Wang C.-C.Tseng K.-C.Tzeng I.-S.JIA-HORNG KAO2021-09-042021-09-0420210929-6646https://www.scopus.com/inward/record.uri?eid=2-s2.0-85094832949&doi=10.1016%2fj.jfma.2020.10.015&partnerID=40&md5=7cfddad451f760fa335f9cfaea90027dhttps://scholars.lib.ntu.edu.tw/handle/123456789/581709Background/Purpose: De novo and early recurrent hepatocellular carcinoma (HCC) have been observed in clinical practice after direct antiviral agents (DAA) treatment. The study aims to investigate the change of cytokines and growth factors after hepatitis C virus (HCV) clearance by DAAs and their impact on the risk of HCC development. Methods: The chronic hepatitis C (CHC) patients with or without HCC who received DAA treatment were prospectively enrolled. The cytokines and growth factors were measured using Bio-Plex Pro? Human Cytokine 27-plex Assay before and 12 weeks off DAA treatment. Results: A total of 37 patients were enrolled for final analysis. There were 11 males (29.7%) and 26 females (70.3%). The mean age was 67.39 ± 10.48 years. 11 (29.7%) patients were HCV-related HCC patients. The HCV genotype included genotype 2 in 26 patients and genotype 1b in 10 patients, and genotype 6 in 1. Among them, 35 (94.6%) patients achieved sustained virologic response (SVR). Two patients with HCC failed to DAA treatment. In HCV-related HCC patients, serum IP-10 level significantly declined after HCV clearance, but no difference in five growth factors including G-CSF, GM-CSF, basic FGF, PDGF-BB, and VEGF. Several cytokines including IP-10 significantly declined after HCV clearance in CHC patients. Conclusion: This study showed only serum IP-10 level, a risk factor of HCC, was significantly declined after HCV clearance and no change in the markers of growth factors in HCV-related HCC patients, suggesting no promotion of HCC using DAA treatment for HCV-related HCC patients. ? 2020 Formosan Medical AssociationCytokine; Direct antiviral agent; Growth factor; Hepatitis C virus; Hepatocellular carcinoma[SDGs]SDG3albumin; antivirus agent; cytokine; daclatasvir; elbasvir plus grazoprevir; eotaxin; fibroblast growth factor 2; gamma interferon; gamma interferon inducible protein 10; granulocyte colony stimulating factor; granulocyte macrophage colony stimulating factor; growth factor; hepatitis B core antibody; hepatitis B surface antigen; interleukin 1 receptor blocking agent; interleukin 10; interleukin 12; interleukin 13; interleukin 15; interleukin 17; interleukin 1beta; interleukin 2; interleukin 4; interleukin 5; interleukin 6; interleukin 7; interleukin 8; interleukin 9; ledipasvir plus sofosbuvir; macrophage inflammatory protein 1alpha; macrophage inflammatory protein 1beta; monocyte chemotactic protein 1; platelet derived growth factor BB; RANTES; ribavirin; sofosbuvir; sofosbuvir plus velpatasvir; tumor necrosis factor; vasculotropin; virus RNA; antivirus agent; cytokine; adult; aged; albumin blood level; antiviral therapy; Article; cancer patient; cancer risk; cancer surgery; Child Pugh score; chronic hepatitis C; clinical article; data analysis software; female; genotype; Hepatitis C virus genotype 1; Hepatitis C virus genotype 2; Hepatitis C virus genotype 6; Hepatitis C virus subtype 1b; human; liver cell carcinoma; liver cirrhosis; male; middle aged; nonhuman; prospective study; protein blood level; protein expression; radiofrequency ablation; retrospective study; sustained virologic response; very elderly; viral clearance; viral RNA blood level; complication; genetics; Hepacivirus; hepatitis C; liver cell carcinoma; liver tumor; Aged; Antiviral Agents; Carcinoma, Hepatocellular; Cytokines; Female; Hepacivirus; Hepatitis C; Humans; Liver Neoplasms; Male; Middle Agedjournal article10.1016/j.jfma.2020.10.015331296212-s2.0-85094832949