Open AccessPlasma nitrate/nitrite and endothelin‐1 in patients with liver cirrhosis
Author(s) -
Curgunlu Aslı,
Vural Pervin,
Canbaz Mukaddes,
Erten Nilgun,
Karan M. Akif,
Tascioglu Cemil
Publication year - 2005
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.20074
Subject(s) - cirrhosis , nitric oxide , medicine , gastroenterology , ascites , nitrite , liver disease , endothelin receptor , nitrate , endocrinology , chemistry , receptor , organic chemistry
Abstract 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 ( P <0.01 and P <0.001) 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 ( P< 0.05), and in the Child C subgroup vs. either subgroup A or B ( P <0.05). 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 ( P <0.05 and P <0.01). 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. J. Clin. Lab. Anal. 19:177–181, 2005. © 2005 Wiley‐Liss, Inc.