Alcoholic gastritis is an acute or chronic inflammatory and destructive disease of the stomach resulting from the abuse of alcoholic beverages. It is manifested by pain in the epigastric region, vomiting, changes in appetite. Diagnosis is based on anamnestic data, instrumental (mainly endoscopic) and laboratory research methods. Treatment consists in the complete rejection of alcohol intake, compliance with a sparing diet and the appointment of therapy aimed at normalizing the function of the gastrointestinal tract and eradication of concomitant helicobacteriosis in its presence.
K29.2 Alcoholic gastritis
To date, there are no official epidemiological data on the prevalence of alcoholic gastritis (reactive alcoholic gastropathy). The distribution of this pathology by age groups is heterogeneous, but it has been statistically established that over time the frequency of chronic forms increases, reaching a maximum at the age of over 60 years. Acute forms are registered mainly in young people of working age. The sex ratio (male/female) is approximately 3:1. Alcoholic gastritis due to its frequent detection in people who abuse alcohol, at the suggestion of WHO, is included in the ICD as a separate nosological form.
Causes of alcoholic gastritis
The most pronounced destructive effect on the gastric mucosa is provided by strong alcoholic beverages, which include 20% ethanol or more (vodka, cognac, liqueur). Stomach cells have high reparative capabilities, so the development of gastritis depends on both the amount of alcohol consumed and the duration of abuse. With an alcoholic excess, an acute form develops mainly, and with constant long–term intake, a chronic form develops.
Of particular importance in the development of alcoholic gastritis is the presence of risk factors. The leading role is assigned to the gram-negative bacterium Helicobacter pylori, which is responsible for dystrophic processes and a decrease in the functional activity of the mucous membrane. Spicy and hot food, nonsteroidal anti-inflammatory drugs, duodenogastric reflux are the main factors of aggression that damage the inner layer of the stomach.
Alcohol is a powerful chemical irritant, has both direct and indirect damaging effects on the gastrointestinal tract. Acetaldehyde, being a metabolite of ethanol, has a direct membranotoxic effect by activating lipid peroxidation, reducing the activity of ion pumps and combining with hydrophobic groups of the phospholipid layer of cells (fluidization), which morphologically manifests itself as a violation of the ordering of cell membranes. These changes lead to the blocking of the respiratory chain, as a result of which apoptosis of epithelial cells is activated.
The indirect damaging effect is associated with the effect of ethanol on the central nervous system. As a result, the coordinating function of the cerebral cortex in relation to subcortical structures, in particular the hypothalamus, is disrupted. There is a dysfunction of the autonomic nervous system. An increase in sympathetic influences leads to an increase in the concentration of glucocorticoids in the blood, which increase the sensitivity of the mucosa to the action of ulcerogenic factors, a decrease in organ perfusion, trophic disorders and subsequently to the occurrence of erosions. The strengthening of parasympathetic influences is manifested by the increased activity of APUD-system G-cells responsible for gastrin secretion.
The above changes are represented by a violation of digestion in the stomach and a decrease in all its functions. Due to the discoordination of secretion, the volume of gastric juice and hydrochloric acid increases. Due to disorders of motor activity, antiperistaltic waves occur, which are accompanied by heartburn. Violation of reservoir and evacuation functions leads to a delay in food masses, manifested by nausea, vomiting. Another important function of the stomach, which decreases with gastritis, is excretory, it consists in extrarenal excretion of metabolites from the bloodstream (urea, creatinine).
Alcoholic gastritis symptoms
The acute form occurs 6-12 hours after an alcoholic excess. The first symptoms are anxiety, weakness, nausea. Patients note a feeling of rapid satiety and heaviness in the epigastric region, a decrease in appetite. Vomiting often occurs at the peak of nausea, vomit has a meager volume, contains mucus, and often bile. As a result of alcohol intoxication, chills with subfebrile temperature are possible. The chronic form is manifested by long-existing pain of a dull, dragging, aching nature that occurs shortly after eating. Gastric dyspepsia syndrome with increased secretory activity is represented by heartburn, acid belching, and with secretory insufficiency – nausea, belching air, food, rotten.
It is possible to develop intestinal dyspepsia, clinically manifested by flatulence, rumbling, pain near the navel. This form of gastritis is almost always accompanied by a violation of the stool and intestinal dysbiosis. With a hyperacid state, there is a tendency to constipation, with a reduced one, diarrhea is noted.
The most common complication of alcoholic gastritis is peptic ulcer, which is the main cause of gastrointestinal bleeding. With a prolonged course of gastritis, atrophy of the mucous membrane occurs, including the fundal glands responsible for the secretion of the internal Castle factor. Hypo- or vitamin deficiency B12 develops, pernicious anemia. Following atrophy, as a rule, epithelial metaplasia occurs, the risk of malignancy of which is 13%. Increased secretion of gastrin, high acidity of chyme can lead to the manifestation of acute pancreatitis.
Diagnostics of alcoholic gastritis
In the presence of a characteristic anamnesis, diagnosis is not difficult. The diagnosis of alcoholic gastritis is based not on subjective complaints of the patient, but on the results of laboratory, instrumental studies with biopsy and morphological verification. Diagnosis is carried out by a gastroenterologist and consists of the following stages:
- Clinical survey and examination. Patients complain of manifestations of gastric and intestinal dyspepsia, which, as a rule, occur after a certain period of time after consuming a large amount of alcohol. The objective status is characterized by pallor, dryness of the skin, soreness in the epigastrium during palpation. The tongue is overlaid with a pale grayish coating.
- Laboratory tests. The results of the general analysis of blood and urine have no specific changes. There are signs of maldigestion in the coprogram (the presence of digestible and an increase in indigestible dietary fibers). Biochemical analysis provides information about concomitant damage to the pancreas, liver and changes in lipid (increased LDL, TAG), protein (decrease in total protein, dysproteinemia) and carbohydrate (increase in glucose) metabolism.
- Gastrointestinal endoscopy. The gold standard for the diagnosis of “gastritis” is the endoscopic method – FGDS. It allows not only to visually determine the nature and localization of mucosal changes, but also to take biopsies (at least 5 fragments) for histological examination. The morphological feature of alcoholic gastritis is the accumulation of filaments of an intermediate type in the mucous membrane.
Ultrasound of the liver, gallbladder, pancreas is used to diagnose concomitant pathology. In order to prescribe adequate drug therapy, differential diagnosis is carried out. First of all, it is necessary to exclude functional dyspepsia, which can manifest itself as pain, vomiting, decreased appetite. In peptic ulcer disease, the clinic is similar, but usually more pronounced, and the pain syndrome depends on the location of the ulcer (body, bottom, 12 duodenum).
Alcoholic gastritis treatment
The goals of therapy are relief of acute condition and prevention of complications, treatment of alcohol dependence, eradication of H. pylori, normalization of functional activity of the stomach. To achieve these goals, a chemically and mechanically sparing diet is prescribed, which is of the greatest importance in acute gastritis. Treatment is carried out on an outpatient basis, in the presence of complications – in inpatient.
Complete abstinence from alcohol is an important component of diet therapy and significantly increases its effectiveness. The method of heat treatment of food provided for by therapeutic nutrition includes steaming, cooking and extinguishing are also used.
In case of exacerbation of the disease, diet No. 1 according to Pevsner is prescribed: food should be liquid, semi-liquid and involves the complete exclusion from the diet of any products with a high content of dietary fiber, spices, carbonated drinks. The frequency of feeding 5-6 times a day in small portions. In remission, dietary recommendations are gradually expanding and becoming less strict – diet No. 2, which excludes fried, smoked, canned food.
In any form of alcoholic gastritis, in addition to therapeutic nutrition, drug therapy is necessary aimed at normalizing acid-base balance, restoring stomach protection factors and eliminating dyspeptic disorders. Pharmacological treatment includes:
- Proton pump inhibitors. These include medicines such as omeprazole, rabeprazole. These drugs affect the final stage of hydrochloric acid synthesis, inhibit both basal and stimulated its secretion. They are a mandatory component of hyperacid therapy.
- Histamine receptor blockers. Typical representatives of this group are ranitidine, famotidine. They inhibit the production of pepsin and hydrochloric acid. Due to side effects and less ability to maintain pH compared to proton pump inhibitors, they are rarely prescribed in practical gastroenterology.
- Gastroprotectors. They form protective films on the surface of erosions, increase the amount of prostaglandins, mucus, and bicarbonate, as a result of which the resistance of the mucosa to aggression factors increases. An additional therapeutic effect is associated with the accumulation of epidermal growth factor, which enhances the regeneration of the damaged mucous membrane.
- Eradication of Helicobacter pylori. To do this, a standard triple scheme is used using proton pump inhibitors, antibacterial agents from a number of macrolides, penicillins, and if it is ineffective, quadrotherapy, in which a group of antibiotics (metronidazole, tetracycline) is changed and a gastroprotector is added.
- Prokinetics. Block D2 receptors, eliminating disorders of gastroduodenal motility (insufficient peristaltic activity and decreased stomach tone). This group of drugs has an antiemetic effect due to a combination of peripheral action and blockade of chemoreceptors of the trigger zone of the vomiting center. A typical representative is domperidone.
Physiotherapy measures help to remove signs of inflammation, normalize secretory and motor functions. Vegetocorrective (dyadinamotherapy, electroson), anti-inflammatory (low-intensity UHF therapy, high-frequency magnetotherapy) methods are used. Various methods of reparative regeneration (decimeter waves, infrared laser therapy) are also used.
Prognosis and prevention
With timely treatment, the prognosis is favorable in most cases, determined by the presence or absence of concomitant alcoholic lesions of the liver, pancreas and the degree of histological rearrangement in the stomach. The prognosis becomes doubtful with precancerous changes in the mucous membrane (intestinal meta-, dysplasia) against the background of atrophic gastritis. Primary prevention involves the rationalization of lifestyle, the organization of proper nutrition, the exclusion of alcohol, tobacco, medicines. Secondary prevention consists in conducting a course of H. eradication. pylori and FGDS screening once every 2 years.