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

BACKGROUND AND AIM: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: This study suggests a close interaction among MDA, endotoxin, and NOx and that these substances are also associated with hemodynamic derangement in cirrhosis.