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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, OBJECTIVE, METHODS, RESULTS. Meshes: Adolescent, Adult, Anemia, Sickle Cell, Bilirubin, Female, Gallstones, Genotype, Gilbert Disease, Glucuronosyltransferase, Humans, Male, Middle Aged, Risk Factors, Tunisia, Young Adult, beta-Thalassemia.
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Does gilbert syndrome act as a risk factor of developing gallstone among β hemoglobinopathy Tunisian patients? Context: As a result of chronic hemolysis, hyperbilirubinemia is often observed, leading to the formation of pigment cholelithiasis which could be busted by the presence of uridine diphosphoglucuronosyltransferase 1A1 defects. Herein, we investigated the effect of glibert mutation on the occurrence of pigment cholelithiasis in Tunisian patients with beta (β) hemoglobinopathy including sickle cell anemia and β thalassemia (minor). Our study included 151 subjects divided in 75 SCA patients and 76 β thalassemia patients. Both groups of patients were divided into two sub-groups according to the presence or absence of cholelithiasis. The relationship between A(TA)nTAA variation of UGT1A1 gene, the serum bilirubin level and the occurrence of cholilithiasis was investigated. Our results show a significant association between genotypes carrying variant (TA)7 and hyperbilirubinemia (p<0.05). Furthermore, we demonstrated a significant association between (TA)6/(TA)7 and (TA)7/(TA)7 genotypes with cholelithiasis among sickle cell anemia and thalassemia patients (p<0.05).
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Altogether, our data provide evidence that genotypes (TA)6/(TA)7 and (TA)7/(TA)7 and (TA)7 variant present a risk factor of developing gallstone among β hemoglobinopathy Tunisian patients. Final Decision: yes