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Drug induced immune haemolytic anaemia in the Berlin Case‐Control Surveillance Study
Author(s) -
Garbe Edeltraut,
Andersohn Frank,
Bronder Elisabeth,
Klimpel Andreas,
Thomae Michael,
Schrezenmeier Hubert,
Hildebrandt Martin,
SpäthSchwalbe Ernst,
Grüneisen Andreas,
Mayer Beate,
Salama Abdulgabar,
Kurtal Hanife
Publication year - 2011
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2011.08784.x
Subject(s) - medicine , odds ratio , drug , fludarabine , diclofenac , case control study , pharmacovigilance , antibiotics , gastroenterology , immunology , adverse effect , chemotherapy , pharmacology , cyclophosphamide , microbiology and biotechnology , biology
Summary Drug‐induced immune haemolytic anaemia is a rare but serious condition. This study investigated the possibility of drug aetiology of immune haemolytic anaemia (IHA) in 134 patients with new onset of IHA who were identified in the Berlin Case‐Control Surveillance Study between 2000 and 2009. Single drugs related to IHA in three or more patients and assessed more than once as a certain or probable cause of IHA in a standardized causality assessment included diclofenac, fludarabine, oxaliplatin, ceftriaxone and piperacillin. In a case‐control study including all 124 IHA cases developed in outpatient care and 731 controls, significantly increased odds ratios (OR) were observed for beta‐lactam antibiotics (OR = 8·8; 95% confidence interval [CI] 3·2–25·2), cotrimoxazole (OR = 6·5; CI 1·1–37·9), ciprofloxacin (OR = 6·9, CI 1·3–38·5), fludarabine (OR = 22·2; CI: 2·8–454·5) and lorazepam (OR = 5·3; CI: 1·2–21·2). Excluding new onset cases with a chronic IHA disease course, an increased risk became also apparent for diclofenac with an OR of 3·1 (CI 1·3–7·0). This is the first case‐control study investigating drugs as risk factors for IHA. It corroborates an increased risk for several drugs that have been implicated as a cause of IHA in the standardized causality assessment of individual cases.