{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T02:44:39Z","timestamp":1792032279028,"version":"4.4.0"},"reference-count":43,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2019,8,1]],"date-time":"2019-08-01T00:00:00Z","timestamp":1564617600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000033","name":"Institute of Musculoskeletal Health and Arthritis","doi-asserted-by":"publisher","award":["MOP77700"],"award-info":[{"award-number":["MOP77700"]}],"id":[{"id":"10.13039\/501100000033","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Arthritis &amp; Rheumatology"],"published-print":{"date-parts":[[2019,9]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To determine the incidence of inflammatory arthritis and autoantibody prevalence in Indigenous North American people.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Unaffected relatives of Indigenous North Americans with rheumatoid arthritis (\n                      <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\n                      ) from central Canada and Alaska were systematically monitored from 2005 to 2017. Rheumatoid factor (\n                      <jats:styled-content style=\"fixed-case\">RF<\/jats:styled-content>\n                      ) and anti\u2013citrullinated protein antibodies (\n                      <jats:styled-content style=\"fixed-case\">ACPA<\/jats:styled-content>\n                      s) were tested at every visit, and a subset was tested for\n                      <jats:styled-content style=\"fixed-case\">ACPA<\/jats:styled-content>\n                      fine specificity using a custom multiplex assay. Multistate models based on all available study visits were developed to determine the likelihood of transitioning between autoantibody states, or to inflammatory arthritis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Eighteen of 374 relatives (4.8%) developed inflammatory arthritis during follow\u2010up (after a mean \u00b1\n                      <jats:styled-content style=\"fixed-case\">SD<\/jats:styled-content>\n                      of 4.7 \u00b1 2.4 years), yielding a transition rate of 9.2 cases\/1,000 person\u2010years. Thirty percent of those who developed inflammatory arthritis were seronegative at baseline, but all were seropositive at inflammatory arthritis onset. Although 30% of\n                      <jats:styled-content style=\"fixed-case\">ACPA<\/jats:styled-content>\n                      \/\n                      <jats:styled-content style=\"fixed-case\">RF<\/jats:styled-content>\n                      double\u2010seropositive individuals developed inflammatory arthritis (after 3.2 \u00b1 2.2 years), the majority of these individuals did not develop inflammatory arthritis. Multistate modeling indicated a 71% and 68% likelihood of\n                      <jats:styled-content style=\"fixed-case\">ACPA<\/jats:styled-content>\n                      and\n                      <jats:styled-content style=\"fixed-case\">RF<\/jats:styled-content>\n                      seropositive states, respectively, reverting to a seronegative state after 5 years, and a 39% likelihood of an\n                      <jats:styled-content style=\"fixed-case\">ACPA<\/jats:styled-content>\n                      \/\n                      <jats:styled-content style=\"fixed-case\">RF<\/jats:styled-content>\n                      double\u2010seropositive state becoming seronegative. Fine specificity testing demonstrated an expansion of the\n                      <jats:styled-content style=\"fixed-case\">ACPA<\/jats:styled-content>\n                      repertoire prior to the development of inflammatory arthritis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Despite a high incidence of inflammatory arthritis in this cohort of at\u2010risk relatives of Indigenous North Americans with\n                      <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\n                      , a large proportion of autoantibody\u2010positive individuals do not develop inflammatory arthritis and revert back to an autoantibody\u2010negative state.\n                    <\/jats:p>\n                  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