Evidence map›Paper›PMID 33754220›Full record

SynthesisClinical rheumatology2021

Ankylosing spondylitis risk factors: a systematic literature review.

Mark C Hwang, Lauren Ridley, John D Reveille

Open access · greenAbstract readSystematic Review
In one paragraph

Synthesis in Clinical rheumatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 5 pooled it
16.3field-weighted citation impact, top 1% 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

82 citing papers in PubMed, 5 syntheses or guidelines pooled it, 143 citations in OpenAlex.

  1. Pooled it
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  4. Non-genetic biomarkers for ankylosing spondylitis: An umbrella review.Journal of clinical laboratory analysis · 2022
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22 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Mark C HwangDepartment of Internal Medicine, Division of Rheumatology, McGovern Medical School at The University of Texas Health Science Center, 6431 Fannin, MSB 1.150, Houston, TX, 77030, USA.
Lauren RidleyDepartment of Internal Medicine, Division of Rheumatology, McGovern Medical School at The University of Texas Health Science Center, 6431 Fannin, MSB 1.150, Houston, TX, 77030, USA.
John D ReveilleDepartment of Internal Medicine, Division of Rheumatology, McGovern Medical School at The University of Texas Health Science Center, 6431 Fannin, MSB 1.150, Houston, TX, 77030, USA. John.D.Reveille@uth.tmc.edu.ORCID http://orcid.org/0000-0001-5950-0913
The University of Texas Health Science Center at Houston · USThe University of Texas Health Science Center · US

Funding

The Genetic Basis of AS SusceptibilityP01AR052915 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI REVEILLE, JOHN DUFFIN · 2006 to 2016
$10.9M
Institutional Career Development CoreKL2TR003168 · NCATS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MILLER, CHARLES C · 2019 to 2023
$4.9M
NCATS NIH HHS KL2 TR003168NIAMS NIH HHS P01 AR052915Novartis Pharmaceuticals Corporation N/A
6 · The paper itself

Abstract

Radiographic axial spondyloarthritis (also known as ankylosing spondylitis [AS]) is a chronic immune-mediated arthritis characterized by inflammation of the axial skeleton, peripheral joints, and entheses. It is estimated that 1 in every 200 people are affected by AS, making it an important healthcare and socioeconomic issue. In this review, we aim to explore the current understanding of AS risk factors and provide a comprehensive update. Multiple search strings were used to identify articles of interest published in PubMed between January 1, 2013, and February 1, 2021. On the basis of the literature review and analysis, we present up-to-date information on the risk factors of developing AS and our viewpoints on disease onset and progression. Multiple genetic and nongenetic risk factors have been suggested in the onset of AS. HLA-B27 is known to have a strong association with the disease, but other genes have been implicated in disease development. Aside from genetics, other factors are thought to be involved; up to 70% of patients with AS have subclinical intestinal inflammation, suggesting that the origin of the disease may be in the gut. The exact mechanism by which AS onset begins is most likely complex and multifactorial. Key Points • It remains unclear how interactions between genes, microbes, mechanical stress, gender, and other environmental and lifestyle factors predispose patients to the development of ankylosing spondylitis (AS). • The exact mechanisms of AS are complex and multifactorial which will require much future research • Recognizing the risk factors, as well as understanding gene-environment interactions, may offer valuable insights into the etiology of AS and have important implications for diagnosis and treatment strategies.

Indexed as

SpondylarthritisSpondylitis, AnkylosingHLA-B27 AntigenHumansInflammationRisk FactorsHLA-B27 AntigenAnkylosing spondylitisGeneticsHLA-B27PathogenesisRadiographic axial spondyloarthritisRisk factors

Identifiers

PMID33754220
PMCPMC9044547
OpenAlexW3138796149

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.