The aim of present study was to evaluate relationships between degree of portal hypertension, severity of the disease, and bleeding status in patients with liver cirrhosis. Patients and methods. All study patients with liver cirrhosis underwent hepatic venous pressure gradient measurements, endoscopy, clinical and biochemical evaluation. Liver function was evaluated according to Child-Turcotte-Pugh (Child’s) scoring system. Patients with decompensated cirrhosis (presence of severe ascites, acute variceal bleeding occurring within 14 days, hepatorenal syndrome, cardiopulmonary disorders, transaminase levels >10 times higher the upper normal limit), active alcohol intake, use of antiviral therapy and/or beta-blockers were excluded from the study.
. One hundred twenty-eight patients with liver cirrhosis (male/female, 67/61; mean age, 53.8±12.7 years) were included into the study. Etiology of cirrhosis was viral hepatitis, alcoholic liver disease, cryptogenic and miscellaneous reasons in 57, 49, 14, and 8 patients, respectively. Child’s stages A, B, and C of liver cirrhosis were established in 28 (21.9%), 70 (54.9%), and 30 (23.4%) patients, respectively. The mean hepatic venous pressure gradient significantly differed among patients with different Child’s classes: 13.8±5.3 mm Hg, 17.3±4.6 mm Hg, and 17.7±5.05 mm Hg in Child’s A, B, and C classes, respectively (P
=0.003). The mean hepatic venous pressure gradient in patients with grade I, II, and III varices was 14.8±4.5, 16.1±4.3, and 19.3±4.7 mm Hg, respectively (P
=0.0001). Since nonbleeders had both small and large esophageal varices, patients with large varices were analyzed separately. The mean hepatic venous pressure gradient in patients with large (grade II and III) varices was significantly higher than that in patients with small (grade I) varices (17.8±4.8 mm Hg vs 14.6±4.8 mm Hg, P
=0.007). Thirty-four (26.6%) patients had a history of previous variceal bleeding; all of them had large (20.6% – grade II, and 79.4% – grade III) varices. In patients with large varices, the mean hepatic venous pressure gradient was significantly higher in bleeders than in nonbleeders (18.7±4.7 mm Hg vs 15.9±4.7 mm Hg, P
. Hepatic venous pressure gradient correlates with severity of liver disease, size of varices, and bleeding status. Among cirrhotics with large esophageal varices, bleeders have a significantly higher hepatic venous pressure gradient than nonbleeders. Hepatic venous pressure gradient measurement is useful in clinical practice selecting cirrhotic patients at the highest risk of variceal bleeding and guiding to specific therapy.