Affiliation:
1. Department of Medicine, University of Utah College of Medicine, Salt Lake City, Utah.
2. University of Utah College of Medicine, Salt Lake City, Utah.
3. Assistant Professor of Medicine, University of Utah College of Medicine, Salt Lake City, Utah.
Abstract
Abstract
1. Two patients with microcytic hypochromic anemia, hyperferremia, and hemosiderosis have been described .A partial hematologic remission was observed in both patients following the administration of pyridoxine.
2. Interruption of pyridoxine therapy resulted in reticulocytopenia, a decline in the concentration of hemoglobin and a decrease in free erythrocyte protoporphyrin. Increased excretion of kynurenine and kynurenic acid, but not xanthurenic acid, was observed in the urine of one of the patients following administration of tryptophane. The excretion of tryptophane metabolites was within normal limits in the second patient.
3. Reinstitution of pyridoxine therapy was followed by reticulocytosis, an increase in free erythrocyte protoporphyrin and an increase in the concentration of hemoglobin. The excretion of tryptophane metabolites in the urine following the administration of tryptophane was within normal limits in both patients. However, microcytosis, hypochromia, anemia and hyperferremia persisted.
4. The administration of brewer’s yeast, Valentine’s liver extract, calcium disodium ethylenediamine tetra-acetic acid, ethinyl estradiol, pantothenic acid, pyridoxal, pyridoxamine, ascorbic acid, niacin, riboflavin, glutamic acid and tryptophane failed to elicit a further hematologic response.
5. These patients have been compared with the seven other reported cases of "pyridoxine-responsive" anemia.
Publisher
American Society of Hematology
Subject
Cell Biology,Hematology,Immunology,Biochemistry
Cited by
22 articles.
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