ReviewCurrent rheumatology reports2004
The genetic basis of spondyloarthritis.
Review in Current rheumatology reports, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00081562 (Family Studies of the Genetics of Ankylosing Spondylitis), which is not on this map. Cited by 2 papers.
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.
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.
Family Studies of the Genetics of Ankylosing Spondylitis
Who cites it
2 citing papers in PubMed, 21 citations in OpenAlex.
- Outcomes in Juvenile-Onset Spondyloarthritis.Frontiers in medicine · 2021Review
- Targeting tumor necrosis factor receptors in ankylosing spondylitis.Annals of the New York Academy of Sciences · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spondyloarthritis tends to cluster in families and, to a great extent, is associated with human leukocyte antigen (HLA) B27. In fact, the population frequency of spondyloarthritis in most groups is proportional to that of HLA-B27. But the frequency of HLA-B27 in the population-at-large far exceeds that of spondyloarthritis, suggesting other genetic factors also are operative. Other major histocompatibility complex genes have been implicated, especially HLA-DR, though linkage to HLA-B27 confounds the analysis of this in many studies. Genome-wide scans have implicated regions on chromosomes 2q, 6p, 6q, 10q, 11q, 16q, 17q, and 19q in ankylosing spondylitis, on 4, 6p, and 17q in psoriasis, and on 7q and 16q in inflammatory bowel disease. The search for non-major histocompatibility complex candidate genes has been complicated by inadequate power, because of the small effect they exert on overall disease susceptibility, although recent studies are revealing promising candidates that must be confirmed by other groups.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.