Gastritis vitamin

Saltzman JR, Kemp JA, Golner BB, Pedrosa MC, Dallal GE, Russell RM Effect of hypo-chlorhydria due to omeprazole treatment or atrophic gastritis on protein-bound vitamin B12 absorption. J Am CollNutr 1994 13 584-591. 

A frequent cause of vitamin B12 deficiency is atrophic gastritis leading to a lack of intrinsic factor. Besides megaloblastic anemia, damage to mucosal linings and degeneration of myelin sheaths with neurological sequelae will occur (pernicious anemia). 

The answer is d. (Hardman, pp 1331-1333.) Iron-deficiency anemia usually occurs in infants undergoing rapid growth. In adults in a late stage, it may result in a bowel syndrome associated with gastritis and hypochlo-rhydria (Plummer-Vinson syndrome). Characteristically, all iron-deficiency anemias are associated with a hypochromic microcytic blood profile. Infestation with the tapeworm D. latum is accompanied by a hyperchromic macrocytic anemia, which is treatable with vitamin B12. Bleeding syndromes are treated with iron. 

Individuals with chronic alcoholism are prone to gastritis and have increased susceptibility to blood and plasma protein loss during drinking, which may contribute to anemia and protein malnutrition. Alcohol also reversibly injures the small intestine, leading to diarrhea, weight loss, and multiple vitamin deficiencies. 

The gastritis and chronic pancreatitis associated with chronic alcoholism may result in a reduction of the amount of vitamin B12 absorbed but this has not been found to result in a clinical deficiency (M4). Alcohol can also cause damage to the ileum. Lindenbaum and Lieber gave alcohol to human volunteers for periods of 13—37 days and found that absorption of the vitamin was impaired in six of eight volunteers and this was not corrected by the addition of intrinsic factor or pancreatin (L10,L11). Biopsy of the ileum showed ultra-structural evidence of mitochondrial damage (Rll). It has been shown previously that folate deficiency may result in a reduction in the serum vitamin B12 level (H16) and the low serum vitamin B12 levels found in some alcoholics is probably secondary to folate depletion, which is common in this condition (L12). How folate is able to influence the serum vitamin B12 level is not clear. 

Patients with severe atrophic gastritis may have impaired absorption of vitamin B12 and a reduced serum level of the vitamin, but this is not accompanied by either megaloblastic anemia or neuropathy. Parietal-cell antibodies have been found in 33% of patients with gastritis, none of these patients having pernicious anemia (12, V4). Intrinsic factor antibodies were not found, and this was not surprising since it is rare to find antibodies to intrinsic factor in the absence of pernicious anemia. Patients with superficial gastritis usually have normal vitamin B12 absorption and normal serum levels of the vitamin. 

Other causes of gastric atrophy, such as those due to Helicobacter pylori,AIDS, or radiation injury, can lead to a similar outcome but from different pathogenic mechanisms. Therefore, vitamin B12 deficiency, resulting in neurological, psychiatric, metabolic, and hematological disorders, can arise from any one of the many causes listed in Table 28-1. For this reason, the term pernicious anemia (PA) is used here to describe only the classical disease that is associated with IF deficiency due to autoimmune gastritis. 

Parietal cells also secrete intrinsic factor, which is necessary for the absorption of vitamin B12. Vitamin B12 is a cofactor of enzymes which synthesise tetrahydrofolic acid, which in turn is needed for the synthesis of DNA components. An impairment of DNA synthesis will affect rapidly dividing cell populations, among them the haematopoietic cells of the bone marrow, which may result in pernicious anaemia. This condition may result from a destruction of the gastric mucosa by, for example, autoimmune gastritis or the resection of large parts of the lower ileum, which is the main site of vitamin B12 absorption, or of the stomach. 

Pernicious anemia is the megaloblastic anemia due specifically to vitamin B12 deficiency, in which there is also spinal cord degeneration and peripheral neuropathy. It is a disease of later life. Only about 10% of patients are under age 40 by the age of 60, about 1% of the population is affected, rising to 2% to 5% of people over age 65, as a result of atrophic gastritis and thus impaired absorption of vitamin B12 (Section 10.7.1). 

Atrophic gastritis will cause decreased secretion of gastric acid before there is any impairment of intrinsic factor secretion. This means that the absorption of crystalline vitamin B12, as used in the Schilling test, is normal but the absorption of protein-bound vitamin B12 from foods will be impaired (Section 10.7.1), and the Schilling test will give a false-negative result. 

G23. Glass, G. B. J., Uchino, H., Schwartz, G., Study of vitamin Bj2 binders in the gastric juice of normals, of patients with pernicious anemia and of those with atrophic gastritis and histamine-fast anacidity. Proc. VIII Intern. Congr. Hematol., Tokyo, 1960 pp. 956-969. Pan Pacific Press, Tokyo (1961). 

Vitamin B12 deficiency most frequently is seen in people over 60 years of age (11). Deficiency of vitamin B12 in younger adults is rare, but can occur as a result of reduced absorption of vitamin B12, for example in pernicious anemia, atrophic gastritis type B, long-term use of blockers of acid secretion, or short bowel syndrome after resection of the terminal ileum (18,19). Vitamin B12 deficiency in children usually depends on inborn defects of vitamin Bi2 metabolism or on insufficient support during pregnancy and breastfeeding. 

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