Drug-induced autoimmune hemolytic anemia

Authors
Citation
Jc. Homberg, Drug-induced autoimmune hemolytic anemia, PRESSE MED, 28(13), 1999, pp. 703-708
Citations number
50
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
PRESSE MEDICALE
ISSN journal
07554982 → ACNP
Volume
28
Issue
13
Year of publication
1999
Pages
703 - 708
Database
ISI
SICI code
0755-4982(19990403)28:13<703:DAHA>2.0.ZU;2-S
Abstract
Autoantibody production: The production of autoantibodies can only occur if immune tolerance is circumvented. Thus drug-induced autoimmune hemolytic a nemia requires that the drug have an effect on both autoantigens and on the Immune system. An example, methyldopa: Methyldopa is a hypotensive agent which,induces maj or production of anti-Rh IgC antierythrocyte autoantibodies, antinuclear an tibodies and an ii-actin antibodies. These autoantibodies generally appear 6 months after treatment onset and are observed in 20% of treated patients. Hemolysis is however exceptional and is only clinically or biologically pe rceptible in 1 to 2% of the patients who become immunized. induced lupus ha s been reported as have been several dozen cases of drug-induced hepatitis with anti-actin autoantibodies. Drugs inducing hemolytic anemia: Besides methyldopa, other drugs known to i nduce hemolytic anemia include levodopa used for Parkinson's disease, mefen amic acid, a nonsteroidal antiinflammatory drug, interferon-alpha, used in chronic viral hepatitis, cyclosporin used for the prevention of graft rejec tion and the treatment of certain autoimmune diseases, and fludarabin, used in chronic lymphoid leukemia. Therapeutic strategy: If there is no clinical or biological expression, the drug can be continued, excepting fludarabin where regular controls are nee ded. If hemolytic anemia is patent, the drug must be discontinued. transfus ion and corticosteroid therapy should be envisaged.