Evidence map›Paper›PMID 30445483›Full record

ReviewRheumatology (Oxford, England)2018

Progress in our understanding of the pathogenesis of ankylosing spondylitis.

Davide Simone, M Hussein Al Mossawi, Paul Bowness

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Rheumatology (Oxford, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07130331 (Efficacy and Influencing Factors Analysis of Secukinumab in Patients With Axial Spondyloarthritis in a Real-World Setting), which is not on this map. Cited by 68 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 6 pooled it
11.1field-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.

NCT07130331 completednot on this mapstarted 2020, after this paper: background citation

Efficacy and Influencing Factors Analysis of Secukinumab in Patients With Axial Spondyloarthritis in a Real-World Setting

TypeobservationalSponsorThe Affiliated Nanjing Drum Tower Hospital of Nanjing University Medical SchoolRan2020 to 2025Enrolled200ConditionsAxial Spondylarthritis (axSpA), SecukinumabArmsSecikinumab
3 · Its place in the literature

Who cites it

68 citing papers in PubMed, 6 syntheses or guidelines pooled it, 162 citations in OpenAlex.

  1. Pooled it
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  4. Lack of association between TNF polymorphism and ankylosing spondylitis susceptibility in HLA-B27-positive population: a meta-analysis.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2021
    Pooled it
  5. The association of polymorphisms in TNF and ankylosing spondylitis in common population: a meta-analysis.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2021
    Pooled it
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8 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 1 institution in 1 country.

Davide SimoneNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
M Hussein Al MossawiNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
Paul BownessNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
University of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AS is a common rheumatic condition characterized by inflammation and new bone formation. The pathogenesis of AS is likely multifactorial and has not been fully elucidated to date. A major genetic role has been demonstrated. The strongest genetic association is with HLA B27. Numerous other associated genetic polymorphisms have been identified, including those affecting the type 17 immune pathway, although the precise link between genetics and pathogenesis remains unexplained. Several immunological alterations, together with recent therapeutic advances, support a central role for IL-23- and IL-17-producing immune cells in disease pathogenesis. Recently, perturbations of gut microbiota of AS patients have further catalysed research and offer potential for future therapeutic intervention. In this review we outline the genetic basis of AS and describe the current hypotheses for disease pathogenesis. We synthesize recent experimental research data and clinical studies to support a central role for the type 17/23 immune axis in AS.

Indexed as

Gastrointestinal MicrobiomeGenetic Predisposition to DiseaseHLA-B27 AntigenHumansInterleukin-17Interleukin-23Polymorphism, GeneticSpondylitis, AnkylosingHLA-B27 AntigenInterleukin-17Interleukin-23

Identifiers

PMID30445483
PMCPMC6238220
OpenAlexW2905523412

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

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.