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- W2020432999 abstract "Enhanced erythrocyte destruction in sickle cell anemia results in chronic hyperbilirubinemia. Only a subset of patients develop cholelithiasis. UGT1A1 promoter polymorphism is associated both with unconjugated bilirubin level and elevated risk for cholelithiasis in such subset. Here, we investigated the role of α-thalassemia, yet another genetic factor that modulates hemolysis, in conferring protection from cholelithiasis. We show that, although α-thalassemia is associated with modest reduction in hemolysis and unconjugated bilirubin level, UGT1A1 polymorphism outweighs its effect on cholethiogenesis in sickle cell anemia patients. Am. J. Hematol. 81:377–379, 2006. © 2006 Wiley-Liss, Inc." @default.
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- W2020432999 date "2006-01-01" @default.
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- W2020432999 title "UGT1A1 polymorphism outweighs the modest effect of deletional (−3.7 kb) α-thalassemia on cholelithogenesis in sickle cell anemia" @default.
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- W2020432999 doi "https://doi.org/10.1002/ajh.20574" @default.
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