Increased plasma malondialdehyde in patients with viral cirrhosis and its relationships to plasma nitric oxide, endotoxin, and portal pressure.

Abstract

Increased oxidative stress is involved in the development of portal hypertension in cirrhosis. Our study aimed to assess the relationship between oxidative stress and hemodynamic parameters in cirrhotic patients.
Forty-two patients with viral cirrhosis and 24 normal controls were enrolled. Measurements of plasma levels of malondialdehyde (MDA), nitrite/nitrate (NOx), endotoxin, and activities of superoxide dismutase (SOD) were carried out in all subjects. Systemic and splanchnic hemodynamic measurements were carried out in cirrhotic patients.
Plasma levels of MDA, endotoxin, and NOx were significantly higher in cirrhotic patients than in normal controls (900 +/- 751 versus 226 +/- 16 nM, P < 0.01; 62.0 +/- 26.0 versus 14.8 +/- 4.1 pg/mL, P < 0.01; 50.5 +/- 22.6 versus 15.0 +/- 9.2 nM, P < 0.01, respectively). Activities of SOD were significantly decreased in cirrhotic patients compared with in normal controls (2.62 +/- 0.7 versus 6.8 +/- 0.4 U/mL). Further, plasma levels of MDA in cirrhotic patients were significantly positively associated with hepatic venous pressure gradient (HVPG) (r = 0.35; P = 0.025), wedge hepatic venous pressure (WHVP) (r = 0.42; P = 0.007), and hepatic sinusoid resistance (HSR) (r = 0.33; P = 0.033). Plasma MDA levels also correlated positively with plasma endotoxin (r = 0.71, P < 0.001) and NOx (r = 0.55, P < 0.001) levels in the cirrhotic patients. Multiregression analysis showed that the independent and strongest factors to predict HVPG, WHVP, and HSR are plasma levels of NOx, MDA, and endotoxin, respectively.
This study suggests a close interaction among MDA, endotoxin, and NOx and that these substances are also associated with hemodynamic derangement in cirrhosis.