Original Article
Single institution experience of sorafenib for advanced HCC in a US tertiary care hospital
Abstract
Background: Sorafenib is first line chemotherapy for advanced hepatocellular carcinoma (HCC). There are little real-world experiences with sorafenib done on US population except for the US arm of the GIDEON study, a phase IV multi-national study. In this context, we present a single institution experience with sorafenib for HCC in a tertiary inner-city safety-net hospital of Chicago.
Methods: We retrospectively analyzed electronic medical records of patients with HCC (confirmed with radiographic criteria and/or biopsy) who received sorafenib from 2009 to 2016. We collected data regarding the demographics, characteristics of tumor, liver cirrhosis, duration of treatment with sorafenib, reported adverse effects with sorafenib and laboratory investigations done at the time of sorafenib initiation. Overall survival was calculated from the time of sorafenib initiation and cases were censored at the date of last follow up, if date of death was not known. Kaplan-Meier curves were estimated to evaluate the prognostic significance of various clinical variables.
Results: Fifty-nine patients received sorafenib in the study period and the median overall survival was 7 months (25–75 percentile =3–15 months). Alcohol was the leading cause of cirrhosis, 64% of them had Child-Turcotte-Pugh (CTP) class A cirrhosis or did not have cirrhosis and 73% had Barcelona stage C HCC at the time of sorafenib initiation. Close to half of them suffered from adverse effects of sorafenib, most common being those involving skin and gut. Patients with CTP class A cirrhosis or no cirrhosis (median OS 39 vs. 16 months, log rank test 3.913, P=0.048), absence of extrahepatic spread (EHS) (median OS 39 vs. 9 months, log rank test 5.632, P=0.018) and hepatitis C virus (HCV) infection (median OS 39 vs. 9 months, log rank test 5.015, P=0.025) had better survival.
Conclusions: Overall survival of patients with HCC treated with sorafenib in US is lower than those observed in cohorts from Europe or Japan. HCV infection could be a marker of benefit in those treated with sorafenib for HCC. Further studies to confirm this association and understand it’s pathophysiologic basis could be useful in development of other therapeutic options for advanced HCC.
Methods: We retrospectively analyzed electronic medical records of patients with HCC (confirmed with radiographic criteria and/or biopsy) who received sorafenib from 2009 to 2016. We collected data regarding the demographics, characteristics of tumor, liver cirrhosis, duration of treatment with sorafenib, reported adverse effects with sorafenib and laboratory investigations done at the time of sorafenib initiation. Overall survival was calculated from the time of sorafenib initiation and cases were censored at the date of last follow up, if date of death was not known. Kaplan-Meier curves were estimated to evaluate the prognostic significance of various clinical variables.
Results: Fifty-nine patients received sorafenib in the study period and the median overall survival was 7 months (25–75 percentile =3–15 months). Alcohol was the leading cause of cirrhosis, 64% of them had Child-Turcotte-Pugh (CTP) class A cirrhosis or did not have cirrhosis and 73% had Barcelona stage C HCC at the time of sorafenib initiation. Close to half of them suffered from adverse effects of sorafenib, most common being those involving skin and gut. Patients with CTP class A cirrhosis or no cirrhosis (median OS 39 vs. 16 months, log rank test 3.913, P=0.048), absence of extrahepatic spread (EHS) (median OS 39 vs. 9 months, log rank test 5.632, P=0.018) and hepatitis C virus (HCV) infection (median OS 39 vs. 9 months, log rank test 5.015, P=0.025) had better survival.
Conclusions: Overall survival of patients with HCC treated with sorafenib in US is lower than those observed in cohorts from Europe or Japan. HCV infection could be a marker of benefit in those treated with sorafenib for HCC. Further studies to confirm this association and understand it’s pathophysiologic basis could be useful in development of other therapeutic options for advanced HCC.
