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UGT1A1 polymorphism outweighs the modest effect of deletional (−3.7 kb) α-thalassemia on cholelithogenesis in sickle cell anemia

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 alpha-thalassemia, yet another genetic factor that modulates hemolysis, in conferring protection from cholelithiasis. We show that, although alpha-thalassemia is associated with modest reduction in hemolysis and unconjugated bilirubin level, UGT1A1 polymorphism outweighs its effect on cholethiogenesis in sickle cell anemia patients.
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https://hal.univ-antilles.fr/hal-03265334
Contributor : Marc Romana <>
Submitted on : Wednesday, June 23, 2021 - 3:00:35 PM
Last modification on : Wednesday, June 30, 2021 - 9:40:16 PM

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Jean Pierre Diara, Vicky Chaar, Lysiane Kéclard, Maryse Etienne-Julan, Jean Diara, et al.. UGT1A1 polymorphism outweighs the modest effect of deletional (−3.7 kb) α-thalassemia on cholelithogenesis in sickle cell anemia. American Journal of Hematology, Wiley, 2006, 81 (5), pp.377-379. ⟨10.1002/ajh.20574⟩. ⟨hal-03265334⟩

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