Prolonged Clinical Use of a Heme Oxygenase Inhibitor: Hematological Evidence for an Inducible but Reversible Iron-Deficiency State.

HEME oxygenase; IRON deficiency anemia; BILIRUBIN; CHEMICAL inhibitors

Abstract. The heme oxygenase inhibitor tin (Sn[sup 4+])-mesoporphyrin, administered to two 17-year-old Crigler-Najjar type I patients during a 400-day study to lower plasma bilirubin levels, also produced changes, beginning Is approximately equal to 50 days after initiation of treatment, in hematological and iron metabolism indices consistent with the development of iron deficiency anemia. These indices were responsive to iron supplementation and reverted to normal after termination of inhibitor treatment. Tin-mesoporphyrin enhances biliary heme excretion and inhibits intestinal heme oxygenase when administered orally or parenterally; the changes in blood indices could thus reflect, in part, blockade of heme catabolism and therefore of uptake of heine-derived iron, by intestinal epithelium. This action of the inhibitor suggests that such agents may facilitate studies involving aberrant metabolism of heme-derived iron in humans and that they merit further investigation with respect to their potential value in enhancing iron disposal in certain disorders such as those related, for example, to transfusion-induced iron overload states. Pediatrics 1993;91:537-539; tin-mesoporphyrin, heme oxygenase inhibitors, iron deficiency. [ABSTRACT FROM AUTHOR]

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