In a randomized controlled trial, addition of simvastatin to standard therapy did not reduce rebleeding, but was associated with a survival benefit for patients with Child-Pugh class A or B cirrhosis. Survival was not the primary end point of the study, so these results require validation. The incidence of rhabdomyolysis in patients receiving 40 mg/d simvastatin was higher than expected. European Clinical Trial Database ID: EUDRACT 2009-016500-24; ClinicalTrials.gov ID: NCT01095185.

In 30-50% of patients with portal thrombosis, no underlying etiology is found. The recent reports of new hereditary clotting defects are contributing to the understanding of this problem, but they only justify a small number of idiopathic cases. Instead, anticoagulant protein C resistance, caused by a mutation in the V factor gene, appears to be at least 10 times more common than any of the other known inherited deficiencies of anticoagulant proteins. In spite of that, extensive thrombosis of portomesenteric or hepatic venous circulation has been rarely described in this hereditary clotting defect. We report a typical case of familial and recidivant deep vein thrombosis in a young man heterozygous for the factor V Leiden mutation (Arg506-Gln), who developed an acute portal and mesenteric vein thrombosis. The patient was discharged with an oral anticoagulant treatment and remains asymptomatic 2 years later. In conclusion, the high prevalence of the factor V Leiden in young and aged patients with idiopathic vein thrombosis and the case here described makes it obligatory to consider this disorder in patients with portal and/or mesenteric vein thrombosis, especially in those without evident etiology.