IN 1956 Harris and his associates1 described the first patient with a spontaneously occurring sideroblastic anemia in whom a hematologic response to large doses of pyridoxine was obtained. Subsequently, many other patients with sideroblastic anemias responsive to pyridoxine were found. These patients had in common hypochromic and usually microcytic red cells, erythroid hyperplasia of the bone marrow, increased iron stores and ringed sideroblasts in the bone marrow.2 Occasionally, the bone marrow resembled that seen in untreated pernicious anemia. Some of these patients had had 1 or more relatives with a similar disorder; their pedigrees usually suggested a sex-linked recessive mode . . .
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Spitzer et al. (1966) studied this question.
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