Chronic gastritis caused by Helicobacter pylori

Helicobacter pylori (Helicobacter pylori) is the main pathogenic microorganism of the stomach, which causes gastritis, peptic ulcer, adenocarcinoma of the stomach and low-grade gastric lymphoma.

Chronic gastritis caused by Helicobacter pylori can be asymptomatic or cause varying degrees of severity of dyspepsia. The diagnosis is established by a respiratory test with urea labeled C14 or C13, and morphological studies of biopsy specimens during endoscopy. Treatment of chronic gastritis caused by Helicobacter pylori is the use of proton pump inhibitors and two antibiotics.

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What causes chronic gastritis caused by Helicobacter pylori?

Helicobacter pylori is a spiraling, gram-negative microorganism that has adapted to reproduction in an acidic environment. In developing countries, it is the cause of chronic infections and is usually acquired in childhood. In the US, infection is less common in children, but the incidence increases with age: approximately 50% of people aged 60 years are infected. Infection is especially common in African Americans and Hispanic people.

The microbe was sown from a stool, saliva and plaque, suggesting an oral or fecal-oral transmission of the infection. Infection tends to spread in families and in shelter residents. Nurses and gastroenterologists are at high risk: bacteria can be transmitted through insufficiently disinfected endoscopes.

Pathophysiology of chronic gastritis caused by Helicobacter pylori

Influence of Helicobacter pylori infection (Helicobacter pylori) varies depending on localization within the stomach. The predominance of infection in the antrum of the stomach leads to an increase in the secretion of gastrin, most likely because of a local decrease in the synthesis of somatostatin. The resulting hypersecretion of hydrochloric acid predisposes to the development of a prepyloric and duodenal ulcer. Infection prevailing in the body leads to atrophy of the gastric mucosa and a decrease in acid production, possibly due to an increase in local secretion of interleukin 1b. Patients with a predominant infection in the body are predisposed to stomach ulcer and adenocarcinoma. Some patients have a combined infection of the antrum and the body of the stomach with the combined clinical manifestations. Many patients with Helicobacter pylori infection do not develop any significant clinical manifestations.

Ammonia produced by Helicobacter pylori, allows the body to survive in its acidic environment of the stomach and destroy the mucous barrier. Cytotoxins and mucolytic enzymes (eg, bacterial protease, lipase) produced by Helicobacter pylori can play a role in damage to the mucosa and subsequent ulcerogenesis.

Infected people are 3-6 times more likely to have stomach cancer. Helicobacter pylori infection is associated with the intestinal type of adenocarcinoma of the body and the antral part of the stomach, but not the cancer of the cardiac department. Other associated malignancies include gastric lymphoma and mucosal associated lymphoid tissue (MALT-lymphoma), a monoclonal restricted B-cell tumor.

Diagnosis of chronic gastritis caused by Helicobacter pylori

Screening examination of asymptomatic patients does not guarantee the establishment of a diagnosis. Studies are performed to assess the course of peptic ulcer and gastritis. Usually, a post-treatment examination is also performed to confirm the death of the microorganism. Differentiated studies are conducted to verify the diagnosis and the effectiveness of treatment.

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Non-invasive tests for Helicobacter

Laboratory tests for helicobacter and programmed serological tests of antibodies to Helicobacter pylori have a sensitivity and specificity of more than 85% and are considered non-invasive tests of choice in the primary verification of Helicobacter pylori infection (Helicobacter pylori). However, since the qualitative definition remains positive up to 3 years after successful therapy and the quantitative levels of antibodies do not significantly decrease within 6-12 months after treatment, serological studies to evaluate the effectiveness of the treatment are usually not used.

When determining urea in exhaled air, 13C or 14C labeled urea is used. In an infected patient, the body metabolizes urea and releases labeled CO ₂, which is exhaled and can be quantified in exhaled air 20-30 minutes after oral administration of labeled urea. Sensitivity and specificity of the method is more than 90%. The respiratory test for Helicobacter (for urea) is well suited to confirm the death of a microorganism after treatment. False negative results are possible with the previous use of antibiotics or proton pump inhibitors; so follow-up studies should be conducted more than 4 weeks after antibiotic therapy and 1 week after therapy with proton pump inhibitors. H2-blockers do not affect the test results.

Invasive tests for Helicobacter

Gastroscopy is used for biopsy sampling of mucosal fragments to perform a rapid urea test (BTM or urease test) and histological staining of the biopsy specimen. Bacterial sowing has limited use because of the low stability of the microorganism.

A rapid test for urea, in which the presence of bacterial urea in biopsies causes a change in coloration in special media, is a method of selecting the diagnosis of tissue samples. Histological staining of biopsy specimens should be performed in patients with negative BTM results, but with clinical suspicion of infection, as well as with previous antibiotic therapy or with proton pump inhibitor drugs. Rapid urea test and histological staining have a sensitivity and specificity of more than 90%.

Treatment of chronic gastritis caused by Helicobacter pylori

Patients with complications (eg, gastritis, ulcer, malignancy) need the appointment of treatment aimed at the destruction of the microorganism. Elimination of Helicobacter pylori may even in some cases lead to the cure of lymphoma from mucosally-associated lymphoid tissue (but not another malignant process associated with infection). The treatment of an asymptomatic infection is controversial, but the recognition of the role of Helicobacter pylori in the development of cancer has led to the recommendation of preventive treatment.

Treatment of chronic gastritis caused by Helicobacter pylori (Helicobacter pylori) requires the use of mixed therapy, usually including antibiotics and acid suppressants. Proton pump inhibitors suppress H. Pylori and increase the pH of the stomach, increasing the concentration of medication in the tissues and the effectiveness of antibacterial drugs, creating an adverse environment for H. Pylori.

The use of three drugs is recommended. Oral administration of omeprazole 20 mg 2 times a day or lansoprazole 30 mg twice a day, clarithromycin 500 mg twice a day and metronidazole 500 mg 2 times a day or amoxicillin 1 g 2 times a day for 14 days are cured infection in more than 95% of cases. This mode has excellent tolerance. Ranitidine bismuth citrate 400 mg orally two times a day, can be used as a blocker of H ₂ histamine receptors to increase the pH.

Therapy with four drugs with proton pump inhibitor 2 times a day, tetracycline 500 mg and basic salicylic acid or bismuth citrate 525 mg 4 times a day and metronidazole 500 mg 3 times a day is also effective, but more cumbersome.

Infected patients with duodenal or gastric ulcer need a prolonged inhibition of acidity for at least 4 weeks.

Treatment of chronic gastritis caused by Helicobacter pylori (Helicobacter pylori) should be repeated if H. Pylori is retained. In case of ineffectiveness of repeated courses of treatment, some authors recommend endoscopic preparation of a culture for the study of its sensitivity to drugs.