Viral eradication reduces all-cause mortality in patients with chronic hepatitis C virus infection who had received direct-acting antiviral therapy.

direct‐acting antiviral hepatitis C virus liver‐related mortality non‐liver‐related mortality sustained virological response

Journal

Liver international : official journal of the International Association for the Study of the Liver
ISSN: 1478-3231
Titre abrégé: Liver Int
Pays: United States
ID NLM: 101160857

Informations de publication

Date de publication:
02 Sep 2024
Historique:
revised: 01 08 2024
received: 23 06 2024
accepted: 22 08 2024
medline: 3 9 2024
pubmed: 3 9 2024
entrez: 3 9 2024
Statut: aheadofprint

Résumé

The impact of hepatitis C virus (HCV) eradication via direct-acting antiviral (DAA) therapy on overall mortality, particularly non-liver-related mortality, is understudied. We recruited 4180 patients with chronic HCV infection who achieved sustained virological response (SVR) (HCV eradication) through DAA therapy (n = 2501, SVR group) or who did not receive antiviral therapy (n = 1679, non-SVR group); 1236 from each group were chosen using propensity score matching. Causes of death and all-cause mortality, including non-liver-related diseases, were investigated. Of the 4180 patients, 592 died during the follow-up period. In the SVR group, the mortality rates from liver-related and non-liver-related diseases were 16.5% and 83.5%, respectively. Compared to the non-SVR group, mortality rates from liver-related and non-liver-related diseases were 50.1% and 49.9%, respectively (p < .001). In non-cirrhotic patients, multivariable analysis revealed that SVR was an independent factor associated with both liver-related (hazard ratio [HR], .251; 95% confidence interval [CI], .092-.686) and non-liver-related (HR, .641; 95% CI, .415-.990) mortalities. In cirrhotic patients, multivariable analysis revealed that SVR remained an independent factor significantly associated with liver-related mortality (HR, .151; 95% CI, .081-.279). In propensity score-matched patients, the eradication of HCV (SVR group) decreased both liver-related (p < .001) and non-liver-related mortality (p = .008) rates compared to persistent HCV infection (non-SVR group). The elimination of HCV via DAA therapy reduced not only liver-related mortality but also non-liver-related mortality in patients with chronic HCV.

Sections du résumé

BACKGROUND AND AIMS OBJECTIVE
The impact of hepatitis C virus (HCV) eradication via direct-acting antiviral (DAA) therapy on overall mortality, particularly non-liver-related mortality, is understudied.
METHODS METHODS
We recruited 4180 patients with chronic HCV infection who achieved sustained virological response (SVR) (HCV eradication) through DAA therapy (n = 2501, SVR group) or who did not receive antiviral therapy (n = 1679, non-SVR group); 1236 from each group were chosen using propensity score matching. Causes of death and all-cause mortality, including non-liver-related diseases, were investigated.
RESULTS RESULTS
Of the 4180 patients, 592 died during the follow-up period. In the SVR group, the mortality rates from liver-related and non-liver-related diseases were 16.5% and 83.5%, respectively. Compared to the non-SVR group, mortality rates from liver-related and non-liver-related diseases were 50.1% and 49.9%, respectively (p < .001). In non-cirrhotic patients, multivariable analysis revealed that SVR was an independent factor associated with both liver-related (hazard ratio [HR], .251; 95% confidence interval [CI], .092-.686) and non-liver-related (HR, .641; 95% CI, .415-.990) mortalities. In cirrhotic patients, multivariable analysis revealed that SVR remained an independent factor significantly associated with liver-related mortality (HR, .151; 95% CI, .081-.279). In propensity score-matched patients, the eradication of HCV (SVR group) decreased both liver-related (p < .001) and non-liver-related mortality (p = .008) rates compared to persistent HCV infection (non-SVR group).
CONCLUSIONS CONCLUSIONS
The elimination of HCV via DAA therapy reduced not only liver-related mortality but also non-liver-related mortality in patients with chronic HCV.

Identifiants

pubmed: 39223936
doi: 10.1111/liv.16093
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Grant-in-Aid from the Japan Agency for Medical Research and Development

Informations de copyright

© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Références

WHO. Hepatitis C. World Health Organization (WHO). Accessed March 7, 2024. https://www.who.int/news‐room/fact‐sheets/detail/hepatitis‐c
Westbrook RH, Dusheiko G. Natural history of hepatitis C. J Hepatol. 2014;61:S58‐S68.
Adinolfi LE, Restivo L, Guerrera B, et al. Chronic HCV infection is a risk factor of ischemic stroke. Atherosclerosis. 2013;231:22‐26.
Mason AL, Lau JY, Hoang N, et al. Association of diabetes mellitus and chronic hepatitis C virus infection. Hepatology. 1999;29:328‐333.
Marcellin P, Boyer N, Gervais A, et al. Long‐term histologic improvement and loss of detectable intrahepatic HCV RNA in patients with chronic hepatitis C and sustained response to interferon‐alpha therapy. Ann Intern Med. 1997;127:875‐881.
Niederau C, Lange S, Heintges T, et al. Prognosis of chronic hepatitis C: results of a large, prospective cohort study. Hepatology. 1998;28:1687‐1695.
Yoshida H, Arakawa Y, Sata M, et al. Interferon therapy prolonged life expectancy among chronic hepatitis C patients. Gastroenterology. 2002;123:483‐491.
Kasahara A, Tanaka H, Okanoue T, et al. Interferon treatment improves survival in chronic hepatitis C patients showing biochemical as well as virological responses by preventing liver‐related death. J Viral Hepat. 2004;11:148‐156.
Hsu YC, Lin JT, Ho HJ, et al. Antiviral treatment for hepatitis C virus infection is associated with improved renal and cardiovascular outcomes in diabetic patients. Hepatology. 2014;59:1293‐1302.
Arase Y, Suzuki F, Suzuki Y, et al. Sustained virological response reduces incidence of onset of type 2 diabetes in chronic hepatitis C. Hepatology. 2009;49:739‐744.
Akahane T, Kurosaki M, Itakura J, et al. Real‐world efficacy and safety of sofosbuvir + ribavirin for hepatitis C genotype 2: a nationwide multicenter study by the Japanese red cross liver study group. Hepatol Res. 2019;49:264‐270.
Mashiba T, Joko K, Kurosaki M, et al. Real‐world efficacy of elbasvir and grazoprevir for hepatitis C virus (genotype 1): a nationwide, multicenter study by the Japanese red cross hospital liver study group. Hepatol Res. 2019;49:1114‐1120.
Tahata Y, Sakamori R, Urabe A, et al. Clinical outcomes of direct‐acting antiviral treatments for patients with hepatitis C after hepatocellular carcinoma are equivalent to interferon treatment. Hepatol Res. 2020;50:1118‐1127.
Drafting Committee for Hepatitis Management Guidelines, the Japan Society of Hepatology. Japan Society of Hepatology guidelines for the management of hepatitis C virus infection. Hepatol Res. 2019;2020(50):791‐816.
Kanwal F, Kramer J, Asch SM, Chayanupatkul M, Cao Y, El‐Serag HB. Risk of hepatocellular cancer in HCV patients treated with direct‐acting antiviral agents. Gastroenterology. 2017;153:996‐1005.
Nahon P, Layese R, Bourcier V, et al. ANRS CO12 CirVir group. Incidence of hepatocellular carcinoma after direct antiviral therapy for HCV in patients with cirrhosis included in surveillance programs. Gastroenterology. 2018;155:1436‐1450.
Janjua NZ, Wong S, Darvishian M, et al. The impact of SVR from direct‐acting antiviral‐ and interferon‐based treatments for HCV on hepatocellular carcinoma risk. J Viral Hepat. 2020;27:781‐793.
Seko Y, Moriguchi M, Hara T, et al. Presence of varices in patients after hepatitis C virus eradication predicts deterioration in the FIB‐4 index. Hepatol Res. 2019;49:473‐478.
Inoue‐Shinomiya E, Murakawa M, Asahina Y, et al. Association of serum interferon‐λ3 levels with hepatocarcinogenesis in chronic hepatitis C patients treated with direct‐acting antiviral agents. Hepatol Res. 2019;49:500‐511.
Asahina Y, Drafting Committee for Hepatitis Management Guidelines, the Japean Society of Hepatology. JSH Guidelines for the Management of Hepatitis C Virus Infection, 2019 Update; protective effect of antiviral therapy against Hepatocarcinogenesis. Hepatol Res. 2020;50:775‐790.
Nagaoki Y, Imamura M, Teraoka Y, et al. Impact of viral eradication by direct‐acting antivirals on the risk of hepatocellular carcinoma development, prognosis, and portal hypertension in hepatitis C virus‐related compensated cirrhosis patients. Hepatol Res. 2020;50:1222‐1233.
Yoshiji H, Nagoshi S, Akahane T, et al. Evidence‐based clinical practice guidelines for liver cirrhosis 2020. Hepatol Res. 2021;51:725‐749.
O'Shea RS, Dasarathy S, McCullough AJ, Practice Guideline Committee of the American Association for the Study of Liver Diseases; Practice Parameters Committee of the American College of Gastroenterology. Alcoholic liver disease. Hepatology. 2010;51:307‐328.
Tada T, Kumada T, Toyoda H, et al. Viral eradication reduces all‐cause mortality in patients with chronic hepatitis C virus infection: a propensity score analysis. Liver Int. 2016;36:817‐826.
Sterling RK, Lissen E, Clumeck N, et al. Development of a simple noninvasive index to predict significant fibrosis in patients with HIV/HCV coinfection. Hepatology. 2006;43:1317‐1325.
Butt AA, Yan P, Lo Re V, et al. Liver fibrosis progression in hepatitis C virus infection after seroconversion. JAMA Intern Med. 2015;175:178‐185.
Heimbach JK, Kulik LM, Finn RS, et al. AASLD guidelines for the treatment of hepatocellular carcinoma. Hepatology. 2018;67:358‐380.
Kokudo N, Takemura N, Hasegawa K, et al. Clinical practice guidelines for hepatocellular carcinoma: the Japan Society of Hepatology 2017 (4th JSH‐HCC guidelines) 2019 update. Hepatol Res. 2019;49:1109‐1113.
Fine JP, Gray RJ. A proportional hazards model for the subdistribution of a competing risk. J Am Stat Assoc. 1999;94:496‐509.
Kanda Y. Investigation of the freely available easy‐to‐use software ‘EZR’ for medical statistics. Bone Marrow Transplant. 2013;48:452‐458.
Tong MJ, el‐Farra NS, Reikes AR, Co RL. Clinical outcomes after transfusion‐associated hepatitis C. N Engl J Med. 1995;332:1463‐1466.
Yano M, Kumada H, Kage M, et al. The long‐term pathological evolution of chronic hepatitis C. Hepatology. 1996;23:1334‐1340.
Kobayashi M, Tanaka E, Sodeyama T, Urushihara A, Matsumoto A, Kiyosawa K. The natural course of chronic hepatitis C: a comparison between patients with genotypes 1 and 2 hepatitis C viruses. Hepatology. 1996;23:695‐699.
Cacoub P, Renou C, Rosenthal E, et al. Extrahepatic manifestations associated with hepatitis C virus infection. A prospective multicenter study of 321 patients. The GERMIVIC. Groupe d'Etude et de Recherche en Medecine Interne et Maladies Infectieuses sur le Virus de l'Hepatite C. Medicine (Baltimore). 2000;79:47‐56.
Cacoub P, Gragnani L, Comarmond C, Zignego AL. Extrahepatic manifestations of chronic hepatitis C virus infection. Dig Liver Dis. 2014;46:S165‐S173.
Kozuka R, Tamori A, Enomoto M, et al. Risk factors for liver‐related and non‐liver‐related mortality following a sustained virological response after direct‐acting antiviral treatment for hepatitis C virus infection in a real‐world cohort. J Viral Hepat. 2023;30:374‐385.
Hamill V, Wong S, Benselin J, et al. Mortality rates among patients successfully treated for hepatitis C in the era of interferon‐free antivirals: population based cohort study. BMJ. 2023;382:e074001.

Auteurs

Toshifumi Tada (T)

Department of Gastroenterology, Japanese Red Cross Society Himeji Hospital, Himeji, Japan.

Masayuki Kurosaki (M)

Department of Gastroenterology and Hepatology, Musashino Red Cross Hospital, Tokyo, Japan.

Hidenori Toyoda (H)

Department of Gastroenterology and Hepatology, Ogaki Municipal Hospital, Gifu, Japan.

Nobuharu Tamaki (N)

Department of Gastroenterology and Hepatology, Musashino Red Cross Hospital, Tokyo, Japan.

Yutaka Yasui (Y)

Department of Gastroenterology and Hepatology, Musashino Red Cross Hospital, Tokyo, Japan.

Shinichiro Nakamura (S)

Department of Gastroenterology, Japanese Red Cross Society Himeji Hospital, Himeji, Japan.

Nami Mori (N)

Department of Gastroenterology, Hiroshima Red Cross Hospital and Atomic-bomb Survivors Hospital, Hiroshima, Japan.

Keiji Tsuji (K)

Department of Gastroenterology, Hiroshima Red Cross Hospital and Atomic-bomb Survivors Hospital, Hiroshima, Japan.

Hironori Ochi (H)

Center for Liver-Biliary-Pancreatic Disease, Matsuyama Red Cross Hospital, Matsuyama, Japan.

Takehiro Akahane (T)

Department of Gastroenterology, Japanese Red Cross Ishinomaki Hospital, Ishinomaki, Japan.

Haruhiko Kobashi (H)

Department of Gastroenterology, Japanese Red Cross Okayama Hospital, Okayama, Japan.

Hideki Fujii (H)

Department of Gastroenterology, Japanese Red Cross Kyoto Daiichi Hospital, Kyoto, Japan.

Hiroyuki Marusawa (H)

Department of Gastroenterology and Hepatology, Japanese Red Cross Osaka Hospital, Osaka, Japan.

Masahiko Kondo (M)

Department of Gastroenterology, Japanese Red Cross Otsu Hospital, Otsu, Japan.

Naohito Urawa (N)

Department of Hepatology, Japanese Red Cross Ise Hospital, Ise, Japan.

Hideo Yoshida (H)

Department of Gastroenterology, Japanese Red Cross Medical Center, Tokyo, Japan.

Yasushi Uchida (Y)

Department of Gastroenterology, Japanese Red Cross Matsue Hospital, Matsue, Japan.

Atsuhiro Morita (A)

Department of Gastroenterology, Japanese Red Cross Kyoto Daini Hospital, Kyoto, Japan.

Chitomi Hasebe (C)

Department of Gastroenterology, Japanese Red Cross Asahikawa Hospital, Asahikawa, Japan.

Akeri Mitsuda (A)

Department of Gastroenterology, Tottori Red Cross Hospital, Tottori, Japan.

Chikara Ogawa (C)

Department of Gastroenterology and Hepatology, Takamatsu Red Cross Hospital, Takamatsu, Japan.

Ryoichi Narita (R)

Department of Gastroenterology, Oita Red Cross Hospital, Oita, Japan.

Yoshihito Kubotsu (Y)

Department of Internal Medicine, Karatsu Red Cross Hospital, Saga, Japan.

Tomomichi Matsushita (T)

Department of Gastroenterology, Japanese Red Cross Gifu Hospital, Gifu, Japan.

Masaya Shigeno (M)

Department of Gastroenterology, Japanese Red Cross Nagasaki Genbaku Hospital, Nagasaki, Japan.

Eisuke Okamoto (E)

Department of Gastroenterology, Masuda Red Cross Hospital, Masuda, Japan.

Kazuhiko Okada (K)

Department of Gastroenterology, Toyama Red Cross Hospital, Toyama, Japan.

Toyotaka Kasai (T)

Department of Gastroenterology, Fukaya Red Cross Hospital, Saitama, Japan.

Toru Ishii (T)

Department of Gastroenterology, Japanese Red Cross Akita Hospital, Akita, Japan.

Michiko Nonogi (M)

Department of Gastroenterology, Tokushima Red Cross Hospital, Tokushima, Japan.

Satoshi Yasuda (S)

Department of Gastroenterology and Hepatology, Ogaki Municipal Hospital, Gifu, Japan.

Yuichi Koshiyama (Y)

Department of Gastroenterology and Hepatology, Ogaki Municipal Hospital, Gifu, Japan.

Takashi Kumada (T)

Department of Nursing, Gifu Kyoritsu University, Gifu, Japan.

Namiki Izumi (N)

Department of Gastroenterology and Hepatology, Musashino Red Cross Hospital, Tokyo, Japan.

Classifications MeSH