Evidence map›Paper›PMID 28219691›Full record

ReviewGastroenterology2017

Hepatitis B Reactivation Associated With Immune Suppressive and Biological Modifier Therapies: Current Concepts, Management Strategies, and Future Directions.

Rohit Loomba, T Jake Liang

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 331 papers, 13 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
331citing papers in PubMed, 13 pooled it
35.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

331 citing papers in PubMed, 13 syntheses or guidelines pooled it, 577 citations in OpenAlex.

  1. Hepatitis B Virus Reactivation Risk With IL-17, IL-23/IL-12, or JAK Inhibitors: A Systematic Review and Meta-Analysis.Liver international : official journal of the International Association for the Study of the Liver · 2026
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271 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Rohit LoombaDivision of Gastroenterology, Department of Medicine, University of California at San Diego, La Jolla, California.
T Jake LiangLiver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. Electronic address: jliang@nih.gov.
National Institutes of Health · USUniversity of California, San Diego · US

Funding

Molecular Mechanisms Of Hepatitis B Viral Pathogenesis And PersistenceZIADK054500 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI LIANG, T. JAKE · 2009 to 2025
$20.3M
QUS Technology for Diagnosis and Grading of Hepatic Steatosis in NAFLDR01DK106419 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LOOMBA, ROHIT, SIRLIN, CLAUDE B · 2015 to 2019
$3.4M
GENETIC EPIDEMIOLOGY OF NONALCOHOLIC FATTY LIVER DISEASEK23DK090303 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LOOMBA, ROHIT · 2011 to 2014
$721k
NIDDK NIH HHS K23 DK090303NIDDK NIH HHS R01 DK106419
6 · The paper itself

Abstract

Hepatitis B reactivation associated with immune-suppressive and biological therapies is emerging to be an important cause of morbidity and mortality in patients with current or prior exposure to hepatitis B virus (HBV) infection. The population at risk for HBV reactivation includes those who either currently are infected with HBV or have had past exposure to HBV. Because curative and eradicative therapy for HBV is not currently available, there is a large reservoir of individuals at risk for HBV reactivation in the general population. HBV reactivation with its potential consequences is particularly a concern when these people are exposed to either cancer chemotherapy, immunosuppressive or biologic therapies for the management of rheumatologic conditions, malignancies, inflammatory bowel disease, dermatologic conditions, or solid-organ or bone marrow transplantation. With the advent of newer and emerging forms of targeted biologic therapies, it has become important to understand the mechanisms whereby certain therapies are more prone to HBV reactivation. This review provides a comprehensive update on the current concepts, risk factors, molecular mechanisms, prevention, and management of hepatitis B reactivation. In addition, we provide recommendations for future research in this area.

Indexed as

Virus ActivationAntiviral AgentsBiological ProductsHepatitis B, ChronicHepatitis B virusHistone Deacetylase InhibitorsHumansImmunosuppressive AgentsProteasome InhibitorsProtein Kinase InhibitorsRisk FactorsRituximabSecondary PreventionTumor Necrosis Factor-alphaAntiviral AgentsBiological ProductsHistone Deacetylase InhibitorsImmunosuppressive AgentsProteasome InhibitorsProtein Kinase InhibitorsRituximabTumor Necrosis Factor-alphaChronic Hepatitis BCirrhosisFulminant Hepatic FailureGuidelinesLiver DiseaseLiver FailureMortalityViral Hepatitis

Identifiers

PMID28219691
PMCPMC5501983
OpenAlexW2590941489

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.