Post-treatment alpha fetoprotein and platelets predict hepatocellular carcinoma development in dual-infected hepatitis B and C patients after eradication of hepatitis C
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Ming-Lun Yeh1,2,3, Ching-I Huang2, Chung-Feng Huang2,3, Meng-Hsuan Hsieh2,3,5, Ming-Yen Hsieh2, Zu-Yau Lin2,3, Shinn-Cherng Chen2,3, Jee-Fu Huang2,3, Po-Lin Kuo1, Hsing-Tao Kuo6,7,*, Chia-Yen Dai1,2,3,4,5,*, Ming-Lung Yu2,3,4,8 and Wan-Long Chuang2,3,4
1Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
2Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
3School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
4Lipid Science and Aging Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan
5Department of Occupational and Environmental Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
6Division of Hepatogastroenterology, Department of Internal Medicine, Chi-Mei Medical Center, Tainan, Taiwan
7Department of Senior Citizen Service Management Chia Nan University of Pharmacy and Science, Tainan, Taiwan
8Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan
*These authors contributed equally to this work
Chia-Yen Dai, email: [email protected]
Hsing-Tao Kuo, email: [email protected]
Keywords: hepatocellular carcinoma, incidence, hepatitis B virus, hepatitis C virus, dual infection
Received: August 02, 2017 Accepted: September 21, 2017 Published: January 13, 2018
We investigated the long-term risk of hepatocellular carcinoma (HCC) in dual-infected hepatitis B and C patients after eradication of hepatitis C virus (HCV). A total of 164 (62% male, median age, 50.5 years) hepatitis B and C dual-infected patients who achieved HCV sustained virological response were recruited. Half the patients were HCV genotype 1 with a median viral load of 5.5 log10 IU/mL, and 22.6%had an HBV DNA level ≥ 2000 IU/mL before therapy. HCC developed in 14 patients (8.5%), with an annual incidence of 1.38% per person-year. The 3-year, 5-year, 10-year, and 15-year cumulative probabilities were 2.5%, 5.1%, 12.6%, and 22.7%, respectively. Six months after treatment, a Cox regression hazard analysis revealed platelet level (HR: 0.98, 95% CI: 0.957–0.999, P = 0.038) and AFP level (HR: 1.20, 95% CI: 1.031–1.400, P = 0.019) to be independent factors in HCC. A higher 10-year cumulative risk of HCC was detected in patients with 6-month post-treatment AFP levels > 5.0 ng/mL and platelet levels < 130 x1000/μL (54.9%), compared to patients with neither (8.6%). Although the risk of HCC is low, surveillance of HCC is encouraged in dual-infected patients after eradication of HCV. Post-treatment AFP and platelet levels predict HCC development.
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