Symptoms / Complaints

As a complication of chronic gastritis type B and C a gastric ulcer can occur, which can lead to acute gastric bleeding. As already described for acute gastritis, gastric bleeding can have different effects. Clues can be hidden (occult) blood in the stool, tar stools, as a coffee grounds-like mass or light blood in the vomit.

Due to the persistent immune-controlled inflammation in type B gastritis, the mucous membrane recedes over time (atrophy). Due to its chronic irritation it changes into a different tissue. The pathologist refers to this process as metaplasia of the tissue.

This tissue tends to degenerate malignantly more often and can therefore lead to gastric cancer (gastric CA). Autoimmune gastritis (type A) also leads to severe atrophy of the mucous membrane and even to a three to six-fold increased risk of developing stomach cancer. In type A gastritis, the lack of gastric acid results in an increased stimulus to the G-cells, which then secrete more gastrin. This excess hormone stimulus can cause other tissues to degenerate malignantly, resulting in the development of hormone-producing tumours, so-called carcinoids.

Diagnosis

Clear indications of the suspected diagnosis of gastritis can be obtained during the patient interview (anamnesis) by asking about medication and consumption habits (alcohol, nicotine). In type A gastritis, the causative autoantibodies in the blood are often found, which are directed against cells and the intrinsic factor. The lack of intrinsic factor can be diagnosed by means of a Schilling test.

Anemia (pernicious anemia), which can be seen in the blood count, can also be an additional indication of type A gastritis. In most cases, only a gastroscopy provides final clarity about the diagnosis and the extent of the mucous membrane damage. The 13C-urea breath test can be used for the diagnosis of Helicobacter pylori colonisation.

Otherwise the bacterium is detected in tissue samples of the stomach. This test checks the absorption capacity of vitamin B-12 in the small intestine. First, vitamin B-12 is administered to the gastritis patient and then it is checked how much is absorbed into the blood.

The second step is to give both vitamin B-12 and intrinsic factor and again check the concentration of the vitamin in the blood. If there is more vitamin B-12 in the blood at the second administration, one can assume an intrinsic factor deficiency. However, if there is also little vitamin in the blood at the second attempt, the problem could most likely be with the small intestine and its mucous membrane itself.

The appearance and location of the inflammation alone provides the doctor with important information about the type and cause of the inflammation of the stomach lining. During gastroscopy, the first thing that is noticeable is atrophy of the stomach lining. During the “endoscopy” of the stomach, statements can be made about existing mucous membrane defects (erosions) or ulcers (ulcers).

By taking a tissue sample (biopsy) under the microscope a better statement about the inflammatory process can be made. In the case of a gastritis, the pathologist can see under the microscope a reduction in the surface area of the mucosa with flattening of the mucosal folds and glands. If the bacterium Helicobacter pylori is present, the immigrated inflammatory cells (inflammatory infiltrate) can be detected, especially in the gastric antrum.

A piece of tissue can also be used to perform a urease test. In this test, the piece of tissue is placed in a medium for 3 hours. The ammonia, which is produced by the bacteria‘s own enzyme urease, discolours the medium and thus provides quick and cheap evidence of the bacterium Helicobacter pylori.

In this test, the patient is administered a C13 (or 13C) labelled urea (non-radioactive) through a drink. The patient must then exhale strongly through a straw into a special glass tube. By splitting this urea into CO2 and ammonia, the marked 13C can be measured in the exhaled CO2. This procedure, which is not quite cheap, can be used after antibiotic therapy to check whether the elimination (eradication) of the Helicobacter pylori bacterium was successful. The advantage of this examination is that it is non-invasive and not stressful for the body.