Insufficient nitric oxide production inside the liver contributes to increased intrahepatic vascular resistance (IHVR), which plays an important role in pathogenesis of liver cirrhosis. Statins are proposed to have a promising role in reducing portal hypertension by increasing intrahepatic nitric oxide level, without having the unfavorable effect of systemic vasodilatation, through their upregulating effect on endothelial nitric oxide synthase (eNOS) enzyme.
AIM OF THE WORK
Evaluating the effect of simvastatin on portal hemodynamics in Egyptian HCV- positive cirrhotic patients and its relation to serum eNOS level.
SUBJECTS AND METHODS
Subjects:
40 patients with compensated HCV-liver cirrhosis and portal hypertension received 40 mg of simvastatin daily for 3 months. They were identified based on clinical and laboratory evaluation, abdominal ultrasound, Doppler study of portal vein and upper gastrointestinal endoscopy.
• Patients with liver cirrhosis due to etiologies other than HCV, liver decompensation, non-cirrhotic portal hypertension, hepatic or extrahepatic malignancy, history of direct acting antiviral therapy and history of hypersensitivity to statins were excluded from the study.
Serum levels of CPK and transaminases (TA) were evaluated at baseline and after one week of starting statin therapy. Patients with levels more than three folds the upper limit of normal (ULN) were excluded from the study.