Evidence map›Paper›PMID 19151030›Full record

ReviewRheumatology (Oxford, England)2009

Genetics of bone loss in rheumatoid arthritis--role of vitamin D receptor polymorphisms.

P Ranganathan

Open access · bronzeAbstract readReview
In one paragraph

Review in Rheumatology (Oxford, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Adverse Outcome Pathways Applied to Space Radiation Research.Environmental and molecular mutagenesis · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Inflammation fuels tumor progress and metastasis.Current pharmaceutical design · 2015
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Bone mineral density changes in patients with recent-onset rheumatoid arthritis.Clinical medicine insights. Arthritis and musculoskeletal disorders · 2011
    Article
  15. VITAMIN D RECEPTOR GENE MUTATIONS AND VITAMIN D SERUM LEVELS IN ASTHMATIC CHILDREN.Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo
    Observational
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

1 author at 1 institution in 1 country.

P RanganathanDepartment of Medicine, Division of Rheumatology, Washington University School of Medicine, St Louis, MO 63110, USA. prangana@im.wustl.edu
Washington University in St. Louis · US

Funding

Washington University Institute of Clinical and Translational Sciences (UL1)UL1RR024992 · NCRR · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2007 to 2011
$45.4M
Washington University Institute of Clinical and Translational SciencesUL1TR000448 · NCATS · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2012 to 2016
$41.4M
NCATS NIH HHS UL1 TR000448NCRR NIH HHS UL1 RR024992NCRR NIH HHS UL1RR024992
6 · The paper itself

Abstract

RA is a systemic inflammatory arthritis that leads to local and systemic bone loss. Osteoporosis or the systemic bone loss associated with RA increases the risk for fragility fractures, which can affect quality of life dramatically in RA patients. Although traditional and RA-related risk factors have been defined and studied for osteoporosis associated with RA, genetic factors such as polymorphic variants in the traditional candidate genes for osteoporosis, such as the vitamin D receptor (VDR), type 1 collagen A1 (COLIA1) and oestrogen receptor-alpha (ESR1), have not been well elucidated in RA patients. This review summarizes the currently available literature on the association of VDR polymorphisms with local and systemic bone loss in RA. It also discusses potential targets for genetic research in this area, such as polymorphisms in genes, such as IL-6 (IL6) and TNF receptor type 2 (TNFRSF1B), which control the inflammatory response in RA and may influence bone loss in RA. Defining such genetic factors, in addition to traditional and RA-related risk factors for osteoporosis in RA, may facilitate early identification of patients at high risk for fractures who can then be targeted for treatment.

Indexed as

Polymorphism, GeneticArthritis, RheumatoidFractures, BoneGenetic Predisposition to DiseaseGenotypeHLA-DR AntigensHLA-DRB1 ChainsHumansOsteoporosisReceptors, CalcitriolHLA-DR AntigensHLA-DRB1 ChainsReceptors, Calcitriol

Identifiers

PMID19151030
PMCPMC2722799
OpenAlexW2120642132

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.