(paracetamol + codeine), because of chronic headache. On admission, we observed a moderate normocytic anaemia (Hb 9 g/dl, reticulocytes 0.2%) with some microspherocytes; platelet count was 140 E 09/l, free haemoglobin in plasma 75.8 mg/dl, LDH 2,361 Ul/l, total bilirubin 1.4 mg/dl (conjugated 0.55 mg/dl), urea 193 mg/dl and creatinine 7,73 mg/dl. Acid-base balance, chest and abdominal X-ray, as well as abdominal echography were all normal. The immunohaematologic study on blood drawn at 37°C showed: group A Rh-positive, direct antiglobulin test 3+: IgG (–), IgM (–), IgA (–) and C3d (3+). The antibody screen was negative with non-enzyme-treated cells, in the saline direct test, albumin, antiglobulin phase and with enzyme-treated cells. The eluate gave negative results on antibody screening. In the study of the patient’s serum with red cells (enzyme treated or not), agglutination was observed when Tonopan and Cibalgina (propyphenazone) were added to the incubation mixture, but it did not react when either Algidol or paracetamol or contraceptive substances were added. IHA secondary to propyphenazone was diagnosed. After a short oliguric phase, normalized. Maximum urea concentration was 280 mg/dl and maximum creatinine, 12.2 mg/dl. Fourteen days after admission, urea was 85 mg/dl, creatinine 2 mg/dl and Hb 8.3 mg/dl. Twenty-three cases of IHA induced by NSAID have been published until now [1–8]. Cases due to the immune-complex mechanism have been described in association with ibuprofen [1], diclofenac and mefenamic acid [2], diclofenac [5, 6], tolmetin [1], feprazone [1], acetylsalicylic and aceclofenac [8]. We have not found any IHA case associated with propyphenazone. The complementary and serologic tests performed in our patient confirmed the diagnosis of IHA by an immune-complex mechanism secondary to propyphenazone, since agglutination was only observed when the drug, was added to the Letters to the Editor
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