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Sulindac‐induced immune hemolytic anemia
Author(s) -
Angeles M.L.,
Reid M.E.,
Yacob U.A.,
Cash K.L.,
Fetten J.V.
Publication year - 1994
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1046/j.1537-2995.1994.34394196626.x
Subject(s) - sulindac , medicine , immune system , anemia , hemolytic anemia , immunology , pharmacology , nonsteroidal
Background: Sulindac, a nonsteroidal, anti‐inflammatory, indene‐derived drug, caused life‐threatening immune hemolytic anemia in an individual with back pain. Case Report: A patient was admitted to the hospital with immune hemolytic anemia and kidney and liver failure after several days ingestion of sulindac. The direct antiglobulin test was positive with polyspecific and monospecific anti‐IgG but not with anti‐C3. The eluate did not react in routine tests but reacted strongly after the addition of sulindac. The serum contained a sulindac‐dependent antibody reacting to a titer of 32. The sulindac‐dependent antibody was of both IgG and IgM classes and had no apparent blood group specificity. The antibody agglutinated red cells from humans and chimpanzees but not from chickens, rabbits, or sheep, which implied that a specific component on human and chimpanzee red cells was needed for reactivity. The antibody reacted with red cells treated with trypsin, papain, pronase, dithiothreitol, and sialidase. With aggressive medical care, the patient's condition improved. Conclusion: These findings appear compatible with the so‐called immune complex mechanism for drug‐induced immune hemolytic anemia. Physicians are alerted to the severe nature of this syndrome.