Evidence map›Paper›PMID 30016335›Full record

Trial reportPloS one2018

No association between IFNL3 (IL28B) genotype and response to peginterferon alfa-2a in HBeAg-positive or -negative chronic hepatitis B.

Lai Wei, Heiner Wedemeyer, Yun-Fan Liaw, Henry Lik-Yuen Chan, Teerha Piratvisuth, Patrick Marcellin, Jidong Jia, Deming Tan, Wan-Cheng Chow, Maurizia R Brunetto and 8 more

Open access · goldAbstract readMulticenter StudyRandomized Controlled Trial
In one paragraph

Trial report in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Frontiers in medicine · 2021
    Pooled it
  2. Review
  3. Article
  4. The Association ofInternational journal of molecular sciences · 2024
    Article
  5. Review
  6. Review
  7. Article
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

18 authors at 14 institutions in 12 countries.

Lai WeiPeking University People's Hospital, Peking University Hepatology Institute, Beijing, China.
Heiner WedemeyerDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Yun-Fan LiawLiver Research Unit, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taipei, Taiwan.
Henry Lik-Yuen ChanDepartment of Medicine and Therapeutics, Institute of Digestive Disease and State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, China.
Teerha PiratvisuthNKC Institute of Gastroenterology and Hepatology, Prince of Songkla University, Songklanagarind Hospital, Songkhla, Thailand.
Patrick MarcellinService d'Hépatologie and INSERM CRB3/U773, Université Paris-Diderot, Clichy, France.
Jidong JiaBeijing Friendship Hospital, Capital Medical University, Beijing, China.
Deming TanXiangya Hospital, Central South University, Changsha, Hunan Province, China.
Wan-Cheng ChowDepartment of Gastroenterology & Hepatology, Singapore General Hospital, Singapore, Singapore.
Maurizia R BrunettoHepatology Unit, University Hospital of Pisa, Pisa, Italy.
Moisés DiagoHospital General de Valencia, Valencia, Spain.
Selim GurelDepartment of Gastroenterology, Medical Faculty, Uludag University, Bursa, Turkey.
Viacheslav MorozovMedical Company Hepatolog, LLC, Samara, Russian Federation.
Hua HeRoche Products Ltd, Welwyn, United Kingdom.
Yonghong ZhuGenentech Inc., San Francisco, California, United States of America.
Cynthia WatRoche Products Ltd, Welwyn, United Kingdom.
Bernadette SurujballyBStats Solutions Ltd, Hertfordshire, United Kingdom.
Alexander J ThompsonSt Vincent's Hospital, University of Melbourne, Fitzroy, Victoria, Australia.ORCID 0000-0001-9882-0071
Roche (United Kingdom) · GBAzienda Ospedaliera Universitaria Pisana · ITBursa Uludağ Üni̇versi̇tesi̇ · TRCapital Medical University · CNCentral South University · CNChang Gung University · TWChinese University of Hong Kong · HKHospital General Universitario De Valencia · ESInserm · FRMedizinische Hochschule Hannover · DEPeking University · CNPrince of Songkla University · THSingapore General Hospital · SGThe University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsIt has yet to be firmly established whether host IFNL3 (IL28B) genotype influences interferon responsiveness in patients with chronic hepatitis B. We investigated associations between single-nucleotide polymorphisms (SNPs) in the IFNL3 region and response to peginterferon alfa-2a in 701 patients enrolled in three large, randomized, international studies.

methodsResponses were defined as hepatitis B surface antigen (HBsAg) loss and/or hepatitis B e antigen (HBeAg) seroconversion plus hepatitis B virus (HBV) DNA <2000 IU/ml in HBeAg-positive patients, and HBsAg loss and/or HBV DNA <2000 IU/ml in HBeAg-negative patients (24 weeks after end of treatment). Associations between treatment response and the number of copies of the poor-response allele at three SNPs (rs8099917, rs12980275, rs12979860) were explored with logistic regression models in Asian and white patients.

resultsThe HBeAg-positive and -negative populations comprised 465 (92% Asian, 50% HBV genotype C) and 236 (79% Asian, 41% HBV genotype C) patients, respectively, and had respective response rates of 26% and 47%. The IFNL3 genotype was strongly associated with ethnicity. There was no association between IFNL3 genotype and treatment response in HBeAg-positive or -negative patients. Independent predictors of treatment response were: sex, HBV DNA level and alanine aminotransferase level in HBeAg-positive Asian patients; age in HBeAg-negative Asian patients; and HBV DNA in HBeAg-negative white patients.

conclusionsThis is the largest analysis to date of associations between IFNL3 genotype and peginterferon response in patients with chronic hepatitis B. The data suggest that IFNL3 polymorphism is not a major determinant of the response to peginterferon alfa-2a in either HBeAg-positive or HBeAg-negative patients.

Indexed as

AdultAlanine TransaminaseAntiviral AgentsAsian PeopleDNA, ViralFemaleGene ExpressionGenotypeHepatitis B, ChronicHepatitis B e AntigensHepatitis B Surface AntigensHepatitis B virusHumansInterferon-alphaInterferon LambdaInterferonsAlanine TransaminaseAntiviral AgentsDNA, ViralHepatitis B e AntigensHepatitis B Surface AntigensInterferon-alphaInterferon Lambdainterferon-lambda, humanInterferonsInterleukinspeginterferon alfa-2aPolyethylene GlycolsRecombinant Proteins

Identifiers

PMID30016335
PMCPMC6049926
OpenAlexW2884177497

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.