Plasma nitrate/nitrite and endothelin-1 in patients with liver cirrhosis

✍ Scribed by Aslı Curgunlu; Pervin Vural; Mukaddes Canbaz; Nilgun Erten; M. Akif Karan; Cemil Tascioglu

• Publisher: John Wiley and Sons
• Year: 2005
• Tongue: English
• Weight: 89 KB
• Volume: 19
• Category: Article
• ISSN: 0887-8013
• DOI: 10.1002/jcla.20074

✦ Synopsis

The aims of this study were to examine the plasma nitrate/nitrite (NOx; two end products of nitric oxide metabolism) and endothelin-1 (ET-1) concentrations in patients with liver cirrhosis, and to investigate whether there is a relationship between these two vasoactive parameters and the course of disease. Twenty-eight patients with liver cirrhosis (11 HBV-related, four HCV-related, four alcohol-related, and nine with idiopathic etiology) and 25 healthy subjects (controls) were included in the study. The venous plasma concentrations of NOx and ET-1 were significantly higher (Po0.01 and Po0.001) in the patients with cirrhosis than in the controls. A significant increase in ET-1 was observed in the Child B subgroup vs. Child A (Po0.05), and in the Child C subgroup vs. either subgroup A or B (Po0.05). There were no statistical differences between study subgroups (Child A-C) in the mean of NOx values. Plasma NOx and ET-1 were significantly increased in patients with ascites compared to those without ascites (Po0.05 and Po0.01). Increased nitric oxide synthesis may be a compensation mechanism against endothelial injury. The highest ET-1 levels in Child C and moderately increased ET-1 levels in Child B, and the lower increase of ET-1 levels in Child A patients suggest that plasma ET-1 increases with the progression of the disease. The fact that NOx and ET-1 levels were higher in patients with decompensated cirrhosis (patients with ascites) than in those with compensated cirrhosis (patients without ascites), and the presence of a strong correlation between ET-1, NOx, and the degree of varices, supports the suggestion that there is a relationship between NOx, ET-1, and portal hypertension. Our study demonstrates that increased ET and nitric oxide metabolism is associated with the hemodynamic alterations induced by portal hypertension.