Sampietro M, Lupica L, Perrero L, Comino A, Martinez di Montemuros F, Cappellini M D, Fiorelli G
Istituto di Medicina Interna e Fisiopatologia Medica, Università di Milano, IRCCS Ospedale Maggiore Policlinico, Italy.
Br J Haematol. 1997 Nov;99(2):437-9. doi: 10.1046/j.1365-2141.1997.4113228.x.
We evaluated the effect of Gilbert's syndrome, the most common defect of bilirubin conjugation, on the bilirubin levels of subjects with inherited haematological disorders which cause increased bilirubin production. 57 patients heterozygous for beta-thalassaemia, 21 with G6PD deficiency and 44 controls were examined by typing the TATA-box in the promoter of the gene uridine diphosphate glucuronosyltransferase 1A. Nearly 80% of patients with increased bilirubin levels were heterozygous or homozygous for the UGT1A TA(7) variant associated with Gilbert's syndrome. These findings indicate that Gilbert's syndrome accounts for a large proportion of the variability of bilirubin levels in beta-thalassaemia and G6PD deficiency.
我们评估了最常见的胆红素结合缺陷——吉尔伯特综合征,对因遗传性血液系统疾病导致胆红素生成增加的受试者胆红素水平的影响。通过对尿苷二磷酸葡萄糖醛酸基转移酶1A基因启动子中的TATA盒进行分型,检查了57例β地中海贫血杂合子患者、21例葡萄糖-6-磷酸脱氢酶(G6PD)缺乏症患者和44例对照。胆红素水平升高的患者中,近80%为与吉尔伯特综合征相关的UGT1A TA(7)变异的杂合子或纯合子。这些发现表明,吉尔伯特综合征在β地中海贫血和G6PD缺乏症患者胆红素水平的变异性中占很大比例。