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Quantification of cortisol inactivation in cirrhosis of the liver.

机译:量化肝硬化中的皮质醇失活。

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摘要

Impaired cortisol inactivation in patients with cirrhosis of the liver has been described, but precise data are limited and the pathophysiological significance of this finding has to be elucidated. Therefore, we assessed the main urinary cortisol metabolites using capillary gas chromatography and urinary free cortisol using an enzyme immunoassay in 20 consecutive patients with cirrhosis of the liver and in 28 healthy controls; ratios of cortisol inactivation were calculated (cortisol metabolites/cortisone metabolites, and sum of tetrahydrogenated cortisol metabolites/free urinary cortisol). In patients with cirrhosis free urinary cortisol was normal, whereas the sum of cortisol metabolites was significantly reduced; therefore, cortisol synthesis seems to be adequately adapted to the decreased hepatic inactivation (conjugation, ring A-reduction). A significantly reduced ratio of cortisol metabolites to cortisone metabolites indicating impaired renal 11beta-hydroxysteroid dehydrogenase activity was only found in a subgroup of patients with ascites.
机译:已经描述了肝硬化患者的皮质醇失活受损,但是精确的数据有限,必须阐明这一发现的病理生理意义。因此,我们使用毛细管气相色谱法和酶联免疫法评估了20例连续性肝硬化患者和28例健康对照者的主要尿皮质醇含量和游离尿皮质醇含量。计算皮质醇失活的比率(皮质醇代谢物/可的松代谢物,以及四氢化皮质醇代谢物/游离尿皮质醇的总和)。肝硬化患者的游离尿皮质醇是正常的,而皮质醇代谢产物的总和却明显减少;因此,皮质醇的合成似乎足以适应减少的肝失活(结合,环A减少)。仅在患有腹水的患者亚组中发现皮质醇代谢物与可的松代谢物的比率显着降低,表明肾11β-羟类固醇脱氢酶活性受损。

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