With atrophic gastritis, the gastric mucosa becomes so strangely inflamed that cells secreting acid and enzymes die in it. And also the internal factor that transfers vitamin B12 ceases to work. From this, malignant anemia develops.
The mechanism of such an outrage is more often in an attack on the stomach of our own immunity. It eats away at the stomach for a not very clear reason.
Sometimes the very same helicobacters that cause stomach ulcers can irritate our immunity and arrange atrophic gastritis.
They say that if helicobacters attack young people, they not only trigger atrophic gastritis, but also gradually lead to different types of anemia.
Well, that is, atrophic gastritis is accompanied by a decrease in the amount of acid in the stomach. From this, iron is absorbed worse, and iron deficiency anemia is obtained:
From a lack of intrinsic factor, vitamin B12 is poorly absorbed, and there will be pernicious anemia:
Interestingly, helicobacters, even when they have not damaged the stomach, in an incomprehensible way, disrupt the absorption of iron. There is no atrophy, no bleeding, and for some reason the iron is lost. The mystery of nature.
In fact, stupid helicobacters are digging their own graves. Atrophy gradually leads to the replacement of cells of the gastric mucosa with intestinal cells. This is the same metaplasia that we discussed yesterday:
So helicobacters cannot live in intestinal cells. That is, causing the development of atrophy and metaplasia, they themselves limit the living space.
There is also an opinion that due to a decrease in the amount of acid in the stomach, the place of helicobacters is taken by other microbes, the competition with which helicobacters cannot withstand and gradually die. It turns out that patients with atrophic gastritis have fewer helicobacters than healthy people.
In short, this is what helicobacters need!
