Evidence map›Paper›PMID 27624502›Full record

ArticleHepatology international2017

Hepatitis B virus infection in children of HBV-related chronic liver disease patients: a study of intra-familial HBV transmission.

Hartono Gunardi, Melanie Y Iskandar, Turyadi, Susan I Ie, Pramita G Dwipoerwantoro, Rino A Gani, David H Muljono

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Article in Hepatology international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 25% 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, 15 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Hartono GunardiDepartment of Child Health, Faculty of Medicine, University of Indonesia, Jakarta, Indonesia.
Melanie Y IskandarDepartment of Child Health, Faculty of Medicine, University of Indonesia, Jakarta, Indonesia.
TuryadiEijkman Institute for Molecular Biology, Jalan Diponegoro 69, Jakarta, 10430, Indonesia.
Susan I IeEijkman Institute for Molecular Biology, Jalan Diponegoro 69, Jakarta, 10430, Indonesia.
Pramita G DwipoerwantoroDepartment of Child Health, Faculty of Medicine, University of Indonesia, Jakarta, Indonesia.
Rino A GaniDepartment of Internal Medicine, University of Indonesia, Cipto Mangunkusumo Hospital, Jakarta, Indonesia.
David H MuljonoEijkman Institute for Molecular Biology, Jalan Diponegoro 69, Jakarta, 10430, Indonesia. davidhm@eijkman.go.id.
University of Indonesia · IDEijkman Institute for Molecular Biology · ID

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHBV-infected patients are potential sources of intra-familial transmission. We studied HBV transmission and molecular characteristics within families of HBV-related chronic liver disease (CLD) patients.

methodsFamily members [index cases (ICs), spouses, and 1-18-year-old children] of HBV-related CLD patients were tested for HBsAg, anti-HBc, and anti-HBs. HBsAg-positive subjects were tested for HBeAg/anti-HBe. Anti-HBc-positive children together with their family members were further investigated for HBV DNA. Sequences of positive isolates were analyzed over surface, precore (PC) and basal core promoter (BCP) regions.

resultsAmong 94 children of 46 ICs, the prevalence of HBsAg, anti-HBc, and anti-HBs was 10 (10.6 %), 19 (20.2 %), and 46 (48.9 %), respectively. Thirty-eight (40.4 %) children were seronegative, indicating susceptibility to HBV infection. HBV DNA was identified in all ICs, 4 spouses, and 16 children. Having both parents with HBsAg positive and at least two HBV carriers in the households were significant risk factors of intra-familial transmission. HBV genotype/subtype distributions were comparable between children and ICs/spouses, with predominance of genotype B. The majority of HBV DNA sequences found in children were identical to their corresponding ICs-particularly mothers-including mutation patterns in the surface, PC, and BCP regions. Recognized mutations associated with HBsAg detection and/or vaccination failure, T140I, T143S/M, G145R, and Y161F, were identified in 20 subjects; while mutations linked to HBeAg-defective variants, PC G1896A and BCP A1762T/G1764A, were found in 7 and 11 subjects, respectively.

conclusionsChildren of HBV-related CLD patients were at increased risk of HBV infection through multi-modal transmission routes despite negative parental HBsAg and HBeAg status.

Indexed as

AdolescentCarrier StateChildChild, PreschoolCross-Sectional StudiesDNA, ViralFemaleGenotypeHepatitis B AntibodiesHepatitis B AntigensHepatitis B, ChronicHepatitis B virusHumansMaleMutationPrevalenceDNA, ViralHepatitis B AntibodiesHepatitis B AntigensHepatitis B in childrenHepatitis B virusIntra-familial transmissionMutationTransmission modes of HBV

Identifiers

PMID27624502
OpenAlexW2518799833

What OpenQuestion holds

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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.