045) Considering only patients with severe portal hypertension a

045). Considering only patients with severe portal hypertension at baseline (HVPG ≥ 12mmHg, n=13), the decrease was achieved by 50% of them, all patients in simvas-tatin group. The baseline mean AzBF were 501.2 ± 385 mL/ min in placebo group and 532.7 ± 365 mL/min in simvastatin group, and present

a decrease of 19% and 38%, respectively, at the end of the protocol (p=0.02). Although both HVPG and AzBF reduced after simvastatin use, the correlation between the methods was weak (r=0,39). Two thirds of the patients were taking nonselective beta adrenergic BGJ398 molecular weight blockers and these drugs did not interfere with simvastatin hemodynamic effect. Moderate and severe adverse events did not occur in simvastatin group. CONCLUSION: Simvastatin seems to be safe in liver cirrhosis and can significantly lower portal pressure. This effect is more evident in patients with severe portal hypertension, precisely the group most in need of prevention of its complications. The correlations between the HVPG and the AzBF is weak probably because the azygos system is only one of several drainage pathways in portal hypertension. These

results reinforce the trend of incorporating ALK inhibition statins in the therapeutic arsenal of cirrhotic portal hypertension. Disclosures: The following people have nothing to disclose: Priscila P. Flores, Monica Soldan, Guilherme F. Rezende Introduction: Portal vein thrombosis (PVT) in cirrhosis may aggravate portal hypertension with higher risk of failure to control variceal bleeding(VB) and early rebleeding. Aims: In patients with cirrhosis and PVT without hepatocellular carci-noma(HCC) 1. Analyze the clinical significance of VB at PVT diagnosis. 2. Evaluate influence of VB on mortality at 1 and 3 years. Methods: The study included 65 consecutive cirrhotics with PVT Janus kinase (JAK) without HCC classified into two groups according to presentation at diagnosis of PVT:

variceal bleed(VB) or no variceal bleed(NVB). We compared patients with VB with NVB and controls-74 patients with cirrhosis without PVT with VB at admission and similar Child-Pugh(CP) and MELD scores. Statistical analysis-SPSS 21. Results:Gender: 63%(41)males, age: 58.7±12years. Cirrhosis etiology: Alcohol-62%(40); viral-11%(7); alcohol+viral-12%(8); others- 15%(10). Severity of cirrhosis: CP class:A-19%(12), B-49%(32), C-32%(21). Scores:CP-8(2-15) and MELD-13(6-35). Type of PVT: Acute-88%(57) and chronic-12%(8). Extent of PVT: Main trunk-80%(52); left branch-35%(23); right branch-57%(37); main trunk+branches-31%(20); SMV-28%(18); splenic vein- 19%(12). Anticoagulation after PVT diagnosis was given in 19 patients (varfarin-15, LMWH-4). In 50 patients with follow-up imaging tests, portal vein recanalization(PVR) was noted in 50%(25)(Partial–13, total–12). Median follow-up(FU) 10(0- 376) months. Mortality at end FU 25/65(39%). VB at diagnosis of PVT was noted in 45%(29) patients.

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