Methods: We maintained a de-identified database including mortality outcomes in all patients transplanted at our center since 2006. It was retrospectively Silmitasertib chemical structure reviewed for all LT for HCV cirrhosis and includes: transplant date, date and cause of death, significant co-morbidities, and factors that may have contributed to death. The cause of death was categorized as attributable or not attributable to HCV recurrence. Attributable causes included recurrent HCV with cirrhosis, ascites, or fibrosing cholestatic hepatitis (FCH); also non-compliance, failure to thrive, CMV infection, or renal failure in the context of recurrent HCV.

Non-attributable causes included primary non-function (PNF)/delayed graft function, ischemic reperfusion injury, early hepatic artery thrombosis/abscess, peri-operative deaths, early death from infection, cardiovascular events, hepatocellular carcinoma (HCC) and other cancers, graft versus host disease. Results: From 1/1/2006 to 3/31/14, of 330 patients transplanted at our center, 125 (38%) had underlying HCV of whom 38 have died. Sixteen (42%) deaths in HCV patients were attributable

to HCV; 22 (58%) were not. Non-attributable causes included 14 deaths <6 months after transplant with 4 Selleck PLX4032 peri-operative, 5 recurrent HCC, 3 infection, 2 PNF, 2 bleeding, and 2 suicides. Patients with neither HCV nor HCC had a 3-yr survival of >90%. Without the deaths attributable to HCV, the survival of those transplanted for HCV cirrhosis was 109/125 (87%), the same % as that in non-HCV patients. Conclusion: Treatment of HCV pre-or post liver transplant may improve survival outcomes, however because many of the deaths are not attributable to HCV recurrence, possible improvement is limited. In our series, a running survival of 70% over 8-yr might have been improved to 87% if recurrent HCV could have been else avoided. This may be possible in the era of DAAs. Survival & mortality of

HCV & non HCV liver transplant patients Disclosures: The following people have nothing to disclose: Carmi S. Punzalan, Graham F. Barnard Purpose: Hepatitis C virus (HCV) has been implicated in B cell lymphomagenesis. Antiviral therapy (AVT) is widely accepted in HCV-infected patients (pts) with significant fibrosis/cirrhosis – a sine qua non for hepatocellular carcinoma development. We evaluated the liver disease stages of pts with HCV-associated B-cell non-Hodgkin lymphoma (HCV-NHL). Methods: Pts with HCV-NHL seen at MD Anderson Cancer Center between 2008-2014 were evaluated. Status of underlying liver disease was ascertained within a year of HCV-NHL diagnosis by non-invasive fibrosis markers, radiology or liver biopsy. Advanced liver disease was defined as Metavir fibrosis stage ≥ 3.