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.

Obesity increases the risk of clinical decompensation in cirrhosis, possibly by increasing portal pressure. Whether weight reduction can be safely achieved through lifestyle changes (diet and exercise) in overweight/obese patients with cirrhosis, and if weight loss reducesportal pressure in this setting is unknown. This prospective, multicentric, uncontrolled pilot study enrolled patients with compensated cirrhosis, portal hypertension (hepatic venous pressure gradient, HVPG≥ 6mmHg) and body mass index (BMI)≥26 Kg/m2 in an intensive 16-week lifestyle intervention program (personalized hypocaloric normoproteic diet and 60 min/wk of supervised physical activity). We measured HVPG, body weight and composition, adipokines, health-related quality-oflife and safety data prior and after the intervention. Changes in HVPG and body weight were pre-defined as clinically relevant if ≥10% and ≥5%, respectively. Safety and body weight were re-assessed after 6 months. 60 patients were included and 50 completed the study (56±8 y/o; 62% male; NASH etiology 24%; BMI 33.3±3.2Kg/m2; Child A 92%; HVPG ≥10 mmHg 72%). Lifestyle intervention significantly decreased body weight (average -5.0±4.0 Kg; p<0.0001), by ≥ 5% in 52% and ≥10% in 16%. HVPG also significantly decreased (from 13.9±5.6 mmHg to 12.3±5.2 mmHg, p<0.0001), by ≥10% in 42% and ≥20% in 24%. A ≥10% body weight loss was associated with a greater decrease in HVPG (-23.7±19.9% vs. -8.2±16.6%,p=0.024). No episodes of clinical decompensation occurred. Weight loss achieved at 16-wks was maintained at 6-month;Child and MELD scores did not change.Conclusions. 16-weeks of diet and moderate exercise were safe and reduced body weight and portal pressure in overweight/obese patients with cirrhosis and portal hypertension.

Recent studies have shown that liver cirrhosis (LC) behaves as an acquired hypercoagulable state with increased thrombotic risk. This is why anticoagulation therapy (AT) is now frequently used in these patients. Variceal bleeding is a severe complication of LC. It is unknown whether AT may impact the outcome of bleeding in these patients. Fifty-two patients on AT with upper gastrointestinal bleeding (UGIB) were evaluated. Portal vein thrombosis (PVT) and different cardiovascular disorders (CVDs) were the indication for AT in 14 and 38 patients, respectively. Overall, 104 patients with LC and UGIB not under AT matched for severity of LC, age, sex, source of bleeding, and Sequential Organ Failure Assessment (SOFA) score served as controls. UGIB was attributed to portal hypertension (PH) in 99 (63%) patients and peptic/vascular lesions in 57 (37%). Twenty-six (17%) patients experienced 5-day failure; SOFA, source of UGIB, and PVT, but not AT, were independent predictors of 5-day failure. In addition, independent predictors of 6-week mortality, which was observed in 26 (11%) patients, were SOFA, Charlson Comorbidity index, and use of AT for a CVD. There were no differences between patients with/without AT in needs for rescue therapies, intensive care unit admission, transfusions, and hospital stay. Conclusions: Factors that impact the outcome of UGIB in patients under AT are degree of multiorgan failure and comorbidity, but not AT itself. (HEPATOLOGY 2015;62:575-583) T he use of anticoagulant therapy (AT) for prevention and management of thrombotic events may complicate the management of upper gastrointestinal bleeding (UGIB), increasing the morbidity/mortality associated to it. [1][2][3][4] Until recently, liver cirrhosis (LC) has been considered a hypocoagulant and prohemorrhagic condition owing reduction in platelet count and increase in prothrombin time. Currently, this paradigm has been challenged by the observation that patients with

HVPG monitoring, by stratifying risk and targeting therapy, improves the survival achieved with currently recommended treatment to prevent VRB using β-blockers and ligation. HVPG-guided therapy achieved a greater reduction in PP, which may have contributed to reduce the risk of rebleeding and of further decompensation of cirrhosis, thus contributing to a better survival. (Hepatology 2017;65:1693-1707).