Evidence map›Paper›PMID 25948071›Full record

ReviewArthritis research & therapy2015

Concepts of pathogenesis in psoriatic arthritis: genotype determines clinical phenotype.

Oliver FitzGerald, Muhammad Haroon, Jon T Giles, Robert Winchester

Open access · goldAbstract readReview
In one paragraph

Review in Arthritis research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 5 pooled it
15.8field-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

95 citing papers in PubMed, 5 syntheses or guidelines pooled it, 209 citations in OpenAlex.

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  15. Psoriatic Arthritis: From Diagnosis to Treatment.Journal of clinical medicine · 2025
    Review
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35 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

4 authors at 2 institutions in 2 countries.

Oliver FitzGeraldDepartment of Rheumatology, St Vincent's University Hospital, Elm Park, Dublin, 4, Ireland. oliver.fitzgerald@ucd.ie.
Muhammad HaroonDepartment of Rheumatology, St Vincent's University Hospital, Elm Park, Dublin, 4, Ireland. mharoon301@hotmail.com.
Jon T GilesRheumatology Division, Department of Medicine, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York City, NY, 10032, USA. jtg2122@columbia.edu.
Robert WinchesterRheumatology Division, Department of Medicine, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York City, NY, 10032, USA. rjw8@columbia.edu.
Columbia University · USSt. Vincent's University Hospital · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review focuses on the genetic features of psoriatic arthritis (PsA) and their relationship to phenotypic heterogeneity in the disease, and addresses three questions: what do the recent studies on human leukocyte antigen (HLA) tell us about the genetic relationship between cutaneous psoriasis (PsO) and PsA - that is, is PsO a unitary phenotype; is PsA a genetically heterogeneous or homogeneous entity; and do the genetic factors implicated in determining susceptibility to PsA predict clinical phenotype? We first discuss the results from comparing the HLA typing of two PsO cohorts: one cohort providing the dermatologic perspective, consisting of patients with PsO without evidence of arthritic disease; and the second cohort providing the rheumatologic perspective, consisting of patients with PsA. We show that these two cohorts differ considerably in their predominant HLA alleles, indicating the heterogeneity of the overall PsO phenotype. Moreover, the genotype of patients in the PsA cohort was shown to be heterogeneous with significant elevations in the frequency of haplotypes containing HLA-B*08, HLA-C*06:02, HLA-B*27, HLA-B*38 and HLA-B*39. Because different genetic susceptibility genes imply different disease mechanisms, and possibly different clinical courses and therapeutic responses, we then review the evidence for a phenotypic difference among patients with PsA who have inherited different HLA alleles. We provide evidence that different alleles and, more importantly, different haplotypes implicated in determining PsA susceptibility are associated with different phenotypic characteristics that appear to be subphenotypes. The implication of these findings for the overall pathophysiologic mechanisms involved in PsA is discussed with specific reference to their bearing on the discussion of whether PsA is conceptualised as an autoimmune process or one that is based on entheseal responses.

Indexed as

GenotypeAdultAllelesArthritis, PsoriaticFemaleGene Expression RegulationGenetic Predisposition to DiseaseHLA AntigensHumansMaleMiddle AgedPhenotypePrognosisSeverity of Illness IndexHLA Antigens

Identifiers

PMID25948071
PMCPMC4422545
OpenAlexW1548769791

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.