Nontumorous Portal Vein Thrombosis in Liver Cirrhosis: Possible Role of ß-Blockers.

OBJECTIVE: Nonselective ß-blockers (NSBB) are used in liver cirrhosis (LC) to prevent variceal bleeding because they decrease portal pressure. A main risk factor for the development of portal vein thrombosis (PVT) in LC is decreased portal vein inflow velocity. The aim of our study was to examine retrospectively the incidence of PVT and its correlation with the use of ß-blockers in a cohort of LC patients. SUBJECTS AND METHODS: Data from 230 LC patients (90% Child-Pugh class A), who had been followed up for at least 5 years, were reviewed. The diagnosis of PVT was made by ultrasound. The presence of PVT was evaluated with multiple logistic regression analysis where the independent variables were those significant in the univariate analysis. RESULTS: The prevalence of PVT at baseline was 4.5%, and the incidence was 4.3% at 5 years; among the subjects taking ß blockers, 46.4% were taking NSBB. A total of 19 PVT cases were found. Grade of esophageal varices (p < 0.01), PLT (p < 0.003), INR (p < 0.03), spleen diameter (p < 0.001) and PLT/spleen ratio (p < 0.0005) were significantly associated with PVT. The use of NSBB indicated a higher risk of PVT compared to selective ß-blockers (SBB) (p < 0.05). In logistic regression analysis only the grade of esophageal varices was significant (p < 0.02). Univariate analysis of patients taking ß-blockers showed an association of PVT with grade of esophageal varices (p < 0.01), CP class (p < 0.02), AST (p < 0.03), ALT and albumin (p < 0.02), PLT count and PLT/LD (p < 0.03), longitudinal diameter of the spleen (p < 0.005), ascites (p < 0.05), portal vein (p < 0.0001) and NSBB (OR 8.1; 95% CI 1.7-38.8). CONCLUSION: NSBB seem to play a role in PV thrombogenesis. Further studies are needed, especially in decompensated LC patients.

Hepatocellular carcinoma: comparison of two different periods at the same center.

AIMS: To analyze the main etiological factors and some clinical characteristics of patients with HCC at diagnosis and to compare them with those we described ten years ago. METHODS: 179 patients were included in Group 1, while 132 patients were included in Group 2. For all patients age, sex, serum markers of hepatitis B and C viruses, alcohol consumption, serum alpha feto-protein (AFP) levels and the main liver function parameters at HCC diagnosis were recorded. RESULTS: Mean age was 66.0 years for Group 1 and 69.0 for Group 2 (P=0.005). HCV was responsible for 80.3% of HCC cases in Group 2 versus 72% in Group 1 (P=0.005). HBV alone and co-infection of HCV+HBV decreased, but not significantly. In Group 1 only four patients had an underlying normal liver, while in Group 2 no patients showed an underlying normal liver (P=ns). HCC was more frequently associated with Child class A in Group 2 (P=0.0001), whereas in Group 1 it was more frequently associated with class C (P=0.0001). Staging of HCC correlated inversely when patients of Groups 1 and 2 were compared (P<0.03). AFP serum levels were above normal in 72% of cases in Group 1 and in 41.5% in Group 2 (P=0.0001). CONCLUSION: This study shows that over the last decade a number of characteristics of patients with HCC in our region have changed, particularly age at onset of HCC, staging of underlying liver disease and staging of HCC.