Combination therapy for peptic ulcer disease. Histamine receptor blockers

Without treatment, peptic ulcer disease threatens dangerous complications up to fatal outcome. The disease does not go away on its own, and even in long periods remission pathological changes in tissues continue, although much more slowly. Modern techniques allow you to quickly eliminate characteristic manifestations ulcers, stop effectively possible complications and avoid relapse. The treatment regimen is selected taking into account the phase of the disease, existing complications, severity and other important factors.

Gastric ulcer, treatment

For ulcers, only comprehensive treatment, including diet, drug therapy and limitation of psycho-emotional factors, provides an effect. Individually, these components cannot completely eliminate the disease and provide only short-term relief of symptoms.

Therapy peptic ulcer is based on the following principles:

  • active influence on the cause of the disease;
  • selection medicines taking into account concomitant pathologies;
  • taking into account the individual characteristics of the patient (activity and age of the patient, presence allergic reactions on medications used, body weight);
  • compliance with the treatment regimen;
  • nutrition with mechanical and chemical sparing of the mucous membrane;
  • the use of herbal and physiotherapy;
  • local treatment individual ulcerative formations.

The ulcer was initially treated with H2-blockers, and the same drugs were prescribed to prevent relapse. The sensitivity of bacteria to them was quite high, but due to acidic environment stomach, most blockers lost their effectiveness. And the availability adverse reactions did not allow increasing the concentration of drugs. As a result, instead of monotherapy, they began to use a two-component treatment regimen, combining drugs with a high bactericidal effect and agents that are resistant to an acidic environment.

Then even more was developed efficient scheme– three-component, which is currently considered classic, if the disease is caused by a bacterium Helicobacter pylori. Therapy includes taking proton pump inhibitors (standard dose - 2 times a day, the drug Nexium (esomeprazole) is most often used, but omeprazole, rabeprazole can also be used), antibiotics clarithromycin (500 mg 2 times a day) and amoxicillin (1000 mg 2 times a day).

The second-line regimen, or quadruple therapy, includes taking tripotassium bismuth dicitrate (this is De-Nol, 120 mg 4 times a day), combined with a PPI (at a standard dose 2 times a day), tetracycline (500 mg 4 times a day). day) and metronidazole (500 mg 3 times a day). The duration of quadruple therapy with bismuth preparations is 10-14 days.

Also, second-line therapy is triple with levofloxacin (500 or 250 mg 2 times a day), in addition to it, the patient takes a PPI at a standard dose 2 times a day and amoxicillin 1000 mg 2 times a day. Duration of therapy is 10 days.

Is there some more alternative scheme, where the doctor determines the individual sensitivity of the pathogenic bacterium to antibiotics, then prescribes the drug to which Helicobacter pylori has no resistance. Regardless of the option chosen, the patient must be under the supervision of a physician to avoid various complications and maintain ability to work.

Drug therapy for peptic ulcer disease is divided into two types: treatment acute processes and relapse prevention. Exacerbations are treated with several groups of medications that relieve inflammation and promote healing of ulcers.

Functions and name of the drugBasic properties

Reduces the acidity of stomach contents, relieves painful manifestations, protect epithelial cells. Are different quick action, increase mucus production, accelerate fermentation. If the disease is mild and there is no Helicobacter pylori infection, drug therapy limited to these means

Reduce the acidity of the stomach contents, preventing the movement of hydrogen ions. Currently considered the safest and effective means for peptic ulcer disease

They increase the protective functions of the gastric mucosa, prolong the life of epithelial cells, and increase the amount of glycoproteins in the mucus. Promotes scarring of ulcers and shortens the course of treatment

To prevent relapse (the main cause of ulcers is Helicobacter pylori infection), a special three-component therapy is carried out to completely destroy the causative agent of the disease:


Treatment regimens

Pathologies caused by Helicobacter pylori infection are cured faster than other types of ulcers. The most commonly used are seven-day and ten-day treatment regimens. The classic 14-day regimen is used much less frequently.

10-day scheme

Name of the drugDosage

5 times a day, 108 mg after meals

200 mg 5 times a day after meals

250 mg 5 times after meals

The course of treatment depends on the location of the ulcer: for a gastric ulcer it is 7 weeks, for a duodenal ulcer it is 5 weeks.

If the cause of the ulcer is not the bacterium Helicobacter pylori, the treatment regimen is slightly different. As a rule, this is a two-component therapy, the goal of which is to relieve the symptoms of the disease and ensure scarring of the ulcer.

At the end of the twentieth century. A significant step has been taken towards changes in the principles of treatment of peptic ulcer disease (PU). The success of modern approaches to therapy is associated primarily with the use of new antisecretory drugs and eradication regimens Helicobacter pylori(NR). Currently, pharmacotherapy for ulcers includes more than 500 various drugs and about 1000 of their combinations. Modern concept treatment of ulcer involves active therapeutic tactics, including multicomponent drug regimens And long-term use medications according to indications.

An important component of modern pharmacotherapy for peptic ulcers is the absence of fundamental differences in approaches to the treatment of gastric ulcers and duodenum. The basic principles of therapy for peptic ulcer disease are:

Currently, in the pathogenesis of ulcers, especially duodenal ulcers, great importance give infectious agentH. pylori. Epidemiological data obtained in various countries indicate that 100% of duodenal ulcers and more than 80% of ulcers localized in the stomach are associated with persistent HP.

Many studies confirm that anti-Helicobacter therapy leads to a decrease in the frequency of relapses of gastric ulcer (GUP) and duodenal ulcer (DU). The strategy for treating ulcer using eradication of HP infection has undeniable advantages over therapy with all groups of antiulcer drugs, since it provides long-term remission diseases and possibly complete cure. Anti-Helicobacter therapy is well studied in accordance with the standards evidence-based medicine. Modern approaches to the diagnosis and treatment of infection H. pylori, meeting the requirements of evidence-based medicine, are reflected in the final document of the second Maastricht consensus, adopted in September 2000. The main differences between the current document and the agreement five years ago are several important points.

  • Treatment of infection for the first time H. pylori, and therefore the diseases associated with it, are the responsibility of the doctor general practice, and not to a gastroenterologist, as was previously accepted. The competence of a gastroenterologist includes only those cases where treatment of the disease, including using second-line therapy, was unsuccessful, as well as cases that clearly require specialist intervention.
  • For the first time, two-stage treatment was introduced: when choosing a first-line regimen, the doctor must simultaneously immediately plan reserve therapy.
  • It is recommended to use anti-Helicobacter therapy in patients functional dyspepsia, as well as in cases where long-term therapy with non-steroidal anti-inflammatory drugs is planned.
  • Patients with uncomplicated duodenal ulcer are recommended to be prescribed only recommended courses of anti-Helicobacter therapy, without subsequent use of antisecretory drugs.

The main criterion for choosing anti-Helicobacter therapy is its expected effectiveness, providing a high percentage of eradication (more than 80%).

  • If the treatment regimen used did not achieve eradication, it should not be repeated according to this regimen.
  • If the regimen used does not lead to eradication, this means that the bacterium has acquired resistance to one of the components of the treatment regimen.
  • If the use of one and then another treatment regimen does not lead to eradication, then the sensitivity of the HP strain to the entire range of antibiotics used should be determined.

Accepted by the Russian Gastroenterological Association in 1998. national recommendations on the diagnosis and treatment of Helicobacter pylori infection and mass familiarization of doctors with them have not yet led to a decrease in the number of strategic and tactical errors in determining indications for eradication and choosing adequate anti-Helicobacter regimens (see Table 1).

Table 1. Errors in the treatment of HP infection.

What does a doctor need to know when starting anti-Helicobacter therapy? Every general practitioner, especially those with more than five years of experience, will most likely have to overcome some psychological barrier before prescribing antibiotics to a patient with a peptic ulcer. Today, gastroenterologists and therapists still have different attitudes towards anti-Helicobacter therapy for ulcerative disease. Strict, strict adherence to the anti-Helicobacter treatment regimen is necessary. Their effectiveness has been proven, they correspond to the characteristics of HP and the pharmacokinetics of the drugs, and the side effects of such therapy are also known.

It is better not to carry out anti-Helicobacter therapy at all, rather than to carry it out incorrectly - since in this case, HP resistance to a number of components quickly develops. In this regard, the patient must be told in detail about the upcoming treatment and obtain his consent to cooperate with the doctor. It is also important to assess the patient’s financial capabilities. He should know that thanks to expensive, one-time treatment, it will be possible to achieve stable remission in patients with duodenal ulcer in 70-80% of cases, and in case of ulcerative ulcer - in 50-60%, which is ultimately cost-effective.

Which eradication scheme to choose? If there is a stomach or duodenal ulcer against the background of increased acid production, then preference should be given to classic three-component regimens based on a proton pump blocker (PPI) (omeprazole, etc.). Then it is possible to switch to a single dose of PPI without antibacterial drugs. You should not use regimens containing nitroimidazoles (metronidazole, tinidazole) if you have a history of drugs from this group being prescribed for other indications.

Currently in Russia there is sharp increase number of HP strains resistant to nitroimidazoles. With this in mind urgent task Today, a search for more effective HP eradication regimens seems to be possible. Therefore in last years There is growing interest in the use of macrolides in the treatment of HP-associated diseases. Numerous studies have shown the effectiveness of using macrolide antibiotics for the treatment of HP. These drugs have a high ability to penetrate cells and are intensively released onto the mucous membranes (MS), which increases their effectiveness against HP. In addition, macrolide antibiotics have fewer contraindications, as well as side effects, they have a higher eradication rate than tetracyclines, which can also accumulate in cells. The peculiarity of HP infection is that it is accompanied by hyperacidity.

In this regard, most macrolide antibiotics undergo increased hydrolysis and cannot be used. The exception is clarithromycin, which is resistant to of hydrochloric acid.

Therefore, the purpose of our study was to develop new eradication therapy regimens for duodenal ulcer associated with H. pylori, using omeprazole (O), as well as a combination of amoxicillin (A) and clarithromycin (K). We used the following eradication regimen - Ultop (omeprazole) 20 mg twice a day + Fromilid (clarithromycin) 500 mg twice a day + Hiconcil (amoxicillin) 1000 mg twice a day - a course of seven days. Eradication was 90%. The study showed that the use of fromilid (clarithromycin) is effective and advisable in anti-Helicobacter therapy regimens using PPIs.

Data from numerous studies and the results of their meta-analysis allowed us to conclude that the inclusion of antisecretory drugs in HP infection eradication regimens not only improves HP eradication when combined with antibiotics, but also helps accelerate ulcer scarring and allows for faster elimination of the symptoms of ulcerative dyspepsia. As for the specific mechanisms for increasing the effectiveness of eradication due to the use of antisecretory drugs, then, first of all, with an increase in the pH of the gastric contents, the minimum inhibitory concentration of antibiotics (MIC) decreases and their effectiveness accordingly increases. The viscosity of gastric juice and the concentration of antibiotic in gastric contents also increase, which increases the exposure time of antibacterial drugs to bacteria. H. pylori. We studied the effectiveness of ultope (omeprazole) - pH > 4 of the gastric contents with a single dose of 20 mg lasted for 12-14 hours (see Figure 1).

However, first-generation PPIs do not fully meet the practical needs of clinicians. They are slowly converted into the active form and create the maximum antisecretory effect for eradication only by the fifth to eighth day of therapy. Drugs in this class also include lansoprazole, pantoprazole, rabeprazole and esomeprazole. They bind to enzymes cell wall parietal cells - H+, K+ -ATPase, and are the most by powerful means, controlling gastric acid formation.

Using pH-metry, the effect of a new drug was studied in HP-negative volunteers. dosage form Losek MAPS. After a course of treatment with this drug, the antisecretory effect

V daytime turned out to be even more pronounced than with the use of pantoprazole. However pharmaceutical companies, who continued the search for new, more effective antisecretory agents, created new drug- Nexium. The antisecretory effect of Nexium is superior in severity, speed of onset and duration of action to the similar effect of omeprazole in standard doses of 20 and 40 mg, pantoprazole 40 mg and lansoprazole 30 mg.

In connection with the above, a new PPI, Pariet (rabeprazole), is of great interest. In the treatment of peptic ulcer and duodenum, it is recommended to take pariet at a dose of 40 mg once a day or 20 mg every 12 hours. The most effective, fast-acting antisecretory and antibacterial drug in eradication regimens is pariet at a dose of 20 mg twice a day. It does not need to be prescribed seven days before starting antibiotic treatment, as is the case with other PPIs, since a reliable antisecretory effect is achieved already on the first day of treatment (from the recommendations of the Russian Gastroenterological Association).

Unfortunately, the presence of HP resistance to antibiotics in some patients forces researchers to develop alternative options treatment of patients suffering from peptic ulcer disease associated with H. pylori.

Thus, we have studied the effectiveness of eradication schemes using reserve antibacterial drugs. Best result eradication (90%) was achieved using the following regimen: de-nol 240 mg twice a day, 14 days + tetracycline 1 g/day and furazolidone 200 mg twice a day, seven days.

Quite often the question arises about the need for eradication therapy in elderly and old age. Today, this can be attributed to the fact that with long-term persistence of NRs they develop intestinal metaplasia and atrophy of the gastric mucosa, the risk of developing gastric carcinoma increases. Age characteristics enzymatic activity and atrophic processes in the gastrointestinal tract intestinal tract also change the rate of biotransformation medicines, disrupt their absorption. It was noted that the concentration of ranitidine increases in patients over 60 years of age with concomitant pathology of the hepatopancreatobiliary region.

"Achilles' heel" conservative treatment Peptic ulcer disease is known to have a high complication rate. It has been proven that HP eradication completely prevents complications of peptic ulcer disease. Thus, in the course of four large studies, the course of peptic ulcer disease was studied in patients in whom it manifested itself with bleeding (see Figure 2). As can be seen from the data presented, any other type of treatment does not exclude danger rebleeding, - within a year after the previous bleeding, it recurs in approximately every third patient. In the case of HP eradication, bleeding does not recur at all (see Figure 2).

Evaluation of the effectiveness of eradication is carried out after completion of treatment and is aimed at identifying vegetative and coccal forms H. pylori. The “Recommendations” clearly define the scheme for carrying out this diagnostic stage:

  • timing - no earlier than four to six weeks after the end of the course of anti-Helicobacter therapy, or after treatment of concomitant diseases with any antibiotics or antisecretory agents;
  • diagnosis of eradication is carried out using at least two of the following diagnostic methods, and when using methods that make it possible to directly detect bacteria in biopsy material (bacteriological, histological, urease). It is necessary to study two biopsy specimens from the body of the stomach and one biopsy specimen from the antrum.

The role cannot be underestimated antacids in the treatment of peptic ulcer and duodenum. These drugs, known since ancient times, reduce the acidity of gastric juice due to chemical interaction with acid in the stomach cavity. Preference is given to non-absorbable antacids - almagel, maalox, phosphalugel, talcid, rutacid. With exacerbation of peptic ulcer and duodenum in complex treatment we used rutacid at a dose of 500 mg three times a day + one tablet before bed. While taking this drug, symptoms gastric dyspepsia disappeared

by the end of the first or second day of treatment. Despite the introduction to medical practice modern inhibitors of gastric secretion, antacids retain their importance as effective remedy treatment of patients with peptic ulcer and duodenum.

As a result of treatment, complete clinical and endoscopic remission should be achieved, with negative results HP testing.

It should be noted that we very rarely encounter cases where a patient has an isolated ulcer. Treatment of combined pathology is associated with a number of problems.

Sometimes conservative therapy turns out to be ineffective. This may be due to two factors: the often recurrent course of peptic ulcer disease and the formation of refractory gastroduodenal ulcers. The analysis revealed the reasons for frequent relapses during ulcerative disease, these are HP infection, use of non-steroidal anti-inflammatory drugs, a history of complications of ulcerative ulcer, as well as low compliance. The factors listed above, as well as the latent Zollinger-Ellison syndrome, may be factors contributing to the formation of refractory gastroduodenal ulcers.

In conclusion, we should once again emphasize the extreme importance of developing domestic standards for the treatment of peptic ulcers and duodenal ulcers and their early implementation in the practice of a general practitioner and gastroenterologist. Important arguments in favor of anti-Helicobacter treatment were obtained when assessing the cost/effectiveness ratio. Peptic ulcer is widespread and characterized by a chronic relapsing course. Eradication H. pylori reduces both direct and indirect costs of ulcerative disease, eliminating the need for expensive maintenance treatment with antisecretory drugs, reducing the risk of repeated exacerbations, complications and, in some cases, surgical treatment.

Thus, modern drug therapy Peptic ulcer of the duodenum and gastrointestinal tract can ensure a relapse-free course of these diseases and relieve patients from complications. In most cases, outpatient treatment is sufficient. The success of therapy depends not only on prescribing the optimal drug combination, but also, to a large extent, from its implementation with the participation of the patient.

Literature.
  1. Vertkin A.L., Masharova A.A. Treatment of peptic ulcer disease in a modern clinic // Attending physician, October 2000, No. 8. - pp. 14-19.
  2. Grigoriev P. Ya., Yakovenko E. P., Agafonova A. et al. Pyloric helicobacteriosis: diagnosis, treatment // Attending Physician, June 2002, No. 6. - P. 3-8.
  3. Erashchenko P. P., Snegova E. A., Churilin Yu. Yu. Pharmacoeconomic justification for the use of rabeprazole (Pariet) for peptic ulcer // Clinical pharmacology and therapy, 2001, 10 (1). - pp. 42-46.
  4. Ivashkin V. T. Prevention and treatment chronic diseases upper sections gastrointestinal tract. - M.: "MEDpress - inform", 2002. - P. 127.
  5. Isakov V. A, Shcherbakov P. L. Comments on the Maastricht Agreement." - 2, 2000//V International Symposium "Diagnostics and treatment of diseases associated with H. pylori.", Pediatrics, No. 2, 2002. - P. 5 -7.
  6. Kokueva O. V., Stepanova L. L., Usova O. A. et al. Pharmacotherapy of peptic ulcer disease taking into account concomitant pathology gastrointestinal tract // Experimental and practical gastroenterology, 1/2002. - P. 49-52.
  7. Koltsov P. A., Zadionchenko V. S. Pharmacotherapy of chronic diseases of the digestive system // Practical guide. - M., 2001. - P. 200.
  8. Lapina T. L., Ivashkin V. T. Modern approaches to the treatment of gastric and duodenal ulcers // Russian Medical Journal. - T. 3, No. 1, 2001. -
  9. 10-15.
  10. Lapina T. L. Modern approaches to the treatment of acid-dependent and H. pylori - associated diseases // Clinical perspectives of gastroenterology and hepatology. 1, 2001. -
  11. 21-27.
  12. Pimanov S.I. Esophagitis, gastritis, and peptic ulcer - N. Novgorod, 2000. - 376 p.
  13. Strachunsky L. S., Kozlov S. N. Macrolides in modern clinical practice. - Smolensk, 1998. - 303 p.

I. V. Mayev, doctor medical sciences, Professor MGMSU, Moscow

A stomach ulcer is chronic pathology, often recurrent, the main symptom of which is the formation of an ulcerative defect in the wall of the stomach, penetrating into the submucosal layer. This pathology occurs with alternating periods of exacerbation and remission.

IN developed countries the incidence of the disease is approximately 10-15% among the population, which is very big numbers. There is also a trend towards an increase in pathology among women, although previously it was believed that stomach ulcers were predominantly male disease. Mostly people between 30 and 50 years old suffer from this pathology.

Why and how does an ulcer develop?

Helicobacter pylori infection The main reason for the development of the disease. This spiral-shaped bacterium causes 45-75% of all cases of stomach ulcers. The source of infection is a sick person or a bacteria carrier. The microbe can be transmitted through:
  • saliva (when kissing)
  • dirty dishes
  • food contaminated water
  • poorly sterilized medical instruments(for example, fibrogastroscope)
  • from mother to fetus
Due to taking medications The second most common cause of pathology. These medications include:
  • non-selective non-steroidal anti-inflammatory drugs – acetylsalicylic acid(aspirin), indomethacin, ketoprofen, butadione;
  • corticosteroids – prednisolone, dexamethasone, betamethasone, methylprednisolone;
  • cytostatics – imuran, azathioprine, fluorouracil;
  • potassium preparations – potassium chloride, asparkam;
  • antihypertensive drugs central action– reserpine.
As a complication of various chronic diseases
  • hyperparathyroidism
  • tuberculosis
  • Crohn's disease
  • chronic renal failure
  • diabetes
  • sarcoidosis
  • lungs' cancer
  • chronic viral hepatitis
  • pancreatitis
  • Chronical bronchitis
  • celiac disease
  • syphilis
As a result acute diseases and conditions (so-called “stress ulcers”)
  • all types of shocks
  • extensive burns
  • frostbite
  • sepsis
  • acute renal and
  • injuries
Social reasons
  • negative emotions
  • constant stress
  • gross errors in nutrition
  • alcohol and cigarette abuse
  • financial well-being

What are the types of stomach ulcers?

Symptoms of a stomach ulcer

Signs of pathology can be quite varied; they depend on the size and location of the defect, individual sensitivity to pain, the phase of the disease (exacerbation or remission), the presence of complications, the age of the patient and concomitant pathology.

Pain is the main symptom of a stomach ulcer. The pain syndrome has some features:

  • pain can be early (in the first couple of hours after eating, if the defect is located in the body or cardia of the stomach), late (more than two hours, usually when localized in the pylorus), fasting or hungry (disturbed before meals) and night (usually appear during second half of the night);
  • pain may appear and disappear, depending on the activity of the inflammatory process;
  • pain tends to worsen in spring and autumn;
  • by nature it can be sharp, cutting, pulling, stabbing, blunt, and so on;
  • the pain goes away after taking antisecretory medications and antacids;
  • its intensity varies, from slight indisposition to unbearable sensations;
  • usually experiences pain in the epigastrium, left side chest, behind the sternum, left arm or in the back. Atypical localization pain is right hypochondrium, lumbar region, small pelvis.

It should be remembered that about 20% of patients do not have pain syndrome. This usually happens in old age, when diabetes mellitus, taking NSAIDs.

Other signs of peptic ulcer:

  • heartburn is a burning sensation in the epigastric region. The reason for its appearance is the entry of aggressive acidic gastric contents into the lumen of the esophagus;
  • nausea and vomiting are caused by impaired gastric motility. Vomiting occurs a couple of hours after eating and causes relief;
  • belching is a sudden involuntary reflux of a small amount of gastric juice into the oral cavity. It is characterized by a sour or bitter sensation in the mouth. Belching occurs due to disruption of the cardiac sphincter.
  • loss of appetite– appears due to a violation motor function Gastrointestinal tract or a person consciously refuses to eat for fear of pain;
  • constipation – delay in bowel movements for more than 2 days. Occurs due to increased secretion of hydrochloric acid and retention of food in the stomach;
  • feeling of heaviness in the stomach, occurring after eating;
  • fast saturation;
  • feeling of bloating.

Complications

Like many other diseases, stomach ulcers can have complications, sometimes quite dangerous. These include:

Penetration

Penetration is the destruction of the stomach wall, with the adjacent organ becoming the bottom of the ulcer. This is usually the pancreas. Hydrochloric acid and pepsin destroy its structure, causing acute destructive pancreatitis. The first symptoms of penetration are sharp girdle pain in the abdomen, fever and an increase in alpha-amylase in the blood.

Perforation

Perforation is the destruction of the wall of an organ and the entry of its contents into the abdominal cavity or retroperitoneal space. Occurs in 7-8% of cases. Violation of the integrity of the wall can be caused by heavy lifting, heavy physical labor, consumption of fatty and spicy food, booze. Clinical picture characterized by all the signs of diffuse peritonitis ( general weakness, abdominal pain throughout, intoxication and others).

Plain radiography helps diagnose gastric perforation abdominal cavity V vertical position! On it you can see a disc-shaped clearing (gas) under the dome of the diaphragm.

Malignancy

Malignancy is the degeneration of an ulcer into stomach cancer. This complication occurs infrequently, in approximately 2-3% of patients. It is noteworthy that duodenal ulcers never transform into malignant tumor. As cancer develops, patients begin to lose weight, they develop an aversion to meat foods, and their appetite is reduced. Over time, symptoms of cancer intoxication appear (fever, nausea, vomiting), pallor skin. A person may lose weight to the point of cachexia ( complete exhaustion organism).

Pyloric stenosis

Pyloric stenosis occurs if the ulcerative defect is localized in the pyloric region. The pylorus is the narrowest part of the stomach. Frequent relapses lead to scarring of the mucous membrane and narrowing pyloric region. This leads to disruption of the passage of food into the intestines and its stagnation in the stomach.

There are 3 stages of pyloric stenosis:

  • compensated– the patient has a feeling of heaviness and fullness in the epigastric region, frequent belching sour, but the general condition remains satisfactory;
  • subcompensated– patients complain that even a small meal causes a feeling of fullness and heaviness in the abdomen. Vomiting occurs frequently and provides temporary relief. Patients lose weight and are afraid to eat;
  • decompensated– general condition is severe or extremely serious. The food eaten no longer passes into the intestines due to complete narrowing of the pylorus. Vomiting is profuse, repeated, and occurs immediately after eating foods. Patients are dehydrated, they experience weight loss, impaired electrolyte balance and pH, muscle cramps.

Bleeding

Gastrointestinal bleeding occurs due to destruction of the vessel wall at the bottom of the ulcer (see). This complication is quite common (about 15% of patients). Clinically it manifests itself as vomiting " coffee grounds", melena and common features blood loss.

“Coffee grounds” vomiting gets its name from the fact that blood entering the lumen of the stomach enters chemical reaction with hydrochloric acid. And in appearance it becomes brown-black with small grains.

Melena is tarry or black stool (see). The color of stool is also due to the interaction of blood with gastric juice. However, it should be remembered that some medications (, Activated carbon) and berries (blackberries, blueberries, black currants) can turn the stool black.

Common signs of blood loss include general pallor, decreased blood pressure, . The skin becomes covered with sticky sweat. If the bleeding is not controlled, the person may lose too much blood and die.

How to identify the disease?

The patient's complaints and medical history help the doctor suspect a peptic ulcer. However, in order to accurately diagnose the disease, therapists prescribe a number of special procedures.

Methods for detecting stomach ulcers:

  • General analysis blood— Decrease in the number of red blood cells and hemoglobin (anemia), increased ESR
  • Fibroesophagogastroduodenoscopy (FEGDS)— Using a special rubber tube with a camera (fibrogastroscope), the doctor can with my own eyes see the condition of the mucous membrane digestive tract. This method also allows you to perform a biopsy of the organ wall, that is, pinch off a small piece from it.
  • X-ray of the stomach with contrast— The technique is currently somewhat outdated. Its essence is as follows: the patient drinks a barium contrast mixture. The radiologist then takes a series of pictures that show how the contrast moves through the mucosa. The presentation of a peptic ulcer is usually described as a “niche symptom.”
  • pH-metry and daily monitoring Gastric pH“This is an invasive and painful technique that allows you to assess how aggressive gastric juice is in relation to the mucous membrane.

Methods for identifying Helicobacter:

  • Serological - Detection of antibodies in the blood to H. pylori
  • Radionuclide urease breath test— Based on the release of urea by the microbe, which comes out with the air. The technique is safe; to detect Helicobacter, you only need to breathe into a special container.
  • Stool test - Detection of Helicobacter antigen in stool, used to determine the effectiveness of treatment
  • Rapid urease test— Performed after fibrogastroscopy. The resulting piece of mucous membrane is tested with a special indicator that detects H. pylori

Treatment of stomach ulcers

Therapy for this disease is multicomponent. It is mandatory to eradicate (destruct) Helicobacter pylori, reduce the acidity of gastric juice, eliminate unpleasant symptoms(heartburn, nausea) and prevention of complications.

Antibiotic therapy

When the connection with Helicobacter pyloris peptic ulcer has been proven, treatment cannot be accomplished without the use of antibiotics. Previously, it was believed that treatment should last until the microbe completely disappeared, which was confirmed by:

  • blood test for antibodies
  • sowing
  • urease test for FGDS

Then it turned out that not all types of Helicobacter cause the disease, and their complete destruction cannot be achieved, since when they die in the duodenum and stomach, it moves lower into the intestines, leading to inflammation and severe dysbiosis. Re-infection is also possible when using shared utensils and during the FGDS procedure, which should be performed only according to strict indications.

Today, it is advisable to carry out 1 or 2 courses of antibiotic therapy, if after the first course the bacteria are not killed, a different treatment regimen is selected, the following drugs are used:

  • Macrolides (Clarithromycin)
  • Semi-synthetic penicillins (Amoxicillin)
  • Tetracycline
  • Nitroimidazole derivatives (Metronidazole) for proven Helicobacter infection

Antisecretory drugs

  • Antacids - Almagel, Maalox, sucralfate, queal. They envelop the mucous membrane, also neutralize hydrochloric acid and have an anti-inflammatory effect.
  • H2 blockers histamine receptors — Ranitidine, rhinitis, famotidine, quamatel. Histamine receptor blockers interfere with the action of histamine, interact with parietal cells of the mucosa and increase the secretion of gastric juice. But they have practically ceased to be used because they cause withdrawal syndrome (when symptoms return after stopping therapy).
  • Proton pump blockers- , omez, pantoprazole, rabeprazole, esomeprazole, lansoprazole, controloc, rabeloc, nexium (see more full list). They block the H + /K + -ATPase or proton pump, thereby preventing the formation of hydrochloric acid.
  • Synthetic analogues of prostaglandin E 1 Misoprostol, Cytotec. Inhibits the secretion of hydrochloric acid, increases the formation of mucus and bicarbonates.
  • Selective blockers of M-cholinergic receptors(pirencipin, gastrocepin) reduce the production of hydrochloric acid and pepsin. They are used as an auxiliary therapy for severe pain, side effects include palpitations.

Agents that increase mucosal protection

  • Sucralfate (Venter)- creates protective covering at the bottom of the ulcer
  • Sodium carbenoxolone (biogastron, ventroxol, kaved-s) helps speed up the recovery of the mucous membrane.
  • Colloidal bismuth subcinate— . Forms a peptide bismuth film that lines the wall of the stomach. In addition, bismuth ion has bactericidal effect in relation to Helicobacter.
  • Synthetic prostaglandins (enprostil) stimulate cell restoration and mucus formation.

Other drugs

  • list of probiotics). Prescribed for antibiotic therapy.

The course of treatment for stomach ulcers is 2-6 weeks, depending on general condition and size of the defect.

Treatment regimens

The destruction of H. pylori promotes better scarring of the ulcer. This is the first step in treating peptic ulcers. There are two main schemes antibacterial therapy. They are prescribed step by step, that is, the first-line medications did not work, then they try the second regimen.

1st line of eradication (within a week):

  • Semi-synthetic penicillins (Amoxicillin) 1000 mg twice a day or nitroimidazole derivatives (Metronidazole) 500 mg also twice a day.
  • Macrodids (Clarithromycin) 500 mg twice a day.

In case of failure, a 2nd line of eradication is proposed (1 week):

  • Proton pump inhibitors 20 mg twice a day.
  • Nitroimidazole derivatives (Metronidazole) 500 mg also three times a day.
  • Bismuth subcitrate (De-nol) 120 mg 4 times a day.
  • Tetracyclines (Tetracycline) 0.5 g 4 times a day.

Currently, doctors are developing new methods for treating pathology. A vaccine against Helicobacter is already being tested. For better healing mucosal defects, cytokine drugs, trefoil peptides and growth factors are used.

Nutrition of the sick

Treatment with folk remedies

Fresh milk, soda, decoction of calamus root, all types of nuts, pea powder and carrot juice will help relieve heartburn (see). To neutralize the hydrochloric acid contained in gastric juice, use fresh potato juice. To do this, you need to grate the root vegetable and strain the resulting mass through cheesecloth. Take half a glass of potato juice an hour before breakfast for a week.

Herbal treatment also promotes recovery. Doctors recommend infusions of fireweed, yarrow, marsh cudweed, strawberry and apple leaves, flax seeds, aspen buds, and birch chaga mushroom.

It also has healing properties herbal tea, which includes elecampane rhizome, chamomile flowers, yarrow, marsh cudweed, flax seed, licorice root,. All herbs need to be washed well, dried and poured with boiling water. It is advisable to take a tablespoon 10 minutes before meals. Positive result will not keep you waiting.

The effectiveness of eradication regimens in the treatment of duodenal ulcer associated with Helicobacter pylori is constantly being studied, and new techniques are being developed. This article presents treatment regimens for peptic ulcers using the latest antibacterial drugs that are resistant to hydrochloric acid. All presented treatment regimens for gastric ulcers have undergone numerous clinical trials.

According to 4 international recommendations (Maastricht I, 1996; Maastricht II, 2000; Maastricht III, 2005; Maastricht IV, 2010), eradication treatment is indicated for duodenal ulcer associated with Helicobacter pylori infection. Moreover, the duration of eradication should be from 7 to 14 days, on average 10 days (Maastricht IV) and eradication of H. pylori should be at least 80%.

IN Lately H. pylori resistance to metronidazole reached 82% and clarithromycin 28-29%. Therefore, in eradication regimens, drugs began to appear that replaced metronidazole in the “triple” regimen - amoxicillin, furazolidone, tinidazole, vikram and clarithromycin - josamycin, levofloxacin, rifambutin, dazolic, etc.

Over the course of 15 years, at the Department of Gastroenterology of the Federal State Budgetary Institution UMMC UD of the President of the Russian Federation, they studied different schemes eradication in 435 patients with duodenal ulcer associated with H. pylori: in 90 patients, a “triple” eradication scheme was used, consisting of omeprazole (O), clarithromycin (K), trichopolum (T). In 235 patients, amoxicillin (A), furazolidone (F), tinidazole (TD) and vikram (B) were used instead of T in a “triple” regimen. In 60 patients, vilprafen (VN) and levofloxacin (L) were used instead of K in the “triple” regimen. In 50 elderly and senile patients, 2 eradication schemes were used, consisting of half doses of antibiotics: O + K + A; Sanpraz (S), Dazolic (D) and A

In patients, ulcer scarring was assessed using EGD after 2, 3 and 4 weeks. In biopsy samples from the gastric mucosa, the degree of H. pylori contamination was studied using morphological Giemsa staining and a rapid urease test. The four-component treatment regimen for peptic ulcer disease showed very high results of convalescence. After morphological Giemsa staining of the biopsy specimens, the following were identified: weak degree contamination up to 20 microbial bodies in the field of view (+), moderate from 20 to 50 (++) and pronounced 50 microbial bodies or more (+++). Urease activity was assessed using a rapid urease test in biopsy specimens and positive reaction up to 1 hour was considered a pronounced reaction (+++), from 1 to 3 hours - moderate (++) and from 3 to 24 hours weak (+). The effectiveness and safety of eradication regimens were also assessed.

Three-component treatment regimen for peptic ulcer

A comparative assessment of the effectiveness of 15 eradication regimens in the treatment of duodenal ulcer in the acute stage was carried out. It turned out that 3 regimens, consisting of O+K+T, were effective in 60, 60 and 67% of patients. Thus, the three-component treatment regimen for peptic ulcer showed less successful results. Effective in eradicating H. pylori infection in the gastric mucosa of patients were eradication schemes, where instead of T there were A, F, TD and B (eradication frequency was recorded in 80-97, 90, 87 and 92% of patients), and replacement of K on B and L was accompanied by eradication in 90 and 80% of patients; in 92 and 80% of elderly and old people with half doses of antibiotics on regimens of O+K+A and C+D+A.

Side effects were recorded from 15 to 30%, short-term, associated in most cases with effective blockade of gastric secretion and went away on their own.

The most effective eradication regimens for the treatment of duodenal ulcer associated with H. Pylori:

  • omeprazole + amoxicillin + furazolidone
  • omeprazole + amoxicillin + tinidazole
  • omeprazole + amoxicillin + vikram
  • omeprazole + amoxicillin + levofloxacin
  • omeprazole + amoxicillin + vilprafen
  • omeprazole + amoxicillin + dazolic

Conclusion

Thus, in our studies, 6 treatment regimens using: O+A+F turned out to be more effective; O+A+TD; O+A+B; O+A+L; O+A+VN; O+A+D. Less effective (success<80%) оказались схемы с О+А+М. У пожилых и старых в схемах эрадикации с хорошим эффектом могут и должны быть использованы половинные дозы антибиотиков. Продолжительность эрадикационного лечения должна быть не менее 10 дней.

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 cells of the stomach, 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 (Alfa Normix) 400 mg 2 times a day.
4. Bismuth tripotassium dicitrate (120 mg 4 times a day) for 14 days.