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In contrast to the actual agastric anemia associated with partial or complete anatomical removal of the stomach, we distinguish anemia that develops in conditions of functional agastria, when the anatomically preserved stomach partially or completely turns off from the physiological process of digestion and, in particular, loses the ability to assimilate the external antianemic factor - Vitamin B12.

As a manifestation of functional agastria, we consider the anemia of the pernicious type described by us and N. T. Larchenko in connection with the stricture of the esophagus and the subsequent operation of an antetoracic esophagojejunostomy without additional fistula between the stomach and the jejunum.

In all the cases described, anemia was observed in young girls aged 23-26 years, and in one patient there was a pronounced iron deficiency anemia with latent B12-deficiency, and in 2 patients - anemia of pernicious, B12-deficient type with a cyclically relapsing course.

Pathogenesis. Anemia of patients with artificial esophagus can be called "agastral". Of primary importance is the lesion of the gastric mucosa itself - corrosive gastritis (especially with deep burns with extensive lesions of the gastric mucosa and its slowed regeneration), and the turning off of the gastric digestive phase (“functional agastria”) due to passage of food through esophagio-ano-anastomosis, bypassing the stomach, adversely affects the absorption of iron and vitamin B12. At the same time, in the figurative expression of B. V. Petrovsky, the stomach works as if “idle”, since the juices that are released during the meal, to a large extent can not affect the food masses that enter directly into the jejunum.

The known period (3-5 years), which runs from the time of the operation of creating an artificial esophagus (with the stomach turned off) to the onset of the pernicious-anemic syndrome, is due to the existence in the body (more precisely, in the liver) of reserves of vitamin B12 and folic acid, which can provide for a long time processes of physiological blood formation.
Under these conditions, the implementation of the perniciously-aemic syndrome occurs either due to a deep caustic burn with extensive damage and subsequent atrophy of the gastric mucosa (including the fundus), or due to depletion of vitamin B12 and folic acid in the liver under conditions of functional agastria arising in connection with the operation of esophagojejunostomy, or as a result of exposure to additional factors, such as taking sulfonamides, violating the biosynthesis of folic acid in the intestine (as was the case with s sick).

Treatment. Agastric (agastral) B12-deficiency anemia is treated according to the same principles as the treatment of Addison pernicious anemia — Birmer (see above).

If there are signs of hyposiderosis (erythrocyte hypochromia, hyposideremia, presence of characteristic trophic disorders), combined therapy with vitamin B12 and iron preparations with ascorbic acid, preferably parenterally administered (fercoven) according to the rules of iron deficiency anemia, is prescribed (see above).

Indications for blood transfusion (erythrocyte mass) are the same as for pernicious anemia.

Prevention. Prevention of agastric anemia is timely — even before the onset of B12 symptoms — insufficient supply of vitamin B12 in injections of 100–200? 1-2 times a month, starting from the first months after surgery. Iron preparations are used according to indications (erythrocyte hypochromia, sideropenia).
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