The use of nonselective beta blockers is a risk factor for portal vein thrombosis in cirrhotic patients.

Background/Aim: A reduction in portal vein inflow velocity seems to predispose to the emergence of portal vein thrombosis (PVT). Nonselective ß-blockers (NSBBs), used to prevent variceal bleeding, may increase the development of PVT by reducing portal vein inflow velocity. In this retrospective case-control study, we evaluated the risk factors and clinical features of a first event of PVT in 130 cirrhotics, 19 (15%) with (PVT group) and 111 (85%) without PVT (non-PVT group). Patients and Methods: Patient evaluation and NNBB treatment were carried out according to the AASLD guidelines. Results: PVT was prevalently partial (84%) and asymptomatic (84%). Patients with PVT were treated with different regimens, and resolution of thrombosis was observed in about 50% of the cases. In both groups, HCV was the most frequent cause of cirrhosis and Child-Pugh score A was prevalent. Ascites and esophageal varices were more frequent in the PVT group (P = 0.05 and <0.000, respectively). Treatment with NSBBs was significantly more frequent in the PVT group than in the non-PVT group (P < 0.000). PVT was associated with higher prevalence of chronic renal disease (P = 0.002), higher PT impairment (P = 0.003) and lower AST and ALT (P = 0.000). At multivariate logistic regression analysis, history of esophageal varices (P = 0.007) and NSBB treatment (P = 0.0003) were independent risk factors significantly associated with PVT. Conclusions: Esophageal varices and NSBB treatment were independent risk factors of PVT. Larger studies should evaluate the risk between variceal bleeding and portal vein thrombosis of using NSBBs, particularly in the prevention of first bleeding in nonadvanced liver cirrhosis.

The effect of antiviral therapy on hepatitis C virus-related thrombocytopenia: a case report.

BACKGROUND: Autoimmune thrombocytopenic purpura is an immunological disorder characterized by increased platelet destruction due to presence of anti-platelet autoantibodies. Hepatitis C virus infection, which is one of the most common chronic viral infections worldwide, may cause secondary chronic immune thrombocytopenic purpura. CASE PRESENTATION: We report a case of a 51-year-old Caucasian female with hepatitis C virus infection who developed a severe, reversible, immune thrombocytopenia. Platelet count was as low as 56.000/mm3, hepatitis C virus serology was positive, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase and gamma-glutamyltransferase serum levels were elevated. Disorders potentially associated with autoimmune thrombocytopenic purpura were ruled out. A corticosteroid treatment was started and led to an increase in platelet count. The patient was then treated with pegylated-interferon alpha 2a and ribavirin. After four weeks of treatment hepatitis C virus - ribonucleic acid became undetectable and steroid treatment was discontinued. Six months of antiviral therapy achieved a sustained biochemical and virological response together with persistence of normal platelet count. CONCLUSION: In our case report hepatitis C virus seemed to play a pathogenic role in autoimmune thrombocytopenic purpura. Moreover, the successful response (negative hepatitis C virus - ribonucleic acid) to tapered steroids and antiviral therapy was useful to revert thrombocytopenia.