Okolicsanyi L, Orlando R, Venuti M, Dal Brun G, Cobelli C, Ruggeri A, Salvan A
Am J Physiol. 1981 May;240(5):R266-71. doi: 10.1152/ajpregu.1981.240.5.R266.
The mechanism of fasting hyperbilirubinemia (FH) is not fully understood. We investigated basal bilirubin kinetics in 20 Gilbert's patients and in 7 healthy volunteers. The study was repeated in seven of these Gilbert's patients after 48-h fasting. A two-compartment model proved to be adequate for interpreting crystalline bilirubin kinetics in these individuals. The parameters of bilirubin kinetics were estimated by employing a maximum likelihood parameter estimation technique. Consistency of the model and uniqueness of the estimated parameter values (from the covariance matrix) were shown. Our results confirmed previous observations regarding impaired bilirubin kinetics in Gilbert's patients as compared to controls. The main results obtained from kinetic studies in Gilbert's patients after fasting were i) no modification in the bilirubin clearance, and ii) a more than twice increase of bilirubin turnover. These data indicate that FH is related to an increased bilirubin production (mainly intrahepatic). Furthermore, evidence arises from this study that the bilirubin tolerance test is a useful diagnostic test for Gilbert's syndrome.
禁食性高胆红素血症（FH）的机制尚未完全明确。我们对20例吉尔伯特综合征患者和7名健康志愿者的基础胆红素动力学进行了研究。其中7例吉尔伯特综合征患者在禁食48小时后重复进行了该研究。结果表明，双室模型足以解释这些个体中结晶胆红素的动力学。采用最大似然参数估计技术估算胆红素动力学参数。结果显示了模型的一致性和估计参数值（来自协方差矩阵）的唯一性。我们的研究结果证实了之前关于吉尔伯特综合征患者与对照组相比胆红素动力学受损的观察结果。对吉尔伯特综合征患者禁食后的动力学研究得出的主要结果为：i）胆红素清除率无变化；ii）胆红素周转率增加了两倍多。这些数据表明，FH与胆红素生成增加（主要是肝内生成）有关。此外，该研究表明胆红素耐量试验是诊断吉尔伯特综合征的一项有用检测方法。
