Evidence map›Paper›PMID 11053066›Full record

ArticleAnnals of the rheumatic diseases2000

Recurrence risk modelling of the genetic susceptibility to ankylosing spondylitis.

M A Brown, S H Laval, S Brophy, A Calin

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of the rheumatic diseases, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 6 pooled it
5.2field-weighted citation impact, top 4% 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

99 citing papers in PubMed, 6 syntheses or guidelines pooled it, 279 citations in OpenAlex.

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  3. Associations between interleukin-23R polymorphisms and ankylosing spondylitis susceptibility: a meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012
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39 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 1 country.

M A BrownSpondyloarthritis Research Group, Wellcome Trust Centre for Human Genetics, Roosevelt Drive, Headington, OX3 7BN, UK. mbrown@well.ox.ac.uk
S H Laval
S Brophy
A Calin
Centre for Human Genetics · GBRoyal National Hospital for Rheumatic Diseases · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesIt has long been suspected that susceptibility to ankylosing spondylitis (AS) is influenced by genes lying distant to the major histocompatibility complex. This study compares genetic models of AS to assess the most likely mode of inheritance, using recurrence risk ratios in relatives of affected subjects.

methodsRecurrence risk ratios in different degrees of relatives were determined using published data from studies specifically designed to address the question. The methods of Risch were used to determine the expected recurrence risk ratios in different degrees of relatives, assuming equal first degree relative recurrence risk between models. Goodness of fit was determined by chi(2) comparison of the expected number of affected subjects with the observed number, given equal numbers of each type of relative studied.

resultsThe recurrence risks in different degrees of relatives were: monozygotic (MZ) twins 63% (17/27), first degree relatives 8.2% (441/5390), second degree relatives 1.0% (8/834), and third degree relatives 0. 7% (7/997). Parent-child recurrence risk (7.9%, 37/466) was not significantly different from the sibling recurrence risk (8.2%, 404/4924), excluding a significant dominance genetic component to susceptibility. Poor fitting models included single gene, genetic heterogeneity, additive, two locus multiplicative, and one locus and residual polygenes (chi(2) >32 (two degrees of freedom), p<10(-6) for all models). The best fitting model studied was a five locus model with multiplicative interaction between loci (chi(2)=1.4 (two degrees of freedom), p=0.5). Oligogenic multiplicative models were the best fitting over a range of population prevalences and first degree recurrence risk rates.

conclusionsThis study suggests that of the genetic models tested, the most likely model operating in AS is an oligogenic model with predominantly multiplicative interaction between loci.

Indexed as

Genetic Predisposition to DiseaseModels, GeneticFemaleHumansMajor Histocompatibility ComplexMaleOdds RatioRisk AssessmentRisk FactorsSpondylitis, Ankylosing

Identifiers

PMID11053066
PMCPMC1753017
OpenAlexW2140337653

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.