Vitamin B12 deficiency: pernicious anemia
Vitamin B12 deficiency causes pernicious anemia; the release into the bloodstream of immature precursors of red blood cells (megaloblastic anemia). As dis-cussed below, vitamin B12 deficiency causes functional folate deficiency; this is what disturbs the rapid mul-tiplication of red blood cells, causing immature pre-cursors to be released into the circulation.
The other clinical feature of vitamin B12 deficiency, which is rarely seen in folic acid deficiency, is degen-eration of the spinal cord; hence the name “perni-cious” for the anemia of vitamin B12 deficiency. The spinal cord degeneration is due to a failure of the methylation of one arginine residue in myelin basic protein. About one-third of patients who present with megaloblastic anemia due to vitamin B12 deficiency also have spinal cord degeneration, and about one-third of deficient subjects present with neurological signs but no anemia.
The most common cause of pernicious anemia is failure of the absorption of vitamin B12, rather than dietary deficiency. Classical pernicious anemia is due to failure of intrinsic factor secretion, commonly the result of autoimmune disease, with production of anti-bodies against either the gastric parietal cells or intrin-sic factor. Atrophic gastritis with increasing age also leads to progressive failure of vitamin B12 absorption.
Dietary deficiency of vitamin B12 does occur, rarely, in strict vegetarians (vegans). The rarity of vitamin B12 deficiency among people who have no apparent dietary source of the vitamin suggests that bacterial contamination of water and foods with vitamin B12-producing organisms will provide minimally adequate amounts of the vitamin. The fruit bat develops vitamin B12 deficiency when fed on washed fruit under laboratory conditions, but in the wild micro-bial contamination of the outside of the fruit provides an adequate intake of the vitamin.