{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T23:29:46Z","timestamp":1784071786802,"version":"3.55.0"},"reference-count":70,"publisher":"Springer Science and Business Media LLC","issue":"3","license":[{"start":{"date-parts":[[2009,6,25]],"date-time":"2009-06-25T00:00:00Z","timestamp":1245888000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0\/"},{"start":{"date-parts":[[2009,6,25]],"date-time":"2009-06-25T00:00:00Z","timestamp":1245888000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0\/"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Arthritis Res Ther"],"abstract":"<jats:title>Abstract<\/jats:title><jats:sec>\n                        <jats:title>Introduction<\/jats:title>\n                        <jats:p>Rheumatoid arthritis (RA) is more common in females than males and sex steroid hormones may in part explain this difference. We conducted a case\u2013control study nested within two prospective studies to determine the associations between plasma steroid hormones measured prior to RA onset and polymorphisms in the androgen receptor (<jats:italic>AR<\/jats:italic>), estrogen receptor 2 (<jats:italic>ESR2<\/jats:italic>), aromatase (<jats:italic>CYP19<\/jats:italic>) and progesterone receptor (<jats:italic>PGR<\/jats:italic>) genes and RA risk.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Methods<\/jats:title>\n                        <jats:p>We genotyped <jats:italic>AR<\/jats:italic>, <jats:italic>ESR2<\/jats:italic>, <jats:italic>CYP19<\/jats:italic>, <jats:italic>PGR<\/jats:italic> SNPs and the <jats:italic>AR<\/jats:italic> CAG repeat in RA case\u2013control studies nested within the Nurses' Health Study (NHS), NHS II (449 RA cases, 449 controls) and the Women's Health Study (72 cases, and 202 controls). All controls were matched on cohort, age, Caucasian race, menopausal status, and postmenopausal hormone use. We measured plasma dehydroepiandrosterone sulfate (DHEAS), testosterone, and sex hormone binding globulin in 132 pre-RA samples and 396 matched controls in the NHS cohorts. We used conditional logistic regression models adjusted for potential confounders to assess RA risk.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Results<\/jats:title>\n                        <jats:p>Mean age of RA diagnosis was 55 years in both cohorts; 58% of cases were rheumatoid factor positive at diagnosis. There was no significant association between plasma DHEAS, total testosterone, or calculated free testosterone and risk of future RA. There was no association between individual variants or haplotypes in any of the genes and RA or seropositive RA, nor any association for the <jats:italic>AR<\/jats:italic> CAG repeat.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Conclusions<\/jats:title>\n                        <jats:p>Steroid hormone levels measured at a single time point prior to RA onset were not associated with RA risk in this study. Our findings do not suggest that androgens or the <jats:italic>AR<\/jats:italic>, <jats:italic>ESR2<\/jats:italic>, <jats:italic>PGR<\/jats:italic>, and <jats:italic>CYP19<\/jats:italic> genes are important to RA risk in women.<\/jats:p>\n                     <\/jats:sec>","DOI":"10.1186\/ar2742","type":"journal-article","created":{"date-parts":[[2009,6,25]],"date-time":"2009-06-25T18:13:29Z","timestamp":1245953609000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":50,"title":["A prospective study of androgen levels, hormone-related genes and risk of rheumatoid arthritis"],"prefix":"10.1186","volume":"11","author":[{"given":"Elizabeth W","family":"Karlson","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lori B","family":"Chibnik","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monica","family":"McGrath","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shun-Chiao","family":"Chang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brendan T","family":"Keenan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen H","family":"Costenbader","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patricia A","family":"Fraser","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shelley","family":"Tworoger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan E","family":"Hankinson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I-Min","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie","family":"Buring","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Immaculata","family":"De Vivo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2009,6,25]]},"reference":[{"key":"2582_CR1","doi-asserted-by":"crossref","first-page":"87","DOI":"10.1093\/oxfordjournals.aje.a112878","volume":"111","author":"A Linos","year":"1980","unstructured":"Linos A, Worthington JW, O'Fallon WM, Kurland LT: The epidemiology of rheumatoid arthritis in Rochester, Minnesota: a study of incidence, prevalence, and mortality. 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