Anthony W H Chan1,2, Grace L H Wong3,4,5, Hoi-Yun Chan3,4,5, Joanna H M Tong1,2, Yau-Hei Yu1,2, Paul C L Choi1, Henry L Y Chan3,4,5, Ka-Fai To1,2,4,5, Vincent W S Wong3,4,5. 1. Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong. 2. Li Ka Shing Institute of Health Science, Sir Y. K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong. 3. Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong. 4. Institute of Digestive Disease, Partner State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong. 5. State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.
Abstract
BACKGROUND AND AIMS: Concurrent fatty liver in hepatitis B virus (HBV)-infected patients without significant alcohol intake is a frequent and increasingly alarming problem because of the non-alcoholic fatty liver disease pandemic. The risk of HBV-related hepatocellular carcinoma (HCC) development was increased by concomitant obesity and diabetes. Direct evidence of the hepatocarcinogenic effect of fatty liver in chronic HBV remains elusive. We aimed to evaluate the risk of concurrent histologically proven fatty liver in HBV hepatocarcinogenesis. METHODS: We conducted a retrospective cohort study on a liver biopsy cohort of HBV-infected patients without significant alcohol intake to evaluate the prevalence of concurrent histologically proven fatty liver and its association with subsequent HCC development. We also examined nine polymorphisms on six non-alcoholic fatty liver disease-related candidate genes (ADIPOQ, APOC3, GCKR, LEPR, PNPLA3, and PPARG). RESULTS: Among 270 HBV-infected patients, concurrent fatty liver was found in 107 patients (39.6%) and was associated with metabolic risks, cirrhosis (P = 0.016) and PNPLA3 rs738409 CG/GG genotype (P = 0.002). At a median follow-up of 79.9 months, 11 patients (4.1%) developed HCC, and nine of them had concurrent fatty liver. By multivariable Cox analysis, concurrent fatty liver (HR 7.27, 95% confidence interval: 1.52-34.76; P = 0.013), age, cirrhosis, and APOC3 rs2854116 TC/CC genotype (HR 3.93, 95% confidence interval: 1.30-11.84; P = 0.013) were independent factors predicting HCC development. CONCLUSIONS: Concurrent fatty liver is common in HBV-infected patients and an independent risk factor potentiating HBV-associated HCC development by 7.3-fold. The risk of HBV-related HCC is increased by APOC3 gene polymorphism, and further characterization is required by its role.
BACKGROUND AND AIMS: Concurrent fatty liver in hepatitis B virus (HBV)-infectedpatients without significant alcohol intake is a frequent and increasingly alarming problem because of the non-alcoholic fatty liver disease pandemic. The risk of HBV-related hepatocellular carcinoma (HCC) development was increased by concomitant obesity and diabetes. Direct evidence of the hepatocarcinogenic effect of fatty liver in chronic HBV remains elusive. We aimed to evaluate the risk of concurrent histologically proven fatty liver in HBV hepatocarcinogenesis. METHODS: We conducted a retrospective cohort study on a liver biopsy cohort of HBV-infectedpatients without significant alcohol intake to evaluate the prevalence of concurrent histologically proven fatty liver and its association with subsequent HCC development. We also examined nine polymorphisms on six non-alcoholic fatty liver disease-related candidate genes (ADIPOQ, APOC3, GCKR, LEPR, PNPLA3, and PPARG). RESULTS: Among 270 HBV-infectedpatients, concurrent fatty liver was found in 107 patients (39.6%) and was associated with metabolic risks, cirrhosis (P = 0.016) and PNPLA3rs738409 CG/GG genotype (P = 0.002). At a median follow-up of 79.9 months, 11 patients (4.1%) developed HCC, and nine of them had concurrent fatty liver. By multivariable Cox analysis, concurrent fatty liver (HR 7.27, 95% confidence interval: 1.52-34.76; P = 0.013), age, cirrhosis, and APOC3rs2854116 TC/CC genotype (HR 3.93, 95% confidence interval: 1.30-11.84; P = 0.013) were independent factors predicting HCC development. CONCLUSIONS: Concurrent fatty liver is common in HBV-infectedpatients and an independent risk factor potentiating HBV-associated HCC development by 7.3-fold. The risk of HBV-related HCC is increased by APOC3 gene polymorphism, and further characterization is required by its role.
Authors: Norah A Terrault; Anna S F Lok; Brian J McMahon; Kyong-Mi Chang; Jessica P Hwang; Maureen M Jonas; Robert S Brown; Natalie H Bzowej; John B Wong Journal: Hepatology Date: 2018-04 Impact factor: 17.425
Authors: Mohammed Eslam; Shiv K Sarin; Vincent Wai-Sun Wong; Jian-Gao Fan; Takumi Kawaguchi; Sang Hoon Ahn; Ming-Hua Zheng; Gamal Shiha; Yusuf Yilmaz; Rino Gani; Shahinul Alam; Yock Young Dan; Jia-Horng Kao; Saeed Hamid; Ian Homer Cua; Wah-Kheong Chan; Diana Payawal; Soek-Siam Tan; Tawesak Tanwandee; Leon A Adams; Manoj Kumar; Masao Omata; Jacob George Journal: Hepatol Int Date: 2020-10-01 Impact factor: 6.047
Authors: Clifford G Tepper; Julie H T Dang; Susan L Stewart; Dao M Fang; Kimberly A Wong; Stephenie Y Liu; Ryan R Davis; Doan Y Dao; Jeffrey P Gregg; Natalie J Török; Moon S Chen Journal: Cancer Date: 2018-04-01 Impact factor: 6.860