Lung-Yi Mak1,2, Rex Wan-Hin Hui1, James Fung1,2, Fen Liu3, Danny Ka-Ho Wong1,2, Bofei Li4, Ka-Shing Cheung1,5, Man-Fung Yuen6,7, Wai-Kay Seto8,9,10. 1. Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Pokfulam Road 102, Hong Kong, China. 2. State Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong, China. 3. Department of Gastroenterology and Hepatology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China. 4. Department of Surgery, Queen Mary Hospital, The University of Hong Kong, Hong Kong, China. 5. Department of Medicine, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China. 6. Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Pokfulam Road 102, Hong Kong, China. mfyuen@hkucc.hku.hk. 7. State Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong, China. mfyuen@hkucc.hku.hk. 8. Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Pokfulam Road 102, Hong Kong, China. wkseto@hku.hk. 9. State Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong, China. wkseto@hku.hk. 10. Department of Medicine, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China. wkseto@hku.hk.
Abstract
BACKGROUND: Concomitant chronic hepatitis B infection (CHB) and non-alcoholic fatty liver disease (NAFLD) is common, but the implications of NAFLD on clinical outcomes of CHB, including hepatocellular carcinoma (HCC), are not well-investigated. METHODS: CHB patients were recruited for transient elastography assessment for liver stiffness (LS), and controlled attenuation parameter (CAP), a non-invasive quantification of hepatic steatosis, and were prospectively followed up for development of HCC. Steatosis and severe steatosis were diagnosed by CAP ≥ 248 dB/m and ≥ 280 dB/m respectively, and advanced fibrosis/cirrhosis was diagnosed by LS ≥ 9 kPa. The independent effect of hepatic steatosis on HCC was examined via propensity score matching (PSM) of LS and other significant clinical variables. RESULTS: Forty-eight patients developed HCC among 2403 CHB patients (55.6% male, median age 55.6 years, 57.1% antiviral-treated, median ALT 26 U/L) during a median follow-up of 46.4 months. Multivariate Cox regression analysis showed age (HR 1.063), male (HR 2.032), Albumin-Bilirubin score (HR 2.393) and CAP (HR 0.993) were associated with HCC development. The cumulative probability of HCC was 2.88%, 1.56% and 0.71%, respectively for patients with no steatosis, mild-to-moderate steatosis, and severe steatosis, respectively (p = 0.01). The risk of HCC increased from 1.56 to 8.89% in patients without severe steatosis if advanced fibrosis/cirrhosis was present (p < 0.001). PSM yielded 957 pairs of CHB patients and hepatic steatosis was independently associated with HCC (HR 0.41). CONCLUSION: Reduced hepatic steatosis was significantly associated with a higher risk of incident HCC in CHB infection. Routine CAP and LS measurements are important for risk stratification.
BACKGROUND: Concomitant chronic hepatitis B infection (CHB) and non-alcoholic fatty liver disease (NAFLD) is common, but the implications of NAFLD on clinical outcomes of CHB, including hepatocellular carcinoma (HCC), are not well-investigated. METHODS: CHB patients were recruited for transient elastography assessment for liver stiffness (LS), and controlled attenuation parameter (CAP), a non-invasive quantification of hepatic steatosis, and were prospectively followed up for development of HCC. Steatosis and severe steatosis were diagnosed by CAP ≥ 248 dB/m and ≥ 280 dB/m respectively, and advanced fibrosis/cirrhosis was diagnosed by LS ≥ 9 kPa. The independent effect of hepatic steatosis on HCC was examined via propensity score matching (PSM) of LS and other significant clinical variables. RESULTS: Forty-eight patients developed HCC among 2403 CHB patients (55.6% male, median age 55.6 years, 57.1% antiviral-treated, median ALT 26 U/L) during a median follow-up of 46.4 months. Multivariate Cox regression analysis showed age (HR 1.063), male (HR 2.032), Albumin-Bilirubin score (HR 2.393) and CAP (HR 0.993) were associated with HCC development. The cumulative probability of HCC was 2.88%, 1.56% and 0.71%, respectively for patients with no steatosis, mild-to-moderate steatosis, and severe steatosis, respectively (p = 0.01). The risk of HCC increased from 1.56 to 8.89% in patients without severe steatosis if advanced fibrosis/cirrhosis was present (p < 0.001). PSM yielded 957 pairs of CHB patients and hepatic steatosis was independently associated with HCC (HR 0.41). CONCLUSION: Reduced hepatic steatosis was significantly associated with a higher risk of incident HCC in CHB infection. Routine CAP and LS measurements are important for risk stratification.
Authors: R W H Hui; W-K Seto; K-S Cheung; L-Y Mak; K S H Liu; J Fung; D K-H Wong; C-L Lai; M-F Yuen Journal: J Viral Hepat Date: 2017-08-25 Impact factor: 3.728
Authors: Lung-Yi Mak; Vania Cruz-Ramón; Paulina Chinchilla-López; Harrys A Torres; Noelle K LoConte; John P Rice; Lewis E Foxhall; Erich M Sturgis; Janette K Merrill; Howard H Bailey; Nahum Méndez-Sánchez; Man-Fung Yuen; Jessica P Hwang Journal: Am Soc Clin Oncol Educ Book Date: 2018-05-23
Authors: Jung Won Yun; Yong Kyun Cho; Jung Ho Park; Hong Joo Kim; Dong Il Park; Chong Il Sohn; Woo Kyu Jeon; Byung Ik Kim; Byung Ho Son; Jun Ho Shin Journal: Liver Int Date: 2009-01-22 Impact factor: 5.828