18% to 152%) (Table 2) The prevalence was slightly higher when

18% to 1.52%) (Table 2). The prevalence was slightly higher when the subject and all their relatives were the same sub-division for

White/Eurasian, but slightly lower for Niger-Congo (Bantu). For both these sub-divisions, almost 90% of subjects had themselves and all relatives classed within the sub-division. For subjects born in the United Kingdom, the frequency of HLA-B*5701 was 8.32% (95% CI 5.99% to 10.64%) and for those born in Uganda it was 2.40% (0.82% to 6.82%) (Fig. 1). Importantly, none of the 215 subjects from Zimbabwe nor the 55 from Zambia was HLA-B*5701 positive. No other countries where at least 50 subjects were born were reported. In total, 1479 subjects PLX4032 cost had both a central laboratory and a local laboratory test result. Only one result differed between the two laboratories. This subject was classed as HLA-B*5701 negative by the central laboratory but positive at the local laboratory. On further analysis this was demonstrated to be an HLA-B*570301 reported as HLA-B*5701 (on two separate occasions) by the local laboratory methods. No serious adverse events were reported during this study. HLA-B*5701 is an important pharmacogenetic predictor of the ABC hypersensitivity reaction and is also associated with other adverse drug reactions, such as flucloxacillin-induced liver injury [12]. The overall

adjusted prevalence of HLA-B*5701 in the United Kingdom selleck chemical was found to be 4.55% (95% CI 3.49% to 5.60%). This is lower than two smaller studies from Brighton and Sussex University Hospitals and the Chelsea & Westminster Clinic in London where unweighted overall rates of 7.7% and 7.3%, respectively, were previously reported [5,13]. The prevalences Dehydratase found among our White patients (7.95%) were very similar to both these studies. However, these two studies also reported much higher proportions of White patients in their cohorts (71% and 81% respectively). Additionally the high rates reported among Black patients from the Chelsea and Westminster cohort (9%) is likely to

have been affected by a high false-positive rate, as the reported test used was unable to distinguish between HLA-B*5701 and HLA-B*5703 (found at higher frequencies in African patients). Eliminating false positives from the Brighton cohort resulted in HLA-B*5701 carriage being reduced from 5.3% to 1.3% among Black African patients. The HLA-B*5701 prevalence identified in our African/American/African heritage subjects is considerably lower than previously reported rates [1] and probably so because of the appropriately represented proportion of Black subjects that were of African origin. As we used full allelic sequencing our results were not affected by HLA-B*5703-associated false positives. In patients from Zimbabwe and Uganda (Zimbabwe 0.0%, Uganda 2.4%), HLA-B*5701 frequency was similar to previously reported rates from those countries [4], although the small sample size may have increased the chance of sampling bias.

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