The leading place in the implementation of the hereditary predisposition is given to the infectious factor – Helicobacter pylori infection, the first report of which appeared about 17 years ago in the journal Lancet.
So how do diverse factors interact with each other? What, in fact, leads to the development of a defect in the gastric mucosa, in the place of which an ulcer forms?
The decisive link in the development of peptic ulcer is the imbalance between the factors of “aggression” and the factors of “protection” of the mucous membrane of the stomach and duodenum.
The factors of aggression include:
- increased production of hydrochloric acid and digestive enzyme – pepsin;
- impaired motility of the stomach and duodenum (delaying or accelerating the evacuation of acidic contents from the stomach, backfilling of contents from the duodenum into the stomach).
Protection factors are:
- congenital resistance of the mucous membrane to the action of aggressive factors;
- the formation of gastric mucus;
- production of natural alkalis, bicarbonates;
- active restoration of the mucous membrane;
- good blood flow in the wall of the stomach;
- normal content of natural defense factors – prostaglandins in the wall of the mucous membrane;
- immune defense.
As mentioned above, many factors of aggression and defense are genetically prepared for each of us, and the dynamic balance between them is maintained by the coordinated interaction of the nervous and endocrine systems, including the cerebral cortex, hypothalamus, peripheral endocrine glands, and gastrointestinal hormones and polypeptides.
Depending on the violation of the ratio of aggressive and protective factors, peptic ulcer of either the duodenum or stomach occurs. In case of duodenal ulcer, the most important role is played by an increase in the synthesis of hydrochloric acid and pepsin, and in case of gastric ulcer, a decrease in the production of protective factors and motility. This is why duodenal ulcers predominate at a young age.
As for the stress factor and neuropsychic overstrain, in this case there is a violation of the autonomic nervous system. We have already said that a disorder of parasympathetic regulation leads to an increase in the production of hydrochloric acid and pepsin, impaired gastric motility and reverse reflux of acidified food, and spasms of the vessels of the stomach, and disruption of the sympathetic nervous system leads to impaired formation of protective factors.
Protective factors normally inhibit the effect of aggressive ones. The resistance of the mucous membrane is due to its good blood supply, rapid cell recovery in case of damage, and the abundant production of mucus containing substances that neutralize hydrochloric acid. Suppression of acid production with excessive acidification of the vestibule and the initial part of the intestine is called an “acid brake” of secretion.
A realizing factor in the occurrence of an ulcer is an infectious agent – Helicobacter pylori. Global studies conducted in almost all countries of the world showed that HP infection in the population ranges from 30 to 80% in the surveyed regions. Large-scale studies conducted in different countries of the world recently have shown that the share of peptic ulcer associated with HP accounts for 70–80% of duodenal and 50–60% of gastric ulcers. Oddly enough, this microorganism feels great at pH = 1, in the environment that is harmful to most bacteria. And no wonder. Indeed, in the process of its life, this microbe releases products with an alkaline reaction, in particular ammonia.
Ammonia alkalizes the contents of the stomach, thereby provoking an increased release of aggressive hydrochloric acid. In addition, the bacterium releases toxic substances that damage the cells of the mucous membrane, and also affects local immunity.
When predisposing factors are superimposed on the life of the microbe, an ulcer occurs.
In recent years, the attention of a large number of researchers has focused on the role of the damaging effect of acetylsalicylic acid and related drugs – the so-called non-steroidal anti-inflammatory drugs (NSAIDs). Gastroduodenal ulcers occur in 20–25% of patients who take NSAIDs for a long time. This problem has gained particular relevance due to the fact that acetylsalicylic acid has proven to reduce the risk of developing myocardial infarction and is accepted by most patients with coronary heart disease.
However, the protective effect for some body systems turns into a damaging effect on others. Acetylsalicylic acid has a detrimental effect on the protective barriers of the gastric mucosa and reduces the synthesis of protective prostaglandins. That is why, for the prevention of heart attack, the so-called “gastro-protected” acetylsalicylic acid preparations are currently being produced. And as anti-inflammatory drugs are increasingly used drugs with selective action – the so-called cyclooxygenase-2 inhibitors.