Rh blood group-specific antibodies in immune hemolytic anemia induced by
nomifensine
A Salama and C Mueller-Eckhardt
Nomifensine (Merital, Alival; Hoechst, Frankfurt, FRG), an antidepressant
drug, may cause immune hemolytic anemia (IHA) of the so- called immune
complex type that is believed to occur by means of an innocent-bystander
mechanism. In this report we describe findings that are not consistent with
this mechanism in a patient with nomifensine- induced intravascular IHA
associated with renal failure. In vitro studies showed a transitory
positive direct antiglobulin test (DAT) due to IgG, IgM, and C3 fixation.
The causative antibodies were found to be a drug-independent IgM antibody
in the serum and eluate that reacted only with E-positive RBC, although the
patient's RBC were E-negative; an IgG antibody in the serum and initial
eluates that showed a stronger reaction with e-positive than with
e-negative or Rhnull RBC, but only in the presence of ex vivo antigen (ie,
urine containing the drug and all its metabolites); and an IgM antibody in
the serum and initially also on the patient's RBC that, in the presence of
ex vivo antigen as well as in the presence of known metabolites of the
drug, agglutinated all RBC equally strongly, but was hemolytically more
active against E- positive than E-negative cells. Within a few days of
stopping the drug the hemolysis rapidly resolved without administration of
prednisone, the DAT became negative with anti-IgG and anti-IgM, and the
drug- independent anti-E disappeared, but both metabolite-dependent
antibodies remained detectable in the patient's serum. We conclude that the
production and specificity of the causative antibodies in this case were
controlled by a larger antigenic site, presumably consisting of the drug
and/or its metabolites plus RBC antigens, rather than by epitopes of the
drug or metabolites alone.
Volume 68,
Issue 6,
pp. 1285-1288,
12/01/1986
Copyright © 1986 by The American Society of Hematology
