Pyridoxine-responsive anemia conditioned by isonicotinic acid hydrazide.

S INCE THE FIRST report in 1956 of a patient with pyridoxine-responsive anemia, a number of other patients have been reported.”2 The red blood cells usually are hypochromic and microcytic but occasionally they may be macrocytic and accompanied by megaboblastic bone marrow maturation. It is unlikely that many of these patients have a simple dietary deficiency of pyridoxine, since barge doses of the vitamin are needed to elicit a response. Furthermore, this response is commonly incomplete and the hemoglobin concentration and red cell morphology do not return to normal. Thus, the mechanism may be dysmetabolism or impairment of an enzyme system in some way other than by simple coenzyme deficiency. Isonicotinic acid hydrazide ( INFI ) is a pyridoxine antagonist, both in vitro and in vivo, and many of its side effects can be attributed to interference with the proper action of this vitamin.3 It occupies a key position in the therapy of tuberculosis. Although the occurrence of anemia is quite uncommon during INH therapy, two patients have been reported who developed anemia responsive to pyridoxine administration during treatment of tuberculosis with INH.45 A third patient, whose anemia originally responded to small doses of pyridoxine, suffered a recurrence of anemia during therapy of tuberculosis with INH. When administration of this drug was stopped and relatively small doses of pyridoxine (5 mg./day, i.m.) were given, there was a reticulocytosis followed by marked hematologic improvement.6’7 It is the purpose of this paper to describe three additional patients who had pyridoxine-responsive anemia while being treated for tuberculosis with INH.