Effect of the citrovorum factor in pernicious anemia
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ADMINISTRATION of steroids to patients with Addisonian pernicious anemia in relapse often produces a hematologic response.1 There is an improvement in vitamin B12 absorption2 3 4 and with it an increase in secretion of intrinsic factor5 and a decline in the amount of intrinsic-factor antibody in the blood.6 The absorption of vitamin B12 after total gastrectomy is not improved by steroid therapy.7 There is good evidence that gastric atrophy is the result of an autoimmune process. It is also possible that the final failure of vitamin B12 absorption in pernicious anemia follows the development of antibodies against intrinsic factor. . . .
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THE absorption of ordinary amounts of vitamin B12 from the gastrointestinal tract is normally dependent on the presence of the intrinsic factor of Castle in the gastric secretions. A lack of intrinsic factor results in deficient absorption of vitamin B12 and the clinical picture of pernicious anemia. In the treatment of this condition it has been necessary either to administer vitamin B12 parenterally or to add intrinsic factor to the vitamin B12 given by mouth to ensure proper absorption. If, however, the oral dose of vitamin B12 is increased to more than 1 mg. enough . . .
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Absorption of Vitamin B12alone or with added intrinsic factor was impaired in three patients with vitamin B12malabsorption, two of whom had megaloblastic anemia, thus supporting the diagnosis of intestinal malabsorption rather than pernicious anemia. Yet, presence of serum autoantibodies to parietal cells or intrinsic factor or both indicated concomitant pernicious anemia. Absorption of vitamin B12in the presence of intrinsic factor was restored in two patients by therapy with cyanocobalamin, suggesting that the initial absorptive abnormalities were induced by deficiency of this vitamin. Autoantibodies to parietal cells were also present in one of three patients withDiphyllobothrium latum-caused vitamin B12deficiency. She had concomitant pernicious anemia. Immunologic tasks are valuable aids in differentiating disorders of vitamin B12malabsorption.
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ONCE Addison's pernicious anemia has developed it is usually considered that therapy is necessary for the remainder of the patient's life. Since the absorption of vitamin B12 is apparently dependent upon adequate amounts of intrinsic factor, current concepts imply that intrinsic-factor activity must be reduced below a critical level for a considerable period, usually three to five years, before body stores of vitamin B12 are exhausted and Addison's pernicious anemia develops. This deficiency in intrinsic-factor activity, once it has occurred, is generally considered to persist throughout life. Although this is undoubtedly true of most of the patients in . . .
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Pernicious anemia is a cobalamin deficiency disease caused by a lack of intrinsic factor (IF), which is necessary for the absorption of this vitamin. Because of the extensive hepatic storage of cobalamin, primary dietary deficiency is uncommon, occurring only in strict vegetarians after avoidance of animal products for many months. The most common cause of IF deficiency is gastric atrophy. Total gastrectomy leads to pernicious anemia, and partial gastrectomy does so occasionally. A rare congenital form of pernicious anemia may be the result of an autosomal recessive failure in IF production. It is possible to treat pernicious anemia with oral IF. This was standard practice at one time, but has lost favor because of the difficulty and expense of obtaining IF. For the last 30 or more years, the usual treatment has been 1000 μg of cobalamin administered intramuscularly once every 1 to 3 months. With a retention efficiency of
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Pernicious anemia is a cobalamin deficiency disease caused by a lack of intrinsic factor (IF), which is necessary for the absorption of this vitamin. Because of the extensive hepatic storage of cobalamin, primary dietary deficiency is uncommon, occurring only in strict vegetarians after avoidance of animal products for many months. The most common cause of IF deficiency is gastric atrophy. Total gastrectomy leads to pernicious anemia, and partial gastrectomy does so occasionally. A rare congenital form of pernicious anemia may be the result of an autosomal recessive failure in IF production. It is possible to treat pernicious anemia with oral IF. This was standard practice at one time, but has lost favor because of the difficulty and expense of obtaining IF. For the last 30 or more years, the usual treatment has been 1000 μg of cobalamin administered intramuscularly once every 1 to 3 months. With a retention efficiency of
pernicious anemia
Intrinsic factor
Megaloblastic anemia
Pernicious anaemia
Atrophic gastritis
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