Abstract
Painful sickle cell crises are among the principal manifestations of sickle cell disease. Their treatment routinely requires the use of non-steroidal anti-inflammatory drugs (NSAIDS). These drugs also, however, inhibit the cyclooxygenase cycle in arachidonic acid metabolism, promoting the synthesis of leukotrienes, which have bronchoconstrictive effects. This study took place from March through August, 2007, and included 100 patients of both sexes, aged 2 to 59 years, with any sickle cell phenotype (SS, SC, AS, SFA2, or SAFA2) and treated by NSAIDs in the Immunology and Haematology department of the University Hospital of Cocody. We analysed the characteristics of the respiratory events induced by taking NSAIDs to identify potential risk factors for their occurrence. We found that 5% of these patients presented respiratory symptoms linked to NSAIDs. These appeared within 30 minutes of drug intake for 80%; in 60% of these cases, only corticosteroid and antihistamine treatment resolved these symptoms. The occurrence of respiratory events did not differ by sex; however, younger subjects were more exposed to these respiratory events. All patients with family or individual history of atopy-like hypersensitivity type I events presented these respiratory symptoms when taking NSAIDS for sickle-cell crises.
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