than 80%. In this case, the undoubted advantage is that as part of a weekly course, the full dose of azithromycin is taken over three days, once a day. This is convenient for the patient and reduces the percentage of side effects. In addition, in Russia the cost of azithromycin is lower than that of other modern macrolides.
Ributin, a derivative of rifamycin S, has demonstrated very high activity against H. pylori in vitro. In combination with amoxicillin and pantoprazole, ributin led to 80% eradication in patients treated at least twice (!) with a standard triple regimen.
Despite the fact that the reputation of nitroimidazoles is “tarnished” due to the high percentage of H. pylori strains resistant to them, research into this group of drugs continues. In in vitro experiments, the new nitroimidazole, nitazoxanide, proved to be highly effective against H. pylori, and the development of secondary resistance was not observed. In vivo studies should show how this drug can compete with metronidazole.
As an alternative to multicomponent regimens, several theoretical approaches have long been proposed, for example, drug blockade of urease, an enzyme without which the existence of bacteria is impossible, or blockade of the adhesion of a microorganism to the surface of epithelial cells of the stomach. A drug that inhibits urease has already been created; its activity has been shown in laboratory studies, including in enhancing the effect of antibiotics used in anti-Helicobacter therapy.
Drugs that inhibit H. pylori adhesion - such as rebamipide or ekabet - have been studied in combination with traditional anti-Helicobacter drugs. They statistically significantly increased the percentage of eradication compared to the same regimen without mucoprotective support. The use of dual therapy (proton pump inhibitor + amoxicillin) was abandoned due to low efficiency, and the addition of rebamipide or ecabet significantly increases the percentage of infection eradication. When strains with the phenomenon of multidrug resistance are isolated that are resistant to both metronidazole and clarithromycin, the combination of ecabet or rebamipide with dual therapy may become the treatment of choice.
The opportunities that successful human vaccination against H. pylori infection may offer are difficult to assess due to their magnitude. Advances in the development of a vaccine allow us to hope that vaccination will be available in the coming years. Tested vaccines in animal experiments protect them from infection by H. pylori and related species of the genus Helicobacter, and in some cases lead to the elimination of the microorganism. It has been established that several H. pylori antigens are required for successful immunization. Thanks to the complete decoding of the genome of the microorganism, the selection of these antigens is greatly simplified. In addition, a number of studies are aimed at improving the adjuvant system, which is essential for improving vaccine tolerability.

Aluminum hydroxide + magnesium hydroxide-
Almagel (trade name)
(Balkanpharma)

Omeprazole-
Gastrozol (trade name)
(ICN Pharmaceuticals)

Colloidal bismuth subcitrate
De-nol (trade name)
(Yamanouchi Europe)

Famotidine-
Kvamatel (trade name)
(Gedeon Richter)

Peptic ulcer (PU) is a chronic disease, the main morphological manifestation of which is a recurrent ulcer of the stomach or duodenum (DU), usually occurring against the background of gastritis.

In the pathogenesis of ulcer there is an imbalance between the factors of aggression (acid-peptic factor and Helicobacter pylori (HP)) and defense (gastric and duodenal mucus with all its components - glycoproteins, bicarbonates, immunoglobulins, etc.; high reparative activity of the mucous membrane and adequate its blood supply).

The pathogenetic mechanisms of ulcer formation can be presented as follows.

• Residual organic background and/or psychotraumatic situations and/or depression -> increased tone of the parasympathetic nervous system -> gastric hypersecretion -> formation of a peptic ulcer. Long-term course of PU->depression.
• G-cell hyperplasia as a congenital feature of the patient -> gastric hypersecretion -> formation of an ulcerative defect in DC.
• Colonization of HP in the antrum of the stomach in a patient sensitive to it -> development of G-cell hyperplasia -> gastric hypersecretion -> gastric metaplasia in the duodenum -> colonization of HP in the duodenum >
• Colonization of HP in the antrum of the stomach in a patient sensitive to it -> gastric hypersecretion without G-cell hyperplasia -> gastric metaplasia in the duodenum -> colonization of HP in the duodenum -> formation of an ulcerative defect in the duodenum.
• The possibility of ulcer formation with normal gastric acidity is also shown. The mechanism has not been sufficiently studied and is apparently associated with a decrease in protective mechanisms, for example, impaired microcirculation of the intestinal wall in patients with sympathicotonia.

The etiological factors of ulcers have been reviewed and clarified many times. Thus, the idea expressed in 1910 by Karl Schwartz: “No acid - no ulcer” was modified in 1989 into the following formulation: “No C. pylori - no ulcer” (D.Y. Graham).

Currently, HP is the leading etiological factor in ulcer disease. The frequency of Helicobacter-associated ulcer varies depending on the country (the lower the economic level of the country, the more common helicobacteriosis occurs), on the age of the patient (HP is most often infected at the age of 18-23 years in developed countries and at the age of 5-10 years in economically disadvantaged countries) . Colonization of the gastrointestinal tract (GIT) with Helicobacter does not always lead to the development of a pathological process (gastritis, duodenitis, ulcer, etc.). The body's response to HP depends on the state of a person's immunity, the composition of mucus in the stomach and duodenum, as well as a decrease in the number of receptors on the surface of the stomach that promote adhesion of the microorganism and the virulence of the HP strain (the ability to produce vacuolating toxin (VacA) and cytotoxin-associated protein (CagA), which contribute to the rapid destruction of epithelial cells with the destruction of subepithelial tissues and extracellular matrix).

The second most common cause of ulcers can be the use of NSAIDs and steroid therapy. There are other factors that provoke the development of ulcers - Solinger-Ellison syndrome, liver cirrhosis, Crohn's disease, etc.

The clinical picture of ulcer depends on the location (stomach or duodenum), as well as the age of the child. Thus, according to S.V. Golbits (1997), in the age group from 3 to 14 years, an atypical course is observed in 51.1% of cases, a “silent” course - in 19.5%, and the manifestation of the disease with complications - in 3.3 % children.

The main complaint with ulcer is pain. Its intensity depends on many factors: age, state of the nervous and endocrine systems, localization of the ulcer, and the patient’s individual sensitivity to pain. Gastric ulcers are often characterized by pain that occurs immediately after eating (early pain). Ulcers of the cardial part of the stomach and esophagus may be accompanied by pseudocardial pain, aggravated in the supine position, dysphagia, pain when food passes through the esophagus, and heartburn. With duodenal ulcer, the pain takes on a nocturnal and “hungry” nature, and decreases with food intake. The so-called Moynihan rhythm of pain appears (hunger-pain-eating-light interval-hunger-pain).

Dyspeptic disorders (heartburn, belching, vomiting, nausea) are less common in children than in adults. As the duration of the disease increases, the frequency of dyspeptic symptoms increases. Some patients have decreased appetite. Patients with duodenal ulcers often have a tendency to constipation or unstable stools.

With a long, recurrent course of ulcer, especially in children, asthenia and emotional lability develop.

The main diagnostic method for ulcerative disease is gastroduodenoscopy. In this case, the localization of the ulcer is determined (in a typical variant of duodenal ulcer in children, a single ulcer is localized on the anterior or posterior wall of the duodenum), the size of the ulcerative defect, and its shape. Additional research methods are pH-metry, determination of the patient’s vegetative status, determination of HP. pH-metry allows you to determine the acidity in the stomach and antrum. When performing daily pH measurements, it is possible to determine the daily rhythm of acid formation, which will allow you to prescribe an acid-suppressing drug during the period when acidity is highest.

Invasive and non-invasive methods are used to diagnose Helicobacter pylori infection. The first include:

• endoscopic examination with visual assessment of the condition of the mucous membrane of the stomach and duodenum;
• morphological method - determination of microorganisms in a mucous membrane preparation using special stains (Giemsa, tolluidine blue, Ghent, Warthin-Starry);
• bacteriological method - determining the strain of a microorganism, identifying its sensitivity to the drugs used;
• detection of HP in the mucous membrane of the stomach and duodenum using the polymerase chain reaction method.

Non-invasive methods:

• detection of specific anti-Helicobacter antibodies of classes A and G in the patient’s blood (enzyme-linked immunosorbent assay, rapid tests based on precipitation reactions or immunocytochemistry using capillary blood of patients) and other biological media (feces);
• breath tests with registration of HP waste products (carbon dioxide, ammonia) in exhaled air;
• detection of HP in analyzes of stool, saliva, and dental plaque using the polymerase chain reaction method.

In patients with gastroenterological complaints, dyspepsia, or abdominal pain, at least two non-invasive diagnostic tests should be performed to determine HP.

Therapy for ulcer is aimed at eliminating factors of aggression and is based on the following principles:

• suppression of gastric secretion and/or neutralization of it in the lumen of the stomach;
• anti-Helicobacter therapy;
• correction of the patient’s psychoneurological status;
• stimulation of reparative processes in the mucous membrane of the stomach and duodenum.

The use of drugs that reduce gastric acidity in the treatment of ulcers began a very long time ago. M-anticholinergics were among the first to be used for this purpose. Atropine blocked muscarinic receptors, stopping the effect of vagotonia. However, atropine is a non-selective M-anticholinergic drug that causes serious side effects. To solve this problem, the drug pirencepin (gastrocepin), which is a selective antagonist of M1-cholinergic receptors, was developed. It selectively inhibits the secretion of acid and pepsin, which is under the control of the vagus nerve, suppressing gastric secretion in humans. Unlike atropine, pirenzepine does not cause hypergastrinemia and reduces the concentration of gastrin in the blood during the gastric phase of digestion induced by distension of the gastric fundus or peptone.

The next group of drugs that relieve hyperacidity are H2 blockers. The first antihistamines appeared in the 1950s, but for a long time they had no effect on gastric secretion. In 1966, A. S. F. Ash and H. O. Schild of University College London stated that “no specific antagonists of the stimulatory action of histamine on gastric secretion have now been discovered.” The same scientists introduced the term “H1”, adopted to designate the receptors for which antihistamines of that time were effective, in order to distinguish them from the receptors through which histamine acts on gastric secretion. It was only in 1972 that James Black, a pharmacologist working for Smith Kline and French in Welwyn Garden City (England), after testing about 700 chemical compounds, announced that the compound burimamide, containing an imidazole ring in the side chain, acts on stomach receptors, not influencing H1 receptors. These receptors, later discovered not only in the stomach, were called H 2 receptors. Burimamide inhibited both pentagastrin and histamine-stimulated gastric secretion, which made it possible to identify histamine as the final link in the chain of transmission of stimulating impulses to the parietal cell. For the identification of H2 receptors and the further development of drugs that block them, James Black was awarded the Nobel Prize in 1988.

The first H2 blockers (cimetidine) had pronounced side effects: diarrhea, headache, transient arthralgia and myalgia, in addition - neutropenia and impaired sexual development in boys. In this regard, at present, 1st generation H2 blocker drugs are not used in pediatric practice.

Subsequent generations of drugs (ranitidine, famotidine) do not have these side effects. In general, the frequency of side effects when using them does not exceed 1%. Moreover, the activity of famotidine is 20-60 times higher than the activity of cimetidine and 3-20 times higher than the activity of ranitidine. Compared with ranitidine, famotidine is more effective at increasing pH and reducing gastric volume. It should be noted that the use of H 2 blockers in patients with duodenal ulcer with an initial normal gastrin level can lead to hypergastrinemia. When H 2 blockers are discontinued, a rebound effect occurs, as a result of which the withdrawal is carried out gradually, preferably under the control of daily pH measurements. Despite the pronounced antisecretory effect, H2 blockers do not completely block the synthesis of hydrochloric acid, since they affect only part of the mechanism involved in acid synthesis. At the same time, the secretion caused by histamine is reduced and there is no effect on secretion stimulants such as gastrin and acetylcholine.

Further work made it possible to develop a drug that directly affects the key mechanism of hydrochloric acid secretion - H + /K + -ATPase. Currently, proton pump inhibitors are widely used in gastroenterological practice, which are 2-10 times more effective than H2 blockers. The first proton pump inhibitor drug was omeprazole. Currently, drugs such as omeprazole (Losec, Omez), lansoprazole, pantoprazole, rabeprazole (Pariet) and esomeprazole (Nexium) are widely used.

Proton pump inhibitors (PPIs) in the tubules of parietal cells are converted to tetracyclic sulfenamide and bind to the cysteine ​​groups of the proton pump, which leads to enzyme inhibition and suppression of acid secretion. The restoration of secretion after the use of all proton pump inhibitors occurs due to the synthesis of a new enzyme and the restoration of disulfide bonds, when using pantoprazole - only due to the synthesis of a new enzyme protein. It takes about 18 hours for the parietal cell to synthesize a new enzyme protein. When administered orally, proton pump inhibitors must be protected from the effects of stomach acid, since they are unstable in an acidic environment. Therefore, capsules containing PPIs are coated with a coating that dissolves in an alkaline environment. Bypassing the stomach, they are quickly absorbed in the intestines in an alkaline environment and are redistributed between organs and tissues. Sulfenamide derivatives react with H + /K + -ATPase at different rates, which correlate with the rate of their conversion to sulfenamide and depend on pH: rabeprazole > omeprazole = lansoprazole > pantoprazole. At a pH of 5.0, pantoprazole is the most chemically stable and least activated, while rabeprazole is the least stable and has the greatest potency. At a pH of 4.0, all proton pump inhibitors are active, but rabeprazole will be the most effective. At pH = 3.0, inhibition is provided by all drugs, although pantoprazole will be less effective than the other four. PPI metabolism occurs mainly in the liver with the participation of CYP 2C19 and CYP 3A4, isoenzymes of cytochrome P450. The resulting metabolites are inactive and are excreted from the body. An exception is rabeprazole, which is metabolized without the participation of the CYP 2C19 and CYP 3A4 isoenzymes, which is apparently responsible for the constant value of its bioavailability after the first use. The clearance of omeprazole and esomeprazole is significantly lower than that of other PPIs. This is associated with an increase in the bioavailability of omeprazole and its stereoisomer esomeprazole and an increase in its therapeutic effectiveness. Polymorphism of the gene encoding the 2C19 isoform determines different rates of metabolism of proton pump inhibitors in patients. It is recommended to select the drug under the control of daily pH measurements. PPIs are prescribed 2 times a day immediately before meals.

HP eradication is carried out for all patients with ulcer. Eradication means the complete destruction of microorganisms, determined 6 weeks after treatment.

Currently, schemes based on national and regional recommendations created on the basis of the Maastricht Consensus are used.

• A 3-component treatment regimen for HP infection including colloidal bismuth subcitrate (de-nol) in combination with two antibiotics (clarithromycin and amoxicillin) or one antibiotic and nifuratel (macmiror) or furazolidone;
• A 3-component treatment regimen for HP infection using antisecretory drugs (proton pump blockers or H2-histamine blockers) in combination with two antibiotics (clarithromycin and amoxicillin) or with one antibiotic and nifuratel (Makmiror) or furazolidone;
• Quadruple therapy includes bismuth subcitrate, a PPI (or H 2 blocker) and two antibiotics (clarithromycin and amoxicillin) or one antibiotic and nifuratel (Makmiror) or furazolidone. Quadruple therapy is recommended if the triple regimen is ineffective, with Helicobacter strains resistant to antibiotics.

Treatment is prescribed for 7 days. Due to the possibility of side effects associated with the development of dysbiotic changes in the intestines, probiotics are included in the treatment regimen. The drugs of choice are complex probiotic agents, such as bifiform, linex. The latter contains antibiotic-resistant strains of three types of microorganisms ( Bifidobacterium infantis, Lactobacillus acidophilius, Streptococcus faecium), which allows colonization of the intestine at different levels.

After completion of treatment according to the eradication regimen, the issue of choosing maintenance therapy is decided. In case of multiple, repeated ulcers or a pronounced decrease in protective forces (for example, with long-term use of steroids), continue taking de-nol for up to 21 days. Longer-term PPI therapy is also indicated. With concomitant gastroesophageal reflux disease, with ulcer while taking NSAIDs, steroid drugs, the duration of antisecretory therapy is 6-8 weeks or more.

Antacids for ulcers have little effect on the pH level in the stomach and are prescribed as enveloping agents. In this regard, they choose products that have a gel base - phosphalugel, almagel neo. Take the drugs 3 times a day 1 hour after meals and 1 time at night.

Instead of antacids, you can use the drug smecta. Dioctahedral smectite has an enveloping and high sorbing ability (sorbs bacteria, HP bile acids), improves the rheological properties of mucus, increasing its viscosity, increasing the resistance of the mucous membrane to the effects of pepsin and hydrochloric acid. In addition, dioctahedral smectite has a cytomucoprotective effect. Smecta penetrates the mucous (mucin) layer of the intestine, interacts with the glycocalyx, increases the formation of a protective jelly-like layer and improves its quality. The duration of therapy can vary from 4 weeks (for an uncomplicated newly diagnosed single Helicobacter-associated ulcer) to the need for continuous use (for steroid therapy).

In case of impaired motility of the upper gastrointestinal tract, or inadequate functioning of the sphincters, prokinetics are prescribed. Domperidone (Motilium) and metoclopramide (Cerucal) cause a blockade of central and peripheral dopamine receptors, which prevents the relaxation of smooth muscles of the stomach and upper intestines normally caused by dopamine, and thereby increases the tone of the sphincters of the esophagus of the stomach and upper intestines, accelerating their emptying. due to increased cholinergic effects. The use of metoclopramide in pediatric practice is highly undesirable, as this drug has serious side effects. The only situation when metoclopramide is indispensable is emergency relief of vomiting, due to the fact that other prokinetics are not available in injectable forms. According to research results, cisapride, being a cholinomimetic, can cause the development of long Q-T interval syndrome and, as a consequence, the development of arrhythmia. In this case, secondary long Q-T interval syndrome develops due to a defect in the 3A4 isoenzyme of the cytochrome P 450 system. Therefore, patients suffering from severe gastroesophageal reflux, having a family history of cardiac arrhythmia, and also taking other drugs metabolized through the cytochrome P 450 system are not recommended to prescribe the drug or its administration should be carried out under the control of an electrocardiogram.

The drugs are prescribed 30-60 minutes before meals; as studies have shown, the duration of the course should be at least 1 month.

Correction of psychoneurological status is an obligatory component of ulcer therapy. To do this, cardiointervalography is performed to determine the vegetative status; consultation with a psychoneurologist is required to determine the psycho-emotional status and subsequent prescription of appropriate medications.

Therapy is monitored after 2-3 weeks. Next, maintenance treatment is prescribed. Previously used seasonal therapy is now rarely used. However, standards for maintenance therapy have not been developed. Patients are recommended to keep an observation diary in which to note exacerbations and the factors that provoke them (for example, exams at an educational institution), as well as the fulfillment of doctor’s prescriptions.

A. I. Khavkin, Doctor of Medical Sciences, Professor N. S. Zhikhareva
N. S. Rachkova
Research Institute of Pediatrics and Pediatric Surgery, Moscow

For questions regarding literature, please contact the editor.

The human body is a vulnerable structure that requires constant care. Unfortunately, people often do not pay due attention to the changes occurring in their health. In the majority, gradually developing into a chronic form.

Any use of the medicine is agreed with the supervising physician. The information below is for informational purposes before visiting a specialized medical facility.

Bismuth based circuit

The first regimen includes a multicomponent drug intake:

• denol;
• flemoxin;
• clarithromycin;
• erythromycin.

The course takes several days. The doctor establishes a certain procedure for taking medications, which the patient must follow for the next seven days. For example, on the first day the body is treated with denol and flemoxin. The frequency and dosage are clearly prescribed by the attending physician.

Inhibitor-based regimen

For an e-like regimen, drug treatment of peptic ulcer is determined by the following drugs:

• ompeprazole;
• flemoxin;
• clarithromycin.

The situation with the assignment is similar to that in the description of the first scheme. The doctor determines the dosage, method of handling medications and time of administration. Often the treatment regimen for stomach and duodenal ulcers looks like this: ompeprazole + flemoxin + clarithromycin. Sometimes such alternation undergoes changes depending on the opinion of the employee of the medical institution.

Regimen based on histamine blockers

In the context of the new treatment regimen, other drugs are used. For example, a doctor prescribes the use of famotidine, ranitidine, flemoxin.

Often the structure of the treatment regimen looks like this: Fa+(Ra)+Fl. Changes are at the discretion of the attending physician.

Quad therapy

For many members of the older generation, such a term is unfamiliar. This therapy is already firmly established among the possible treatment regimens offered to the patient.

For conventional therapy, a four-component treatment regimen consisting of 4 antibiotics is considered typical. During quadruple therapy, two antibacterial drugs are used: tetracycline and metronidazole. Fears caused by the reduction of existing treatment drugs will turn out to be unfounded. For effective treatment, these drugs are quite enough.

The duration of the treatment regimen for peptic ulcer disease can be limited to seven days; the result depends on how productive the doctor considers the therapy to be productive and suitable for a particular patient.

Is physical therapy necessary?

The described techniques will help many people get rid of the disease or prevent further development. In addition to these schemes, there is a popular procedure that is very controversial. We are talking about physiotherapy.

The difficulty is that some doctors consider this technique to be of secondary importance. The role of physical therapy is completely undefined; sometimes doctors do not see the need for procedures. Such therapy will not be superfluous, and may help consolidate the results obtained.

Physiotherapy is prescribed as an auxiliary procedure, for example, at the stage of remission. Suitable for prevention:

• magnetic therapy;
• electrosleep;
• hydrotherapy;
• heat therapy.

Although the role of the technique is not defined, selected patients eventually recognize that during these manipulations the necessary tone is returned to the body. In any case, treatment regimens do not negate physiotherapeutic assistance; such measures will help enhance the positive results of treatment for ulcer.

Catad_tema Peptic ulcer - articles

Satellite Symposium within
VIII Russian National Congress "Man and Medicine"
[April 5, 2001]

Modern regimens for eradication therapy of Helicobacter pylori infection

T.L. Lapina
Clinic of Propaedeutics of Internal Diseases, Gastroenterology and Hepatology named after. V.Kh.Vasilenko MMA named after. THEM. Sechenov

To carry out eradication therapy for Helicobacter pylori infection, the doctor must choose the optimal treatment regimen for a particular patient. Often this is not so simple, since it is important to take into account a number of factors: it is necessary to settle on a specific treatment regimen, select specific components of this regimen, establish the duration of treatment, analyze the clinical situation, and reasonably estimate the cost of the drugs included in the regimen.

The basic principles of eradication therapy for H. pylori infection are known. Let us quote them from the text of the “Recommendations for the diagnosis and treatment of Helicobacter pylori infection in adults with gastric and duodenal ulcers” of the Russian Gastroenterological Association and the Russian group for the study of H. pylori: The basis of treatment is the use of combination (three-component) therapy:

• capable of destroying Helicobacter pylori bacteria in controlled studies in at least 80% of cases;
• not causing forced withdrawal of therapy by the doctor due to side effects (acceptable in less than 5% of cases) or the patient stopping taking medications according to the regimen recommended by the doctor;
• effective for a course duration of no more than 7-14 days

Normative documents of health care authorities or expert consensus are intended to provide assistance to practitioners. They are based on clinical experience and data from randomized controlled trials. For a united Europe, such a normative document was the Report of the Consensus Conference on the diagnosis and treatment of diseases associated with H. pylori infection, adopted in Maastricht in 1996. In 1997, authoritative Russian recommendations were adopted. Modern approaches to the diagnosis and treatment of H. pylori infection, meeting the requirements of evidence-based medicine, are reflected in the final document of the conference, which took place in Maastricht on September 21-22, 2000. The European Helicobacter pylori Study Group convened for the second time an authoritative meeting to adopt modern guidance on the problem of H. pylori. In the 4 years since the adoption of the First Maastricht Agreement, significant progress has been made in this area of ​​knowledge, which has forced the updating of previous recommendations.

The Second Maastricht Agreement places gastric ulcer and duodenal ulcer in first place among the indications for anti-helicobacter therapy, regardless of the phase of the disease (exacerbation or remission), including their complicated forms. Eradication therapy for peptic ulcer disease is a necessary therapeutic measure, and the validity of its use in this disease is based on obvious scientific facts. The Second Maastricht Agreement emphasizes that in uncomplicated duodenal ulcers there is no need to continue antisecretory therapy after a course of eradication therapy. A number of clinical studies have shown that after a successful eradication course, ulcer healing does not require further medication. It is also recommended to diagnose H. pylori infection in patients with peptic ulcer disease who are receiving maintenance or course therapy with antisecretory drugs, with the prescription of antibacterial treatment. Carrying out eradication in these patients provides a significant economic effect, which is associated with the cessation of long-term use of antisecretory drugs.

MALT lymphoma, atrophic gastritis, and the condition after gastric resection for cancer are also indicated as indications for eradication therapy. In addition, anti-helicobacter therapy can be indicated for persons who are close relatives of patients with stomach cancer, and carried out at the request of the patient (after detailed consultation with a doctor).

The outcome document of the Maastricht Conference (2000) was the first to suggest that treatment for H. pylori infection should be planned with the possibility of treatment failure in mind. Therefore, it is proposed to consider it as a single block, providing not only first-line eradication therapy, but also in case of persistence of H. pylori - second line at the same time (see Table 1).

It is important to note that the number of possible anti-helicobacter therapy regimens has been reduced. For triple therapy, only two pairs of antibiotics are offered. For quadruple therapy, only tetracycline and metronidazole are prescribed as antibacterial agents.

First line therapy: Proton pump inhibitor (or ranitidine bismuth citrate) in a standard dose 2 times a day metronidazole 500 mg 2 times a day.

Triple therapy is prescribed for at least 7 days.

If treatment is unsuccessful, a Second line therapy: Proton pump inhibitor in a standard dose 2 times a day + Bismuth subsalicylate/subcitrate 120 mg 4 times a day + metronidazole 500 mg 3 times a day + tetracycline 500 mg 4 times a day. Quadruple therapy is prescribed for at least 7 days.

If bismuth preparations cannot be used, triple treatment regimens based on proton pump inhibitors are proposed as a second course of treatment. If the second course of treatment is unsuccessful, further tactics are determined on a case-by-case basis.

The final message of the Consensus Report is that H. pylori-specific antibiotics, probiotics, and vaccines may be part of the anti-Helicobacter therapy in the future, but currently these drugs and treatment approaches are in development and no practical recommendations exist.

The treatment regimen of proton pump blocker + amoxicillin + nitroimidazole derivative (metronidazole) was excluded from the recommendations of the Second Maastricht Agreement. This combination is common in Russia, where metronidazole, due to its low cost and “traditional” use as a “reparant” for peptic ulcer disease, is an almost unchanged anti-Helicobacter agent. Unfortunately, in the presence of a H. pylori strain resistant to nitroimidazole derivatives, the effectiveness of this treatment regimen is significantly reduced, which has been proven not only in European studies, but also in Russia. According to the results of a randomized controlled multicenter study, eradication of infection in the group receiving metronidazole 1000 mg, amoxicillin 2000 mg and omeprazole 40 mg per day for 7 days was achieved in 30% of cases (confidence interval for the 95% probability was 17%-43%) ( V.T. Ivashkin, P.Ya. Grigoriev, Yu.V. Vasiliev et al., 2001). Thus, one can only join the opinion of European colleagues who excluded this scheme from the recommendations.

Unfortunately, eradication therapy for H. pylori infection is not 100% effective. Not all provisions of the Second Maastricht Agreement can be unequivocally agreed with, and without thoughtful analysis they can be transferred to our country.

Thus, Russian doctors often use triple therapy regimens based on bismuth as first-line treatment. A multicenter study of the Russian group for the study of H. pylori (2000) showed the availability and effectiveness of this approach in our country, including the example of the colloidal bismuth subcitrate + amoxicillin + furazolidone regimen.

Anti-Helicobacter therapy must be improved, and the Second Maastricht Agreement is essential for its optimization.

Table 1. SCHEMES FOR ERADICATION THERAPY OF Helicobacter pylori INFECTION
under the Maastricht Agreement (2000)

First line therapy Triple therapy
Pantoprazole 40 mg 2 times a day + clarithromycin 500 mg 2 times a day + amoxicillin 1000 mg 2 times a day or + clarithromycin 500 mg 2 times a day +	Ranitidine bismuth citrate 400 mg 2 times a day + clarithromycin 500 mg 2 times a day + amoxicillin 1000 mg 2 times a day or + clarithromycin 500 mg 2 times a day + metronidazole 500 mg 2 times a day
Second line therapy Quad therapy
Omeprazole 20 mg 2 times a day or Lansoprazole 30 mg 2 times a day or Pantoprazole 40 mg 2 times a day + Bismuth subsalicylate/subcitrate 120 mg 4 times a day + metronidazole 500 mg 3 times a day + tetracycline 500 mg 4 times a day

Literature

1. Recommendations for the diagnosis of Helicobacter pylori in patients with peptic ulcer disease and methods of their treatment. // Russian Journal of Gastroenterology, Hepatology and Coloproctology. – 1998. - No. 1. – p.105-107.
2. Current European concepts in the management of Helicobacter pylori infection. The Maastricht Consensus Report. // Gut. – 1997. – Vol. 41. – P.8-13.