Acute immune hemolysis induced by a degradation product of amphotericin B.
We report here on an eight-year-old boy who first developed acute intravascular hemolysis following therapy with amphotericin B (AmB) and subsequently a delayed hemolytic transfusion reaction due to alloantibodies. Although there is as yet no evidence for metabolism of AmB in vivo, the hemolysis appeared to be the result of sensitization against a degradation product of the drug. The patient's serum contained a hemagglutinating IgM antibody that reacted with all red blood cells (RBC) tested in the presence of plasma obtained from patients receiving AmB (ex vivo antigen), but not in the presence of their urine, AmB itself, or with AmB-pretreated RBC. These findings indicate that the antibody was directed against a degradation product of AmB, presumably a trace metabolite, that has not yet been identified.
Salama
A
A
Department of Internal Medicine, Justus-Liebig-University, Giessen, Federal Republic of Germany.
Burger
M
M
Mueller-Eckhardt
C
C
D000208:Acute Disease; D000666:Amphotericin B / Q000009:adverse effects* / Q000276:immunology / Q000493:pharmacokinetics; D000744:Anemia, Hemolytic, Autoimmune / Q000097:blood / Q000139:chemically induced*; D001711:Biotransformation; D002648:Child; D006386:Hemagglutination Tests; D006454:Hemoglobins / Q000032:analysis; D006801:Humans; D007518:Isoantibodies / Q000032:analysis; D008297:Male
D006454:Hemoglobins; D007518:Isoantibodies; D000666:Amphotericin B