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

American Journal of Hematology
Vicky ChaarMarc Romana

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.

References

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Citations

Dec 24, 2013·Paediatric Respiratory Reviews·Santosh L SarafVictor R Gordeuk
Sep 30, 2008·Drug Metabolism Reviews·Young-Mi AhSang Geon Kim
Oct 5, 2011·Hemoglobin·Swee Lay Thein
Apr 23, 2013·American Journal of Hematology·Vivien A SheehanUNKNOWN BABY HUG Investigators
Nov 19, 2010·Expert Review of Hematology·Kleber Yotsumoto Fertrin, Fernando Ferreira Costa
Dec 17, 2016·European Journal of Haematology·Philippe JolyPhilippe Connes
Apr 5, 2018·Clinical Hemorheology and Microcirculation·Alicia K ChangVivien A Sheehan

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