Evidence map›Paper›PMID 31393374›Full record

Observational studyMedicine2019

Analysis of human leukocyte antigen allele polymorphism in patients with non alcoholic fatty liver disease.

Azza Karrar, Siddharth Hariharan, Yousef Fazel, Ali Moosvi, Mohamad Houry, Zahra Younoszai, Thomas Jeffers, Li Zheng, Otgonsuren Munkhzul, Sharon Hunt and 3 more

Abstract readObservational Study
In one paragraph

Observational study in Medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Journal of clinical medicine · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Myeloid cell MHC I expression drives CD8Frontiers in immunology · 2023
    Article
  11. Liraglutide + PYYJournal of clinical medicine · 2022
    Article
  12. Article
  13. 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

13 authors.

Azza KarrarBetty and Guy Beatty Center for Integrated Research, Inova Health System.
Siddharth HariharanBetty and Guy Beatty Center for Integrated Research, Inova Health System.
Yousef FazelBetty and Guy Beatty Center for Integrated Research, Inova Health System.
Ali MoosviBetty and Guy Beatty Center for Integrated Research, Inova Health System.
Mohamad HouryBetty and Guy Beatty Center for Integrated Research, Inova Health System.
Zahra YounoszaiBetty and Guy Beatty Center for Integrated Research, Inova Health System.
Thomas JeffersBetty and Guy Beatty Center for Integrated Research, Inova Health System.
Li ZhengBetty and Guy Beatty Center for Integrated Research, Inova Health System.
Otgonsuren MunkhzulBetty and Guy Beatty Center for Integrated Research, Inova Health System.
Sharon HuntBetty and Guy Beatty Center for Integrated Research, Inova Health System.
Fanny MongeCenter for Liver Diseases, Department of Medicine, Inova Fairfax Hospital, Falls Church, VA.
Zachary GoodmanCenter for Liver Diseases, Department of Medicine, Inova Fairfax Hospital, Falls Church, VA.
Zobair M YounossiBetty and Guy Beatty Center for Integrated Research, Inova Health System.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human leukocyte antigen (HLA) genes may play a role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) and its progressive form, non-alcoholic steatohepatitis (NASH). The aim of this study was to assess the association of HLA class I and II alleles with NASH and its histological features.Deoxyribonucleic acid (DNA) was extracted from 140 subjects (85 biopsy-proven NAFLD and 55 controls) and genotyped for HLA (-A, -B, -C, -DR1, -DR3, -DQ, and -DP). Liver biopsies were assessed for presence of NASH, degree of fibrosis and inflammation. Multivariate analysis was performed to assess associations between HLA genes and different histologic features of NAFLD.Our data for HLA class I showed that HLA-C*4 was associated with lower risk for histologic NASH and HLA-C*6 was protective against portal fibrosis. Conversely, HLA-B*27 was associated with high-grade hepatic steatosis, while HLA-A*31 was associated with increased risk for advanced fibrosis. Among HLA class II alleles, HLA-DQA1*01 was associated with lower risk for NASH while HLA-DRB1*03 was associated with increased risk for NASH.Our findings indicate that HLA class I and II gene polymorphism may be associated with susceptibility to NASH, fibrosis and other pathologic features and may be involved in the pathogenesis of NAFLD.

Indexed as

AdultAllelesFemaleHistocompatibility Antigens Class IHistocompatibility Antigens Class IIHumansMaleMiddle AgedNon-alcoholic Fatty Liver DiseasePolymorphism, GeneticProspective StudiesHistocompatibility Antigens Class IHistocompatibility Antigens Class II

Identifiers

PMID31393374
PMCPMC6708789

What OpenQuestion holds

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LicenceCC BY
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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.