Gastritis - Chronic gastritis

Chronic gastritis: type A gastritis

Type A gastritis is an autoimmune disease. In this case, so-called autoantibodies against the gastric acid-producing cells of the gastric mucosa (parietal cells) are formed. The parietal cells of the gastric mucosa produce stomach acid, which is essential for digestion. At the same time they produce the so-called intrinsic factor. Only with this intrinsic factor is the uptake of vitamin B12 from the intestine possible. Autoantibodies directed against the parietal cells thus prevent both the production of stomach acid and the absorption of vitamin B12.

The consequences of type A gastritis are decreased gastric acidity (achlorhydria) and anemia (anemia) as a result of vitamin B12 deficiency. Vitamin B12 is essential for the formation of the blood pigment. This form of gastritis is relatively rare, accounting for between three and six percent.

However, autoimmune gastritis may be associated with other autoimmune diseases. Autoimmune gastritis also favors the development of gastric cancer.

Chronic gastritis: Type B gastritis

The most common cause of chronic bacterial gastritis is an infection with the pathogen Helicobacter pylori. About 60 percent of the world's population carry the Helicobacter pylori pathogen in the gastric mucosa. It is a bacterium that produces enzymes involved in cell damage to the gastric mucosa. This pathogen can survive through certain mechanisms in the acid gastric juice and pass through the mucosal wall.

The source of infection is unclear. However, it has been proven that this pathogen can be transmitted from mother to child during pregnancy. Now that the causative agent of gastritis is known, gastritis, like any other bacteria-induced inflammation, can be treated with antibiotics.

Chronic gastritis: type C gastritis

This form of gastric mucositis, like type A gastritis, is also relatively rare. Only about 10 percent of patients with gastritis have type C gastritis. In this form of gastritis, the bile fluids falsely flow into the stomach and not into the small intestine. The reflux of bile fluids is especially common after gastric surgery. The bile fluids change the acidic environment of the stomach and attack the protective layer of the mucous membrane. As a result of this injury, the gastric mucosa may become inflamed.

Certain medicines for the treatment of pain and inflammatory processes such as acetylsalicylic acid or certain rheumatics attack the protective layer of the gastric mucosa and thus cause damage.

Diagnosis of type A & B gastritis

Type A gastritis: In autoimmune gastritis the mucous membrane looks stunted.

Type B gastritis: In this form of gastritis, the reflection shows occasional blotchy redness or small nodular mucosal elevations. In Helicobacter pylori gastritis, in addition to the gastric mucosal inflammation, a gastric ulcer (ulcer ventricles) may be present. The removal of a tissue sample is essential for the rapid urease test. For this, the mucosal sample is placed in a test fluid containing a color indicator and urea.

Helicobacter pylori produces the enzyme urease and is able to split urea. If Helicobacter pylori is present in the tissue sample, the cleavage of the urea will discolour the test fluid red. The test result is considered positive if the discoloration occurred after 24 hours. At high germ colonization, the discoloration takes place after 15 minutes.

Another possibility of diagnosis is the breath test. It serves for the detection of Helicobacter pylori. As gastroscopy can be circumvented with this examination method, this test is preferably used in children. An assessment of the gastric mucosa is not possible with the breath test.

Diagnosis of type C gastritis

In type C gastritis, the gastric mucosa is swollen and covered with blood-stained dark spots. This appearance is mainly found in inflammations caused by analgesics. If the disease is progressing well, even touching these areas with the endoscope can cause bleeding.

In known gastritis, the so-called Schilling test belongs to it. In this study, the patient is given radioactive labeled vitamin B12 for swallowing. As already stated, the vitamin B12 can only be taken in the presence of the intrinsic factor in the end of the small intestine. If autoimmune gastritis is present, the parietal cells are unable to release the intrinsic factor. As a result, the vitamin B12 can not be absorbed. The result is a reduction in vitamin B12 excretion in the urine.

In the second step of the shilling test, the patient is given the radioactive vitamin B12 and the intrinsic factor at the same time. If the radioactive vitamin B12 is detected in the urine, this is the confirmation of autoimmune gastritis with the consequences of pernicious anemia (vitamin B12 anemia). In addition, blood is taken to detect possible anemia. Anemia can be the result of gastric mucosal bleeding or vitamin B12 deficiency. In addition, the determination of antibodies against the parietal cells of the gastric mucosa is recommended for the detection of autoimmune gastritis (type A gastritis).


Autoimmune gastritis favors the development of gastric cancer. Furthermore, it can lead to heavy bleeding from the gastric mucosa. As a result, it can lead to chronic anemia with tiredness, fatigue, laxity, etc. In the worst case, the stomach bleeding can lead to a circulatory shock. In this situation, the bleeding must be stopped immediately via a gastroscopy. If this does not succeed, the person can bleed to death!

Another complication possibility is the development of gastric or duodenal ulcers (ulcer ventriculum and ulcer duodeni). Both ulcer types are characterized by spasmodic, oppressive, pinching or stabbing pain in the upper abdomen. In gastric ulcer, the pain and pressure usually occur shortly after eating, in duodenal ulcer, however, predominantly in an empty stomach.

After eating, the pain disappears for a few hours. But this does not always have to be this way. There is also a lot of pain during the night. Some ulcer patients lack these typical symptoms; There are only uncharacteristic indigestion, belching and heartburn, sometimes nausea with vomiting.

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