Résumé
Increased Endothelin I [ETI] activity may contribute to the complications of cirrhosis and portal hypertension. The main aim of this study was to determine the role of Endothelin I in cirrhotic patient with portal hypertention and hepatopulmonary syndrome. Fifty patients with biopsy proven cirrhosis and 50 normal healthy controls were selected for study. After getting informed consent, two dimensional echocardiography, chest x-ray and pulmonary function test have been done for all cirrhotic patients. Patients with cardiac and pulmonary disease history were excluded from the study and the cirrhotic patients who had proved to have intra-pulmonary vascular dilatation in their contrast echocardiogram were classified as the positive HPS. A total of 100 subject [60 males and 40 females in both case and control group] enrolled in the study. Among cirrhotic patients, 10 subjects with clinical and 7 subjects with sub clinical HPS were detected. The most common etiology of cirrhosis was HBV. Hepatopulmonary syndrome was significantly higher in class C [P=0.007]. There was no significant difference between plasma ETI level in both clinical and subclinical HPS compared to other cirrhotic patients. ET I levels in cirrhotic patients [2.29 pg/ml] were significantly higher in cirrhotic patients compared to that of normal healthy controls [0.85 pg/ml] [P = 0.038]. The effects of HPS on cirrhotic patient's survival are unclear. As to other studies, we found significant increase in plasma Et I level in cirrhotic patients rather that normal subjects, but in contrast to previous study we found no relation between Et I level and HPS. Only further studies with further numbers of cirrhosis-caused HPS patients may bridge up the gap between scientific effort and credibility in this field