Failure of D-thyroxine to increase fetal hemoglobin levels in normal and anemic baboons.
The synthesis of Hb F in baboons after erythropoietic stress is markedly increased. The mechanism of this "reverse switch" is unknown, but erythropoietin is not directly responsible for it. Since D-thyroxine has been reported to cause Hb F increases in marmosets, we determined its effect in normal and anemic baboons whose erythropoiesis, hemoglobin fractions and regulation of hemoglobin synthesis are similar to those of man. No effect was demonstrated in the normal baboons. In the anemic animal the Hb F level did not increase beyond the elevation attributable to the erythropoietic stress itself. It is therefore, unlikely that D-thyroxine will increase Hb F levels in man.
D000740:Anemia / Q000097:blood / Q000188:drug therapy*; D000755:Anemia, Sickle Cell / Q000097:blood / Q000188:drug therapy; D000818:Animals; D003918:Dextrothyroxine / Q000627:therapeutic use*; D004920:Erythropoiesis / Q000187:drug effects; D005319:Fetal Hemoglobin / Q000096:biosynthesis*; D006801:Humans; D010215:Papio
D003918:Dextrothyroxine; D005319:Fetal Hemoglobin