Evidence map›Paper›PMID 21390140›Full record

ArticleWorld journal of gastroenterology2011

Association of core promoter mutations of hepatitis B virus and viral load is different in HBeAg(+) and HBeAg(-) patients.

Andi Utama, Marlinang Diarta Siburian, Sigit Purwantomo, Mariana Destila Bayu Intan, Tri Shinta Kurniasih, Rino Alvani Gani, Wenny Astuti Achwan, Arnelis, Syafruddin A R Lelosutan, Benyamin Lukito and 7 more

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Virus, Exosome, and MicroRNA: New Insights into Autophagy.Advances in experimental medicine and biology · 2022
    Article
  3. Observational
  4. Article
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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

17 authors at 1 institution in 1 country.

Andi UtamaMolecular Epidemiology Division, Mochtar Riady Institute for Nanotechnology, Universitas Pelita Harapan, Lippo Karawaci, Tangerang, 15810, Indonesia. autama@mrinstitute.org
Marlinang Diarta Siburian
Sigit Purwantomo
Mariana Destila Bayu Intan
Tri Shinta Kurniasih
Rino Alvani Gani
Wenny Astuti Achwan
Arnelis
Syafruddin A R Lelosutan
Benyamin Lukito
Tantoro Harmono
Nasrul Zubir
Julius
Soewignjo Soemohardjo
Laurentius Adrianus Lesmana
Ali Sulaiman
Susan Tai
Pelita Harapan University · ID

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo identify the prevalence of hepatitis B e antigen (HBeAg) and to assess the association of hepatitis B virus (HBV) core promoter mutations and viral load in Indonesian patients.

methodsSixty-four patients with chronic hepatitis, 65 with liver cirrhosis and 50 with hepatocellular carcinoma were included in this study. HBeAg and hepatitis B e antibody (HBeAb) tests were performed using enzyme-linked immunosorbent assay and the mutations were analyzed by sequencing. Viral load was measured by real-time polymerase chain reaction.

resultsOf 179 patients, 108 (60.3%) were HBeAg(-) and 86 (79.6%) of these HBeAg(-) patients had been seroconverted. The A1896 mutation was not found in HBeAg(+) patients, however, this mutation was detected in 70.7% of HBeAg(-) patients. This mutation was frequently found when HBeAg was not expressed (87.7%), compared to that found in HBeAg seroconverted patients (65.1%). The A1899 mutation was also more prevalent in HBeAg(-) than in HBeAg(+) patients (P = 0.004). The T1762/A1764 mutation was frequently found in both HBeAg(+) and HBeAg(-) patients, however, the prevalence of this mutation did not significantly differ among the two groups (P = 0.054). In HBeAg(+) patients, the T1762/A1764 mutation was correlated with lower HBV DNA (P < 0.001). The A1899 mutation did not correlate with HBV DNA (P = 0.609). In HBeAg(-) patients, the T1762/A1764 mutation alone was not correlated with HBV DNA (P = 0.095), however, the presence of either the T1762/A1764 or A1896 mutations was associated with increased HBV DNA (P < 0.001).

conclusionThe percentage of HBeAg(-) patients is high in Indonesia, and most of the HBeAg(-) patients had been seroconverted. The A1896 mutation was most likely the major cause of HBeAg loss. The T1762/A1764 mutation alone was associated with lower viral loads in HBeAg(+) patients, but not in HBeAg(-) patients.

Indexed as

MutationViral LoadAdultAlanine TransaminaseDNA, ViralFemaleGenotypeHepatitis B, ChronicHepatitis B e AntigensHepatitis B virusHumansMaleMiddle AgedPromoter Regions, GeneticAlanine TransaminaseDNA, ViralHepatitis B e AntigensHepatitis B e antibodyHepatitis B e antigenHepatitis B virusIndonesiaPrecore/core promoter mutationsViral load

Identifiers

PMID21390140
PMCPMC3042648
OpenAlexW2113781457

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.