Atrophic gastritis is a chronic type A gastritis, in which the number of gastric glands decreases, acid–forming function decreases. It is considered a precancerous condition. It is manifested by heaviness and dull pains in the stomach, nausea, heartburn, dyspeptic phenomena, anemia. The most significant diagnostic methods are: gastroscopy with sampling and histology of biopsies, various studies to determine the presence of helicobacter infection. Gastrography and ultrasound of the abdominal cavity are less informative. Since 90% of stomach atrophy is associated with exposure to helicobacteria, specific treatment includes eradication of infection. Substitution and symptomatic therapy, sanatorium treatment and physiotherapy are prescribed.
K29.4 Chronic atrophic gastritis
Atrophic gastritis is a chronic progressive inflammation of the gastric mucosa, as a result of which the lining glands of the stomach are completely lost, gradual atrophy occurs, followed by metaplasia of mucosal areas. The main sign that indicates a high probability of cancer is not the type of cell rearrangement, but the area of the process – with the prevalence of metaplasia on 20% of the area of the gastric mucosa and more, the probability of developing cancer is almost 100%.
According to the observations of specialists in the field of practical gastroenterology, chronic atrophic gastritis in 13% of cases ends with the development of oncological pathology. Compared with a non-atrophic process, the probability of such a complication in atrophic gastritis is five times higher. The main task of gastroenterologists today is to develop new, simple and non-invasive methods for reliable diagnosis of atrophy, as well as early diagnosis of stomach cancer. It is noted that timely diagnosis and complete eradication of the infectious process after five years lead to the restoration of the gastric mucosa and a significant reduction in the area of metaplasia.
Causes of atrophic gastritis
The main causes of the development of atrophic gastritis are a long-running helicobacter infection and an autoimmune process in which own antibodies damage the G-cells of the stomach (they are the main component of the lining glands). Atrophy of the glandular epithelium can contribute to various concomitant diseases and conditions: uncontrolled medication, alcoholism, stress and severe physical fatigue, various occupational hazards, hereditary features of the gastrointestinal tract, severe background diseases.
H.pylori causes chronic cell damage by weakening the local protective properties of the gastric mucosa, which as a result allows toxins and free radicals to freely penetrate into tissues and damage cell nuclei. At the end of this process, the cells acquire the properties of several types of tissues – the so-called hybrid cells, which have the properties of precancerous. This process is called intestinal metaplasia. Initially, these areas of the mucosa take the form of a small-intestinal epithelium, then a large-intestinal one. The further the metaplasia process has progressed, the more likely it is to develop gastric adenocarcinoma. To date, helicobacter infection is included in the list of biological carcinogens, because without proper treatment, it sooner or later leads to stomach cancer.
The mechanism of development of the autoimmune process is somewhat different. At the same time, antibodies begin to form in the body due to a violation of immunity, which recognize the stomach’s own tissues as foreign. Most often, antibodies are produced to G-cells and Castle factor, which is responsible for the absorption of vitamin B12. Because of this, the acidity of the stomach gradually decreases, the cells are rebuilt and begin to produce mucus instead of hydrochloric acid. Iron and vitamins stop being absorbed in the stomach, severe pernicious anemia develops. If autoimmune gastritis is accompanied by a helicobacter infection, the precancerous condition will develop much faster.
Atrophic gastritis symptoms
Pathology develops slowly, the lesion begins from the bottom of the stomach, passing to its body, and then to the rest of the mucous membrane. At the beginning of the disease, there may not be any special symptoms, which makes it difficult to diagnose and prevents the early start of treatment. After the development of a complete clinical picture, several symptom complexes may be detected in the patient.
Anemic syndrome develops due to impaired absorption of iron and vitamins (especially B12, folic acid) in the stomach cavity. It manifests itself as pronounced weakness, fatigue, drowsiness, constant fatigue (sometimes even the usual activity of the patient is disrupted). The skin and mucous membranes turn pale. The patient notes constant pain in the tongue, burning, the mucous membrane of the tongue becomes varnished. Also, the patient complains of sensitivity disorders in the extremities, usually symmetrical. Dry hair and brittle nails are characteristic, shortness of breath worries with minor loads, stabbing pains in the heart.
Dyspeptic syndrome is manifested by pronounced severity in the epigastrium, less often by dull aching pains in the upper half of the abdomen. Pain is associated with stretching of the walls of the stomach by food masses due to digestive disorders. Also, the patient is concerned about heartburn (throwing acidic contents into the esophagus), regurgitation (throwing food from the stomach into the oral cavity), belching (involuntary escape of air from the stomach). These symptoms are accompanied by nausea, sometimes vomiting, after which the pain in the epigastrium decreases. In the vomit – a large amount of eaten food, mucus, bile. Appetite is significantly reduced.
Digestive disorders spread to other parts of the gastrointestinal tract – abdominal discomfort appears, the stool becomes unstable – constipation is replaced by diarrhea. In the morning, there is an unpleasant taste in the mouth, a constant bad breath worries. The tongue is covered with a grayish coating, teeth prints are visible on it. Impaired digestion and decreased appetite can lead to weight loss, and in the absence of treatment – to severe alimentary dystrophy. Polyhypovitaminosis develops, which leads to a significant decrease in immunity, the addition of various infections.
Today, more and more attention is being paid to the early non-invasive diagnosis of atrophic gastritis. For this purpose, gastroenterologists have developed a special diagnostic panel. During conventional gastroscopy, it is not possible to identify foci of epithelial dysplasia, much less determine their area. Because of this, errors often arise related to both overdiagnosis and underdiagnosis: the area of hyperplasia may be assessed incorrectly, and inflammatory changes may be mistaken for epithelial metaplasia. In order to correctly assess the area of the altered epithelium, take a biopsy from all the altered areas, during gastroscopy, the mucosa is stained (most often with methylene blue) – the dye is well perceived by areas with intestinal metaplasia.
Biohit’s special hematological panel allows you to quickly and effectively determine the degree of epithelial metaplasia, mucosal and lining gland atrophy, and avoid diagnostic errors. In this panel, the level of serum pepsinogen is examined, the ratio of pepsinogen 1 to pepsinogen 2, histamine 17 is determined. A decrease in these indicators indicates a pronounced atrophy of glandular epithelial cells, and a low level of gastrin 17 indicates the death of G-cells of the stomach glands.
At the same time, increased levels of gastrin 17 and pepsinogen 1 are often associated with helicobacter infection. A significant increase in the level of gastrin 17 is most often associated with autoimmune gastritis, in which achlorhydria or hypochlorhydria is observed, the function of the antrum of the stomach is preserved. If there are also foci of atrophy (multifocal atrophy) in the antrum, then the levels of all these indicators will be low. This panel has at least 80% reliability, is used at the initial stages of the examination and allows you to determine the type of gastritis, its localization and cause, identify a precancerous condition and determine the correct treatment tactics.
In comparison with the hematological panel and endoscopic examination with biopsy sampling, other methods of diagnosis of atrophic gastritis are less informative. Thus, during gastrography, the smoothness of the folds of the mucous membrane and the slowing down of the peristalsis of the stomach are noted, its dimensions are reduced. The same pattern is found during ultrasound of the stomach. Intragastric pH-metry detects a decrease in the acidity of gastric juice. To clarify the diagnosis, it is advisable to carry out a daily measurement of acidity.
If malignancy is suspected, MSCT of the abdominal organs should be performed to exclude the tumor process. Also, all necessary studies are carried out to detect H.pylori infection: PCR diagnosis of Helicobacter, a breath test, detection of antibodies to Helicobacter in the blood.
Atrophic gastritis treatment
The main task of a gastroenterologist is to prevent further intestinal metaplasia, cancer transformation. With the timely initiation of treatment of atrophic gastritis, a significant improvement in the condition of the epithelium occurs after five years. A therapeutic diet is necessarily prescribed, which at the initial stage includes chemically, thermally and mechanically sparing food.
After normalization of the condition, the use of chemically active products is allowed: diluted juices (lemon, cabbage, cranberry). Fresh fruits are excluded from the diet, you can only eat bananas. Special requirements are imposed on food – it must be warm (you can not take cold and hot foods), meals should be frequent and fractional. It is necessary to exclude alcoholic beverages and smoking.
When a helicobacter infection is detected, eradication of the infectious agent is a prerequisite for recovery. Modern treatment protocols provide for the appointment of a two- or three-component scheme, including anti-helicobacter antibiotics, proton pump inhibitors, bismuth preparations. Only a complete cure from helicobacteria can lead to the restoration of the mucosa and reduce the risk of malignancy.
Glucocorticoid hormones in atrophic gastritis are prescribed only with the development of B12-folate deficiency anemia. Symptomatic treatment is also prescribed: replacement therapy with natural gastric juice, enzymes, missing vitamins, iron preparations. To stimulate the secretion of hydrochloric acid, it is necessary to drink mineral waters with a high salt content, decoctions of herbs (plantain, wormwood, fennel), acid juices, solutions of citric and succinic acids.
Gastroprotectors, regeneration stimulants (sea buckthorn oil), enveloping agents based on aluminum and bismuth, preparations for improving peristalsis are used. Physiotherapy is actively used: electrophoresis with medications, electro- and magnetotherapy, thermal procedures on the epigastric region. Spa treatment outside the period of exacerbation includes mineral water therapy at balneological resorts.
Prognosis and prevention
The prognosis of atrophic gastritis is worse in patients aged over 50 years – at this age, metaplastic processes develop much faster and more often lead to malignancy. Of great importance for full recovery is the early start of treatment, as well as the degree of eradication of the infectious agent. If, upon repeated examination after a course of anti-helicobacter therapy, microorganisms are detected in the gastric contents, then the course should be repeated. Prevention of the development of atrophic gastritis is the early diagnosis and treatment of H.pylori, compliance with the daily routine and rational nutrition, hand hygiene to prevent infection.