The most common form of cobalamin deficiency, known as pernicious anemia, is now known to be an autoimmune disorder that results from parietal cell destruction. This results in insufficient production of gastric acid and IF and the ensuing malabsorption of cobalamin. Other less common causes of insufficient absorption are hypochlorhydria, gastrectomy, ileo-cecal resection, celiac disease, and chemical incompatibilities with drugs in the gastric milieu. A deficiency of cobalamin can also result from nutritional deficiencies, increased requirements as is seen in pregnancy, as well as a strict vegetarian diet without adequate supplementation. The symptoms of cobalamin deficiency primarily result from potentially irreversible nerve damage, involving sensory, motor, and cognitive functioning, and the megaloblastic anemia that can be confused with that seen in folate deficiency. The ability of folic acid to reverse megaloblastic anemia seen in cobalamin deficiency, without affecting nerve damage, is discussed in the Vitamin B9 section.
Cyanocobalamin is the form most commonly used in the treatment of cobalamin deficiency; however, hydroxo-
cobalamin is equally efficacious. A rare genetic disorder that results in an inability to convert cyanocobalamin to hydroxocobalamin is the only known instance where hy-droxocobalamin would be the preferred treatment.226 Hydroxocobalamin, but not cycanocobalamin, is also used in the treatment of cyanide toxicity. Administration of large doses results in the conversion of hydroxocobalamin to the nontoxic cyanocobalamin effectively reducing plasma levels of cyanide. In this case, 5 to 10 g of IV hy-droxocobalamin may be needed as compared to 1 mg/day in severe pernicious anemia.
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