Evidence map›Paper›PMID 26439405›Full record

ReviewNature reviews. Rheumatology2016

Genetics of ankylosing spondylitis--insights into pathogenesis.

Matthew A Brown, Tony Kenna, B Paul Wordsworth

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 9 pooled it
22.5field-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

156 citing papers in PubMed, 9 syntheses or guidelines pooled it, 276 citations in OpenAlex.

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96 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 2 countries.

Matthew A BrownUniversity of Queensland Diamantina Institute, Translational Research Institute, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, Brisbane, QLD 4102, Australia.
Tony KennaUniversity of Queensland Diamantina Institute, Translational Research Institute, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, Brisbane, QLD 4102, Australia.
B Paul WordsworthNIHR Oxford Musculoskeletal Biomedical Research Unit and Comprehensive Biomedical Research Centre, Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX3 7LD, UK.
Princess Alexandra Hospital · AUNuffield Orthopaedic Centre · GB

Funding

Arthritis Research UK 20402Arthritis Research UK 20796
6 · The paper itself

Abstract

Ankylosing spondylitis (AS), an immune-mediated arthritis, is the prototypic member of a group of conditions known as spondyloarthropathies that also includes reactive arthritis, psoriatic arthritis and enteropathic arthritis. Patients with these conditions share a clinical predisposition for spinal and pelvic joint dysfunction, as well as genetic associations, notably with HLA-B(*)27. Spondyloarthropathies are characterized by histopathological inflammation in entheses (regions of high mechanical stress where tendons and ligaments insert into bone) and in the subchondral bone marrow, and by abnormal osteoproliferation at involved sites. The association of AS with HLA-B(*)27, first described >40 years ago, led to hope that the cause of the disease would be rapidly established. However, even though many theories have been advanced to explain how HLA-B(*)27 is involved in AS, no consensus about the answers to this question has been reached, and no successful treatments have yet been developed that target HLA-B27 or its functional pathways. Over the past decade, rapid progress has been made in discovering further genetic associations with AS that have shed new light on the aetiopathogenesis of the disease. Some of these discoveries have driven translational ideas, such as the repurposing of therapeutics targeting the cytokines IL-12 and IL-23 and other factors downstream of this pathway. AS provides an excellent example of how hypothesis-free research can lead to major advances in understanding pathogenesis and to the development of innovative therapeutic strategies.

Indexed as

Genetic Predisposition to DiseaseAllelesBiomarkersEvidence-Based MedicineHLA-B27 AntigenHumansInterleukin-12Interleukin-23Polymorphism, Single NucleotidePredictive Value of TestsRisk FactorsSensitivity and SpecificitySpondylitis, AnkylosingBiomarkersHLA-B27 AntigenInterleukin-12Interleukin-23

Identifiers

PMID26439405
OpenAlexW1961692905

What OpenQuestion holds

Textmetadata
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.