High Risk of Clinical Relapse in Patients With Chronic Hepatitis B Virus Infection After Cessation of Prophylactic Antiviral Therapy for Rituximab-Containing Chemotherapy.


Journal

The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675

Informations de publication

Date de publication:
14 09 2020
Historique:
received: 02 03 2020
accepted: 07 05 2020
pubmed: 13 5 2020
medline: 6 3 2021
entrez: 13 5 2020
Statut: ppublish

Résumé

Prophylaxis with nucleos(t)ide analogue (NA) is recommended to prevent hepatitis B virus (HBV) reactivation in hepatitis B surface antigen (HBsAg)-positive patients receiving rituximab-based B-cell depletion therapy. However, little is known about the risk of clinical relapse after withdrawal of NA. We retrospectively analyzed 77 noncirrhotic HBsAg carriers with hematological cancer who received rituximab-containing chemotherapy. All of them received either prophylactic entecavir or tenofovir therapy. The risk of clinical relapse and hepatic decompensation after cessation of NA was explored. Clinical relapse and hepatic decompensation developed in 25 (32.5 %) and 11 (14.3 %) of the patients, respectively, and 2 patients died of hepatic decompensation. Most of the hepatic events occurred within 1 year (20 of 25; 80.0%) after stopping NA. A higher pretreatment viral load (≥2000 vs <2000 IU/mL) was associated with increased risks of clinical relapse (hazard ratio, 3.47; 95% confidence interval, 1.56-7.73) and hepatic decompensation (9.91; 2.14-45.92). Of 51 patients with pretreatment viral load <2000 IU/mL, clinical relapse occurred in 10 (19.6 %) and hepatic decompensation in 2 (3.9%). Pretreatment HBV DNA ≥2000 IU/mL is associated with increased risk of liver-related disease after cessation of prophylactic NA therapy in patients who received rituximab-containing chemotherapy.

Sections du résumé

BACKGROUND
Prophylaxis with nucleos(t)ide analogue (NA) is recommended to prevent hepatitis B virus (HBV) reactivation in hepatitis B surface antigen (HBsAg)-positive patients receiving rituximab-based B-cell depletion therapy. However, little is known about the risk of clinical relapse after withdrawal of NA.
METHODS
We retrospectively analyzed 77 noncirrhotic HBsAg carriers with hematological cancer who received rituximab-containing chemotherapy. All of them received either prophylactic entecavir or tenofovir therapy. The risk of clinical relapse and hepatic decompensation after cessation of NA was explored.
RESULTS
Clinical relapse and hepatic decompensation developed in 25 (32.5 %) and 11 (14.3 %) of the patients, respectively, and 2 patients died of hepatic decompensation. Most of the hepatic events occurred within 1 year (20 of 25; 80.0%) after stopping NA. A higher pretreatment viral load (≥2000 vs <2000 IU/mL) was associated with increased risks of clinical relapse (hazard ratio, 3.47; 95% confidence interval, 1.56-7.73) and hepatic decompensation (9.91; 2.14-45.92). Of 51 patients with pretreatment viral load <2000 IU/mL, clinical relapse occurred in 10 (19.6 %) and hepatic decompensation in 2 (3.9%).
CONCLUSIONS
Pretreatment HBV DNA ≥2000 IU/mL is associated with increased risk of liver-related disease after cessation of prophylactic NA therapy in patients who received rituximab-containing chemotherapy.

Identifiants

pubmed: 32396638
pii: 5836326
doi: 10.1093/infdis/jiaa256
doi:

Substances chimiques

Antineoplastic Agents, Immunological 0
Antiviral Agents 0
DNA, Viral 0
Hepatitis B Surface Antigens 0
Rituximab 4F4X42SYQ6
entecavir 5968Y6H45M
Guanine 5Z93L87A1R
Tenofovir 99YXE507IL

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1345-1352

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

Auteurs

Wei-Yuan Chang (WY)

Department of Internal Medicine, National Taiwan University Hospital Hsinchu Branch, Hsinchu, Taiwan.

Yen-Cheng Chiu (YC)

Department of Gastroenterology and Hepatology, National Cheng Kung University Hospital, Tainan, Taiwan.

Fang-Wei Chiu (FW)

Division of Gastroenterology & Hepatology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.

Yao-Chun Hsu (YC)

Division of Gastroenterology and Hepatology, Department of Internal Medicine, E-Da Hospital/I-Shou University, Kaohsiung, Taiwan.

Tai-Chung Tseng (TC)

Division of Gastroenterology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan.

Pin-Nan Cheng (PN)

Department of Gastroenterology and Hepatology, National Cheng Kung University Hospital, Tainan, Taiwan.

Sheng-Shun Yang (SS)

Division of Gastroenterology & Hepatology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.
School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Rong Hsing Research Center for Translational Medicine, National Chung Hsing University, Taichung, Taiwan.
PhD Program in Translational Medicine, National Chung Hsing University, Taichung, Taiwan.

Chun-Jen Liu (CJ)

Division of Gastroenterology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan.
Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.

Tung-Hung Su (TH)

Division of Gastroenterology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan.

Hung-Chih Yang (HC)

Division of Gastroenterology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.
Department of Microbiology, National Taiwan University College of Medicine Taipei, Taiwan.

Chen-Hua Liu (CH)

Division of Gastroenterology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan.

Pei-Jer Chen (PJ)

Division of Gastroenterology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan.
Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.

Ding-Shinn Chen (DS)

Division of Gastroenterology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan.
Genomics Research Center, Academia Sinica, Taiwan.

Jia-Horng Kao (JH)

Division of Gastroenterology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan.
Department of Medical Research, National Taiwan University Hospital, Taipei, Taiwan.
Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.

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