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Familial Clustering of Erosive Hand Osteoarthritis in a Large Statewide Cohort
Author(s) -
Kazmers Nikolas H.,
Meeks Huong D.,
Novak Kendra A.,
Yu Zhe,
Fulde Gail L.,
Thomas Joy L.,
Barker Tyler,
Jurynec Michael J.
Publication year - 2021
Publication title -
arthritis and rheumatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.106
H-Index - 314
eISSN - 2326-5205
pISSN - 2326-5191
DOI - 10.1002/art.41520
Subject(s) - medicine , logistic regression , etiology , incidence (geometry) , population , pedigree chart , odds ratio , cohort , diabetes mellitus , family aggregation , cohort study , epidemiology , disease , genetics , biology , environmental health , physics , optics , gene , endocrinology
Objective Erosive hand osteoarthritis (OA) is a severe and rapidly progressing subset of hand OA. Its etiology remains largely unknown, which has hindered development of successful treatments. This study was undertaken to test the hypothesis that erosive hand OA demonstrates familial clustering in a large statewide population linked to genealogical records, and to determine the association of potential risk factors with erosive hand OA. Methods Patients diagnosed as having erosive hand OA were identified by searching 4,741,840 unique medical records from a comprehensive statewide database, the Utah Population Database (UPDB). Affected individuals were mapped to pedigrees to identify high‐risk families with excess clustering of erosive hand OA as defined by a familial standardized incidence ratio (FSIR) of ≥2.0. The magnitude of familial risk of erosive hand OA in related individuals was calculated using Cox regression models. Association of potential erosive hand OA risk factors was analyzed using multivariate conditional logistic regression and logistic regression models. Results We identified 703 affected individuals linked to 240 unrelated high‐risk pedigrees with excess clustering of erosive hand OA (FSIR ≥2.0, P < 0.05). The relative risk of developing erosive hand OA was significantly elevated in first‐degree relatives ( P < 0.001). There were significant associations between a diagnosis of erosive hand OA and age, sex, diabetes, and obesity (all P < 0.05). Conclusion Familial clustering of erosive hand OA observed in a statewide database indicates a potential genetic contribution to the etiology of the disease. Age, sex, diabetes, and obesity are risk factors for erosive hand OA. Identification of causal gene variants in these high‐risk families may provide insight into the genes and pathways that contribute to erosive hand OA onset and progression.