Evidence map›Paper›PMID 26063382›Full record

SynthesisVirology journal2015

Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis.

Feishu Hu, Sheng Bi, Huadong Yan, Yu Shi, Jifang Sheng

Abstract readMeta-Analysis
In one paragraph

Synthesis in Virology journal, 2015. 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
–field-weighted citation impact
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.

  1. Pooled it
  2. Review
  3. Review
  4. 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

5 authors.

Feishu HuState Key Lab of Diagnostic and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease, The First Affiliated Hospital of Medical School, Zhejiang University, Hangzhou, 310000, China. 06yxsyhfs@163.com.
Sheng BiState Key Lab of Diagnostic and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease, The First Affiliated Hospital of Medical School, Zhejiang University, Hangzhou, 310000, China. 372640052@qq.com.
Huadong YanDepartment of Hepatology, Ningbo No. 2 Hospital, Ningbo, 315010, China. jifangsheng9200@163.com.
Yu ShiState Key Lab of Diagnostic and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease, The First Affiliated Hospital of Medical School, Zhejiang University, Hangzhou, 310000, China. zjushiyu@zju.edu.cn.
Jifang ShengState Key Lab of Diagnostic and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease, The First Affiliated Hospital of Medical School, Zhejiang University, Hangzhou, 310000, China. shengji.fang@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral studies have suggested a relationship between hepatitis B virus (HBV) basal core promoter/pre-core mutations and HBV-induced acute-on-chronic liver failure (ACLF). Therefore, we evaluated this potential relationship using a meta-analysis.

methodsChinese or English studies from 1966 to January 31, 2014 were included in the analysis. A random or fixed-effects model was used to merge the odds ratios (ORs).

resultsWe identified 31 case-control studies containing a total population of 1995 ACLF and 3822 chronic hepatitis B (CHB) patients. Several mutations were significantly correlated with ACLF: T1753V (1.889, 95 % confidence interval (CI) [1.357-2.631]), A1762T (2.696 [2.265-3.207]), G1764A (3.005 [2.077-4.347]), A1762T/G1764A (2.379 [1.519-3.727]), C1766T (1.849 [1.403-2.437]), T1768A (2.440 [1.405-3.494]), A1846T (3.163 [2.157-4.639]), G1896A (2.181 [1.800-2.642]), G1899A (3.569 [2.906-4.385]) and G1896A/A1762T/G1764A (1.575 [1.172-2.116]). Additionally, HBeAg-negative status was also statistically significant for the progression to ACLF (OR = 2.813, 95 % CI = 2.240-3.533, p < 0.001). However, there was no association between ACLF development and HBV genotype.

conclusionsThe HBV basal core promoter/pre-core mutations T1753V, A1762T, G1764A, C1766T, T1768A, A1846T, G1896A and G1899A, and an HBeAg-negative status correlate with an increased risk of HBV-ACLF.

Indexed as

MutationPromoter Regions, GeneticAcute-On-Chronic Liver FailureAdultFemaleHepatitis B e AntigensHepatitis B virusHumansMaleMiddle AgedModels, StatisticalRisk AssessmentYoung AdultHepatitis B e Antigens

Identifiers

PMID26063382
PMCPMC4485863

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.