Heme Synthesis in Pyridoxine-Responsive Anemia

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Abstract
THE typical case of spontaneously occurring pyridoxine-responsive anemia in human beings has been characterized by hypochromic, microcytic red cells, normoblastic proliferation in the bone marrow, hyperferremia, increased iron stores, abnormal tryptophan metabolism and an optimal response to pyridoxine.1 Even after the hemoglobin level has returned to normal, red-cell morphology remains abnormal. Of 72 cases reported by Horrigan and Harris2 only 25 fitted this typical description. The majority of patients demonstrated an incomplete response to vitamin B6. Ten patients had megaloblastic changes in the bone marrow. Some had no demonstrable abnormality of tryptophan metabolism. Others showed partial responses to . . .