BACKGROUND AND OBJECTIVES: Sodium diclofenac is one of the most widely used nonsteroidal anti-inflammatory drugs. Cases of acute haemolytic anaemia have been ascribed to the drug. We describe such a case, mediated by immune complexes. MATERIALS AND METHODS: Standard serologic tests were carried out for blood grouping and the detection and identification of red cell allo- and autoantibodies. Drug-anti-drug complexes were detected with an ex-vivo method. RESULTS: Warm IgG drug-independent red cell and platelet autoantibodies were detected in the serum. At first, the patient was diagnosed as having the Evans syndrome, and corticosteroids were administered. Later, because of the severity of the anaemia, the possibility of an immune complex mechanism was considered. This was confirmed by the detection of diclofenac-dependent antibodies that reacted with RBC only in the presence of urine from a volunteer receiving diclofenac as a source of ex-vivo antigen. The antibodies neither reacted with an in-vitro solution of the drug nor with the volunteer's serum. Diclofenac and corticosteroids were stopped, and the clinical condition of the patient completely normalised within 15 days. CONCLUSIONS: We describe a patient with acute haemolytic anaemia caused by diclofenac through an immune complex mechanism.
BACKGROUND AND OBJECTIVES:Sodium diclofenac is one of the most widely used nonsteroidal anti-inflammatory drugs. Cases of acute haemolytic anaemia have been ascribed to the drug. We describe such a case, mediated by immune complexes. MATERIALS AND METHODS: Standard serologic tests were carried out for blood grouping and the detection and identification of red cell allo- and autoantibodies. Drug-anti-drug complexes were detected with an ex-vivo method. RESULTS: Warm IgG drug-independent red cell and platelet autoantibodies were detected in the serum. At first, the patient was diagnosed as having the Evans syndrome, and corticosteroids were administered. Later, because of the severity of the anaemia, the possibility of an immune complex mechanism was considered. This was confirmed by the detection of diclofenac-dependent antibodies that reacted with RBC only in the presence of urine from a volunteer receiving diclofenac as a source of ex-vivo antigen. The antibodies neither reacted with an in-vitro solution of the drug nor with the volunteer's serum. Diclofenac and corticosteroids were stopped, and the clinical condition of the patient completely normalised within 15 days. CONCLUSIONS: We describe a patient with acute haemolytic anaemia caused by diclofenac through an immune complex mechanism.