期刊
ARTHRITIS AND RHEUMATISM
卷 65, 期 4, 页码 1122-1128出版社
WILEY
DOI: 10.1002/art.37842
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资金
- NIH (National Institute of Arthritis and Musculoskeletal and Skin Diseases) [N01-AR-9-2235]
- NIH (National Center for Research Resources, Clinical and Translational Science Award program) [KL2-RR-024990]
- NIH (National Center for Research Resources, US Public Health Service) [RR-03655]
Objective Familial aggregation of fibromyalgia has been increasingly recognized. The goal of this study was to conduct a genome-wide linkage scan to identify susceptibility loci for fibromyalgia. Methods We genotyped members of 116 families from the Fibromyalgia Family Study and performed a model-free genome-wide linkage analysis of fibromyalgia with 341 microsatellite markers, using the Haseman-Elston regression approach. Results The estimated sibling recurrence risk ratio (s) for fibromyalgia was 13.6 (95% confidence interval 10.018.5), based on a reported population prevalence of 2%. Genome-wide suggestive evidence of linkage was observed at markers D17S2196 (empirical P [Pe] = 0.00030) and D17S1294 (Pe = 0.00035) on chromosome 17p11.2q11.2. Conclusion The estimated sibling recurrence risk ratio (s) observed in this study suggests a strong genetic component of fibromyalgia. This is the first report of genome-wide suggestive linkage of fibromyalgia to the chromosome 17p11.2q11.2 region. Further investigation of these multicase families from the Fibromyalgia Family Study is warranted to identify potential causal risk variants for fibromyalgia.
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