Chronic gastritis

Introduction

In general it can be said that an existing discrepancy between factors that damage the mucous membrane (e.g. gastric acid) and those that protect it (mucous layer) can lead to chronic gastritis.

Types of gastritis

Basically there are 3 different types of chronic gastritis:

  • Type A Gastritis
  • Type B Gastritis
  • Type C Gastritis

The section shows the stomach mucosa enlarged. The mucous membrane defects are clearly visible as red spots in the mucous membrane, as areas of locally increased blood circulation and in some cases bleeding into the mucous membrane tissue of the stomach. As the disease progresses, stomach ulcers may also develop, which can penetrate the stomach wall. Particularly in the chronic form of gastritis there are visible changes in the mucous membrane of the stomach.

Causes

This form is an autoimmune disease in which the body’s own antibodies are directed against the cells (which produce stomach acid) of the stomach lining and destroy them. In some cases, the antibodies are also directed against the intrinsic factor produced by the parietal cells. This substance is later needed to transport vitamin B-12 through the mucous membrane of the small intestine, so a lack of intrinsic factor automatically leads to a lack of vitamin B-12.

This gastritis mainly affects the mucous membrane of the stomach and is therefore also called “corpus gastritis”. In total, type A gastritis accounts for about 5% of all chronic gastritis and is excessively often associated with other autoimmune diseases such as rheumatoid arthritis (rheumatism) and systemic lupus erythematosus. In rheumatoid arthritis, autoantibodies are formed against the joint mucosa.

In type A gastritis, the lining cells are increasingly destroyed in the course of the disease, so that at some point no more gastric acid can be produced. This condition is then called Achylia gastrica or Achlorhydrie (absence of gastric juice). This form of gastritis is caused to 90% by the bacterium Helicobacter pylori.

In the remaining cases, rarer bacteria and viruses can lead to this chronic gastritis. The colonisation of the stomach mucosa by the Helicobacter pylorus bacterium (germ) is very widespread and the number of people colonised increases steadily with age, so that it is assumed that the germ is found in the stomach mucosa in almost 60% of people over 60. This does not mean, however, that everyone falls ill with iner gastric mucosa inflammation.

Often the germ remains undetected precisely because there are no symptoms. The bacterium possesses the enzyme (active protein) urease, which can split urea into ammonia and (carbon dioxide (CO2). The basic ammonia obtained in this way neutralises the hydrochloric acid and thus protects the bacterium from decomposition by gastric acid, thus ensuring its survival in the acidic environment.

The inflammation mainly affects the stomach antrum and is therefore also called “antral gastritis”. Type B – gastritis is the most common chronic gastritis with 85% of cases. The causes of type C gastritis are chemical-toxic factors.

Painkillers such as acetylsalicylic acid (ASS, Aspirin ®) and NSAIDs, such as Voltaren or Ibuprofen, which reduce the blood microcirculation in the gastric mucosa, often cause this type of gastritis, especially in chronically painful patients who are dependent on these drugs on a daily basis. Long-term alcohol and nicotine dependency (abusus) also frequently leads to this form of gastritis. In some cases, bile acid reflux from the duodenum can be the cause of the inflammation.

At 10%, this form is the second most common cause of chronic gastritis and it particularly affects the gastric fundus. A lot of stress is one of the main risk factors for chronic gastritis, in which case we are talking about type C gastritis. Under stress, the body functions at full speed, the adrenal glands release the “alarm messengers” adrenaline and noradrenaline as well as the stress hormone cortisol. Cortisol in turn has a stimulating effect on the stomach lining, so that specific cells (main cells) produce more stomach acid. Excessive acid production can disturb the balance of gastric juice components that are aggressive to the mucous membrane (gastric acid) and protective to the mucous membrane (neutralising protective mucus), so that factors that are aggressive to the mucous membrane predominate and damage the mucous membrane in the long term or permanently and cause inflammation.