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吉尔伯特综合征患者胆红素氧化代谢产物的尿排泄情况。

Urinary excretion of oxidative metabolites of bilirubin in subjects with Gilbert syndrome.

作者信息

Vítek Libor, Kráslová Ivana, Muchová Lucie, Novotný Ladislav, Yamaguchi Tokio

机构信息

Institute of Clinical Biochemistry and Laboratory Diagnostics, First Medical Faculty, Charles University, Prague, Czech Republic.

出版信息

J Gastroenterol Hepatol. 2007 Jun;22(6):841-5. doi: 10.1111/j.1440-1746.2006.04564.x.

DOI:10.1111/j.1440-1746.2006.04564.x
PMID:17565639
Abstract

BACKGROUND AND AIM

Bilirubin is a potent endogenous antioxidant substance. Recent data suggest a direct relationship exists between urinary excretion of biopyrrins, a novel group of bilirubin oxidative metabolites, and severity of oxidative stress. The aim of this study was to evaluate urinary excretion of biopyrrins in subjects with Gilbert syndrome.

METHODS

The study included patients with Gilbert syndrome (n = 33) and healthy blood donors (n = 25). In all subjects complete biochemical tests were conducted along with analysis of urinary excretion of biopyrrins. Linear and logistic regression analyses were used for multiple adjustments of possible confounders/modifiers.

RESULTS

As expected, high serum bilirubin levels were found in the Gilbert syndrome group as compared to controls (27.8 +/- 9.7 vs 9.9 +/- 3.0 micromol/L, P < 0.001). In contrast, urinary levels of biopyrrins were substantially lower in the Gilbert syndrome group as compared to normobilirubinemic control subjects (19.9 +/- 26.0 vs 90.2 +/- 139.1 U/g urinary creatinine, P < 0.001). The Gilbert syndrome group also had very low prevalence odds ratios for urinary biopyrrins above the median of the control values even after adjustment for possibly confounding factors (odds ratio 0.18, 95% confidence interval 0.33-0.94; P = 0.042).

CONCLUSIONS

An inverse relationship was demonstrated between serum bilirubin level and urinary excretion of biopyrrins, which is presumably due to antioxidative effects of elevated serum bilirubin levels in Gilbert syndrome.

摘要

背景与目的

胆红素是一种强大的内源性抗氧化物质。近期数据表明,新型胆红素氧化代谢产物双吡咯啉的尿排泄与氧化应激的严重程度之间存在直接关系。本研究的目的是评估吉尔伯特综合征患者双吡咯啉的尿排泄情况。

方法

该研究纳入了吉尔伯特综合征患者(n = 33)和健康献血者(n = 25)。对所有受试者进行了全面的生化检测以及双吡咯啉尿排泄分析。采用线性和逻辑回归分析对可能的混杂因素/调节因素进行多重校正。

结果

正如预期的那样,与对照组相比,吉尔伯特综合征组的血清胆红素水平较高(27.8±9.7对9.9±3.0微摩尔/升,P < 0.001)。相比之下,与正常胆红素血症对照组相比,吉尔伯特综合征组的双吡咯啉尿水平显著降低(19.9±26.0对90.2±139.1单位/克尿肌酐,P < 0.001)。即使在对可能的混杂因素进行校正后,吉尔伯特综合征组尿双吡咯啉高于对照值中位数的患病率比值比也非常低(比值比0.18,95%置信区间0.33 - 0.94;P = 0.042)。

结论

血清胆红素水平与双吡咯啉尿排泄之间呈负相关,这可能是由于吉尔伯特综合征中血清胆红素水平升高的抗氧化作用所致。

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