Direct-acting antiviral agents do not increase the incidence of hepatocellular carcinoma development: a prospective, multicenter study.


Journal

Hepatology international
ISSN: 1936-0541
Titre abrégé: Hepatol Int
Pays: United States
ID NLM: 101304009

Informations de publication

Date de publication:
May 2019
Historique:
received: 26 10 2018
accepted: 12 02 2019
pubmed: 2 3 2019
medline: 21 1 2020
entrez: 2 3 2019
Statut: ppublish

Résumé

While achieving sustained virological response (SVR) following interferon-based or direct-acting antiviral agent (DAA) treatments reduces the incidence of hepatocellular carcinoma (HCC), an increase in unexpected early occurrence or recurrence of HCC after hepatitis C virus elimination by DAA treatments has been reported. We prospectively investigated the incidence and risk factors of HCC after DAA treatment in a large multicenter cohort in Japan. Patients with chronic hepatitis C with or without cirrhosis who were treated with DAAs and obtained SVR were enrolled. DAAs were administered for 3 or 6 months. A total of 2552 patients were enrolled. Of these, 70 patients (2.7%) developed HCC. The 12-, 24-, and 36-month cumulative HCC incidences were 1.3%, 2.9%, and 4.9% in all patients; 2.5%, 5.2%, and 10.0% in those with cirrhosis; and 0.9%, 2.1%, and 2.9% in those without cirrhosis, respectively. Multivariate analysis revealed age, sex, gamma-glutamyl transpeptidase level, and fibrosis-4 index to be independent factors associated with HCC. Patients with these four factors had an approximately six-to-sevenfold increased risk for HCC development. Five patients with large and early tumor occurrence did not receive contrast imaging examinations before treatment. Although the results of our prospective study suggested that achieving SVR by DAA treatment reduces the incidence of HCC, HCC development still occurs. Careful follow-up is important in patients with risk factors.

Sections du résumé

BACKGROUND BACKGROUND
While achieving sustained virological response (SVR) following interferon-based or direct-acting antiviral agent (DAA) treatments reduces the incidence of hepatocellular carcinoma (HCC), an increase in unexpected early occurrence or recurrence of HCC after hepatitis C virus elimination by DAA treatments has been reported. We prospectively investigated the incidence and risk factors of HCC after DAA treatment in a large multicenter cohort in Japan.
METHODS METHODS
Patients with chronic hepatitis C with or without cirrhosis who were treated with DAAs and obtained SVR were enrolled. DAAs were administered for 3 or 6 months. A total of 2552 patients were enrolled.
RESULTS RESULTS
Of these, 70 patients (2.7%) developed HCC. The 12-, 24-, and 36-month cumulative HCC incidences were 1.3%, 2.9%, and 4.9% in all patients; 2.5%, 5.2%, and 10.0% in those with cirrhosis; and 0.9%, 2.1%, and 2.9% in those without cirrhosis, respectively. Multivariate analysis revealed age, sex, gamma-glutamyl transpeptidase level, and fibrosis-4 index to be independent factors associated with HCC. Patients with these four factors had an approximately six-to-sevenfold increased risk for HCC development. Five patients with large and early tumor occurrence did not receive contrast imaging examinations before treatment.
CONCLUSION CONCLUSIONS
Although the results of our prospective study suggested that achieving SVR by DAA treatment reduces the incidence of HCC, HCC development still occurs. Careful follow-up is important in patients with risk factors.

Identifiants

pubmed: 30820753
doi: 10.1007/s12072-019-09939-2
pii: 10.1007/s12072-019-09939-2
doi:

Substances chimiques

Antiviral Agents 0
Interferons 9008-11-1

Types de publication

Journal Article Multicenter Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

293-301

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Auteurs

Tatsuya Ide (T)

Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume, 830-0011, Japan.

Hironori Koga (H)

Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume, 830-0011, Japan. hirokoga@med.kurume-u.ac.jp.

Masahito Nakano (M)

Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume, 830-0011, Japan.

Satoru Hashimoto (S)

Clinical Research Center, National Hospital Organization Nagasaki Medical Center, 2-1001-1 Kubara, Omura, 856-8562, Japan.

Hiroshi Yatsuhashi (H)

Clinical Research Center, National Hospital Organization Nagasaki Medical Center, 2-1001-1 Kubara, Omura, 856-8562, Japan.

Nobito Higuchi (N)

Division of Gastroenterology, National Kyusyu Medical Center Hospital, 1-8-1 Chigyouhama, Chuou-ku, Fukuoka, 810-8563, Japan.

Makoto Nakamuta (M)

Division of Gastroenterology, National Kyusyu Medical Center Hospital, 1-8-1 Chigyouhama, Chuou-ku, Fukuoka, 810-8563, Japan.

Satoshi Oeda (S)

Liver Center, Saga University Hospital, 5-1-1 Nabeshima, Saga, 849-8501, Japan.

Yuichiro Eguchi (Y)

Liver Center, Saga University Hospital, 5-1-1 Nabeshima, Saga, 849-8501, Japan.

Satoshi Shakado (S)

Department of Gastroenterology and Medicine, Faculty of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.

Shotaro Sakisaka (S)

Department of Gastroenterology and Medicine, Faculty of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.

Yoko Yoshimaru (Y)

Department of Gastroenterology and Hepatology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.

Yutaka Sasaki (Y)

Department of Gastroenterology and Hepatology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.

Yuichi Honma (Y)

Third Department of Internal Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, 807-8556, Japan.

Masaru Harada (M)

Third Department of Internal Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, 807-8556, Japan.

Masataka Seike (M)

Department of Gastroenterology, Faculty of Medicine, Oita University, 1-1 Idaigaoka, Hazama-machi, Yufu, 879-5593, Japan.

Tatsuji Maeshiro (T)

First Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, 207 Azauehara, Nishihara-machi, Nakagashira-gun, 903-0215, Japan.

Satoshi Miuma (S)

Department of Gastroenterology and Hepatology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki, 850-0000, Japan.

Kazuhiko Nakao (K)

Department of Gastroenterology and Hepatology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki, 850-0000, Japan.

Seiichi Mawatari (S)

Digestive and Lifestyle Diseases, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, 890-8544, Kagoshima, Japan.

Akio Ido (A)

Digestive and Lifestyle Diseases, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, 890-8544, Kagoshima, Japan.

Kenji Nagata (K)

Department of Liver Disease, University of Miyazaki Hospital, 5200 Kihara, Kiyotake-machi, Miyazaki, 889-1692, Japan.

Shuichi Matsumoto (S)

Fukuoka Tokushukai Medical Center, 4-5 Sugukita, Kasuga, 816-0864, Japan.

Yuko Takami (Y)

Department of Hepato-Biliary-Pancreatic Surgery and Clinical Research Institute, National Kyushu Medical Center Hospital, 1-8-1 Chigyouhama, Chuou-ku, Fukuoka, 810-8563, Japan.

Tetsuo Sohda (T)

Hepatology Division, Japanese Red Cross Fukuoka Hospital, 3-1-1 Okusu, Minami-ku, Fukuoka, 815-8555, Japan.

Tatsuyuki Kakuma (T)

Biostatistics Center, Kurume University, 67 Asahi-machi, Kurume, 830-0011, Japan.

Takuji Torimura (T)

Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume, 830-0011, Japan.

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