Premium
Predictive score for hepatocellular carcinoma after hepatitis B e antigen loss in patients treated with entecavir or tenofovir
Author(s) -
Lim Tae Seop,
Lee Hyun Woong,
Lee Jung Il,
Kim In Hee,
Lee Chang Hun,
Jang Byoung Kuk,
Chung Woo Jin,
Yim Hyung Joon,
Suh Sang Jun,
Seo Yeon Seok,
Lee Han Ah,
Yu Jung Hwan,
Lee JinWoo,
Kim Sang Gyune,
Kim Young Seok,
Park Soo Young,
Tak Won Young,
Kim Soon Sun,
Cheong Jae Youn,
Jeong Soung Won,
Jang Jae Young,
Rou Woo Sun,
Lee Byung Seok,
Kim Seung Up
Publication year - 2020
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/jvh.13316
Subject(s) - entecavir , hepatocellular carcinoma , medicine , hazard ratio , cirrhosis , gastroenterology , cohort , tenofovir , receiver operating characteristic , hepatitis b virus , hepatitis b , confidence interval , framingham risk score , oncology , immunology , virus , human immunodeficiency virus (hiv) , disease , lamivudine
The risk of developing hepatocellular carcinoma (HCC) after hepatitis B e antigen seroclearance (ESC) remains unclear. We established and validated a new risk prediction model for HCC development after ESC in patients with chronic hepatitis B (CHB) receiving antiviral therapy (AVT). Between 2006 and 2016, 769 patients (training cohort) and 1,061 patients (validation cohort) with CHB who experienced ESC during AVT using entecavir (ETV) or tenofovir disoproxil fumarate (TDF) were recruited. In the multivariate analysis, male sex (hazard ratio [HR] = 2.092; 95% confidence interval [CI] = 1.152‐3.800), cirrhosis (HR = 5.141; 95% CI = 2.367‐11.167) and fibrosis‐4 index (FIB‐4) of >3.25 (HR = 2.070; 95% CI = 1.184‐3.620) were the independent risk factors for HCC development (all P < .05). Accordingly, a novel HCC‐ESC AVT model was developed (1 x [sex: male = 1, female = 0] + 3 x (cirrhosis = 1, noncirrhosis = 0) + 1 x (FIB‐4: >3.25 = 1, ≤3.25 = 0). The cumulative risk for HCC development was significantly different among the risk groups based on the HCC‐ESC AVT category (0‐1, 2‐4 and 5 for the low‐, intermediate‐ and high‐risk groups, respectively) (overall P < .001, log‐rank test). The area under the receiver operating characteristic curve (AUC) for predicting HCC development 3, 5 and 10 years after ESC was 0.791, 0.771 and 0.790, respectively (all P < .05). The predictive value of the HCC‐ESC AVT model was similar in the validation cohort (AUC = 0.802, 0.774 and 0.776 at 3, 5 and 10 years, respectively; all P < .05). Hence, we have developed and validated a new HCC‐ESC AVT model for HCC development, which includes male sex, cirrhosis and FIB‐4 of >3.25 as constituent variables.