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A great deal of data support the direct involvement of the vascular endothelium, complex cellular interactions, and global inflammation-mediated cell activation in triggering vasoocclusive crisis (VOC) in sickle cell disease (SCD) [1]. In the transgenic mice model for SCD, it has been shown that nitric oxide (NO) protects the mice from VOC [2]. Elevated plasma levels of certain proinflammatory cytokines support a role for cytokine-driven inflammation in SCD. The aim of the present study was to evaluate the role of the NOS3 27-bp variable number tandem repeat (VNTR) and IL4 intron-3 VNTR functional polymorphisms in the development of crisis in Indian SCD patients. The study protocol was approved by the Institutional Ethics Committee of the Sickle Cell Institute Chhattisgarh, Raipur, India. Written informed consent was obtained from the study participants. A total of 256 individuals with SCD (55.5% men) were divided into two groups based on the history of VOC. The patients hospitalized with recurrent VOC were considered as the frequent crisis (FC) group (n=140; 54.7%) and patients who had not experienced any VOC during the past 1 year were considered as the infrequent crisis (IFC) group (n=116; 45.3%). Genotyping of the NOS3 27-bp VNTR [3] and IL4 intron-3 VNTR [4] functional polymorphisms was performed and results were compared between the FC and IFC groups.

NOS3 27-bp and IL4 70-bp VNTR Polymorphisms Do Not Contribute to the Risk of Sickle Cell Crisis