Treatment cessation in HBeAg-negative chronic hepatitis B: clinical response is associated with increase in specific proinflammatory cytokines.

Autor: Holmberg M; Department of Infectious Diseases, Vestfold Hospital, Tønsberg, Norway. marte.holmberg@online.no.; Institute of Clinical Medicine, University of Oslo, Oslo, Norway. marte.holmberg@online.no., Aass HCD; Oslo University Hospital, Oslo, Norway., Dalgard O; Institute of Clinical Medicine, University of Oslo, Oslo, Norway.; Akershus University Hospital, Lørenskog, Norway., Samuelsen E; Akershus University Hospital, Lørenskog, Norway., Sun D; Center for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden., Björkström NK; Center for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden., Johannessen A; Department of Infectious Diseases, Vestfold Hospital, Tønsberg, Norway.; Institute of Clinical Medicine, University of Oslo, Oslo, Norway., Reikvam DH; Institute of Clinical Medicine, University of Oslo, Oslo, Norway.; Oslo University Hospital, Oslo, Norway.
Jazyk: angličtina
Zdroj: Scientific reports [Sci Rep] 2023 Dec 18; Vol. 13 (1), pp. 22590. Date of Electronic Publication: 2023 Dec 18.
DOI: 10.1038/s41598-023-50216-y
Abstrakt: Patients with HBeAg-negative chronic hepatitis B may experience an immune response after stopping nucleos(t)ide analogue (NA)therapy, which may potentially trigger HBsAg loss or off-therapy sustained viral control. The immunological mechanisms determining clinical response remain poorly understood. To identify inflammatory signatures associated with defined outcomes, we analysed plasma cytokines and chemokines from 57 HBeAg-negative patients enrolled in the Nuc-Stop Study at baseline and 12 weeks after NA cessation. Clinical response at 12 weeks was classified into four groups: immune control, viral relapse, evolving clinical relapse, and resolving clinical relapse. Twelve weeks after treatment cessation 17 patients (30%) experienced immune control, 19 (33%) viral relapse, 6 (11%) evolving clinical relapse, and 15 (26%) resolving clinical relapse. There was a significant increase in interferon-γ-induced protein 10 (IP-10; p = 0.012) and tumor necrosis factor (TNF; p = 0.032) in patients with evolving clinical relapse. Sparse partial least-squares multivariate analyses (sPLS-DA) showed higher first component values for the clinical relapse group compared to the other groups, separation was driven mainly by IP-10, TNF, IL-9, IFN-γ, MIP-1β, and IL-12. Our results demonstrate that evolving clinical relapse after NA cessation is associated with a systemic increase in the proinflammatory cytokines IP-10 and TNF.Clinical trial registration: ClinicalTrials.gov, Identifier: NCT03681132.
(© 2023. The Author(s).)
Databáze: MEDLINE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje