Risør Louise M, Fenger Mogens, Olsen Niels V, Møller Søren
a Department of Clinical Physiology and Nuclear Medicine, Center of Functional and Diagnostic Imaging and Research 260 , Hvidovre Hospital, University of Copenhagen , Copenhagen , Denmark ;
b Department of Clinical Biochemistry, Hvidovre; Faculty of Health Sciences , University of Copenhagen , Copenhagen , Denmark ;
Scand J Clin Lab Invest. 2016;76(3):234-9. doi: 10.3109/00365513.2015.1137351. Epub 2016 Feb 29.
Erythropoietin (EPO) is produced in the liver during fetal life, but after birth the production shifts to the kidneys. The liver maintains a production capacity of 10% of the total EPO-production, but can be up-regulated to 100%. Previous studies have demonstrated both elevated and reduced concentrations of EPO in cirrhosis. Increased EPO concentrations could be expected due to anemia, hypoxia, renal hypoperfusion, or EPO-mediated hepatoprotective mechanisms. In contrast, poor hepatic production capacity may cause reduced EPO concentrations in cirrhosis. In the present paper we aimed to study hepatic and renal venous concentrations of EPO in relation to the severity of the disease.
We included 24 patients with alcoholic cirrhosis and eight age-matched healthy controls. All had a full catheterization performed with the determination of EPO concentrations in the hepatic, renal and femoral veins and artery. All patients were clinically, biochemically, and hemodynamically characterized.
The median arterial EPO concentrations in the cirrhotic patients and controls were 7.1 mIU/mL (range 3.5-179) and 7.2 mIU/mL (range 3.8-15.3), respectively. In the patient group we found no significant correlations to stage of disease of hemodynamic derangement.
We found no significant differences in EPO concentrations across the liver, kidney, or peripheral circulation in the patient or control groups; and no significant correlations to clinical, biochemical, or hemodynamic characteristics. This suggests that hepatic EPO synthesis is not enhanced in cirrhosis, but larger scale studies are needed to clarify this question.
促红细胞生成素（EPO）在胎儿期由肝脏产生，但出生后其产生部位转移至肾脏。肝脏维持着占EPO总产生量10%的生产能力，但可上调至100%。先前的研究表明肝硬化患者体内EPO浓度既可能升高也可能降低。由于贫血、缺氧、肾脏灌注不足或EPO介导的肝保护机制，EPO浓度升高是可以预期的。相反，肝脏生产能力不佳可能导致肝硬化患者体内EPO浓度降低。在本文中，我们旨在研究EPO的肝静脉和肾静脉浓度与疾病严重程度之间的关系。
我们纳入了24例酒精性肝硬化患者和8例年龄匹配的健康对照。所有人均进行了全面的导管插入术，测定肝静脉、肾静脉、股静脉和动脉中的EPO浓度。所有患者均进行了临床、生化和血流动力学特征分析。
肝硬化患者和对照组的动脉EPO浓度中位数分别为7.1 mIU/mL（范围3.5 - 179）和7.2 mIU/mL（范围3.8 - 15.3）。在患者组中，我们未发现与疾病分期或血流动力学紊乱存在显著相关性。
我们发现患者组和对照组在肝脏、肾脏或外周循环中的EPO浓度无显著差异；且与临床、生化或血流动力学特征均无显著相关性。这表明肝硬化时肝脏EPO合成未增强，但需要更大规模的研究来阐明这一问题。
