Evidence map›Paper›PMID 18257935›Full record

ArticleArthritis research & therapy2008

Common interleukin-6 promoter variants associate with the more severe forms of distal interphalangeal osteoarthritis.

Olli-Pekka Kämäräinen, Svetlana Solovieva, Tapio Vehmas, Katariina Luoma, Hilkka Riihimäki, Leena Ala-Kokko, Minna Männikkö, Päivi Leino-Arjas

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.

  1. Effects ofFrontiers in genetics · 2022
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  8. Genetic Susceptibility to Acute Kidney Injury.Journal of clinical medicine · 2021
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  20. Interleukin-6 genotypes and serum levels in Chinese Hui population.International journal of clinical and experimental medicine · 2014
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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

8 authors at 4 institutions in 2 countries.

Olli-Pekka KämäräinenCollagen Research Unit, Biocenter and Department of Medical Biochemistry and Molecular Biology, University of Oulu, 90220 Oulu, Finland. olli-pekka.kamarainen@oulu.fi
Svetlana Solovieva
Tapio Vehmas
Katariina Luoma
Hilkka Riihimäki
Leena Ala-Kokko
Minna Männikkö
Päivi Leino-Arjas
Finnish Institute of Occupational Health · FIUniversity of Oulu · FIHelsinki University Hospital · FITissue Gene (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe objective of this study was to investigate the relationship of the IL-6 promoter variants G-597A, G-572C and G-174C (rs1800797, rs1800796 and rs1800795, respectively), which have been shown to affect both the transcription and secretion of IL-6, to symptomatic distal interphalangeal (DIP) osteoarthritis (OA).

methodsA total of 535 women aged 45 to 63 years were included. Radiographs of both hands were taken and each DIP joint was evaluated (grade 0 to 4) for the presence of OA. Information on symptoms (pain, tenderness) in each joint was collected by using a self-administered questionnaire. Symptomatic DIP OA was defined by the presence of both radiographic findings of grade 2 or more and symptoms in at least two DIP joints, and symmetrical DIP OA by the presence of radiographic findings of grade 2 or more in at least one symmetrical pair of DIP joints. Common polymorphic loci in the IL-6 gene were amplified and the promoter haplotypes were reconstructed from genotype data with the PHASE program. Logistic regression analysis was used to examine the association between the IL-6 genotypes/diplotypes and the DIP OA outcome.

resultsThe G alleles of two promoter single nucleotide polymorphisms (SNPs) G-597A and G-174C were more common among the subjects with symptomatic DIP OA than among those with no disease (P = 0.020 and 0.024, corrected for multiple testing). In addition, the carriage of at least one G allele in these positions increased the risk of disease (P = 0.006 and P = 0.008, respectively). Carrying a haplotype with the G allele in all three promoter SNPs increased the risk of symptomatic DIP OA more than fourfold (odds ratio (OR) 4.45, P = 0.001). Carriage of the G-G diplotype indicated an increased risk of both symmetrical DIP OA (OR 1.52, 95% confidence interval 1.01 to 2.28) and symptomatic DIP OA (OR 3.67, 95% confidence interval 1.50 to 9.00).

conclusionThe present study showed that the presence of G alleles at common IL-6 polymorphic promoter loci was associated with the more severe DIP OA outcomes, symmetrical and symptomatic.

Indexed as

Genetic VariationHandPromoter Regions, GeneticAllelesFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeHaplotypesHeterozygoteHumansInterleukin-6Middle AgedOsteoarthritisPolymorphism, Single NucleotideSeverity of Illness IndexInterleukin-6

Identifiers

PMID18257935
PMCPMC2374458
OpenAlexW1999040820

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Registered trials

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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.