{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T23:21:24Z","timestamp":1785280884413,"version":"3.55.0"},"reference-count":37,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2025,7,7]],"date-time":"2025-07-07T00:00:00Z","timestamp":1751846400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,7,7]],"date-time":"2025-07-07T00:00:00Z","timestamp":1751846400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Intern Med"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Type 1 diabetes (T1D) increases premature mortality risk, with cardiovascular disease being the leading cause. Chronic inflammation may play a role. Associations between inflammatory biomarkers and mortality are not well\u2010known in T1D.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We evaluated a prospective clinical cohort with T1D without known cardiovascular disease. The inflammatory biomarkers soluble\u2010urokinase\u2010plasminogen\u2010activator\u2010receptor (suPAR) and interleukin\u20106 (IL\u20106) were measured. Patients were stratified by elevated\/low suPAR or IL\u20106, or simultaneously elevated suPAR and IL\u20106. Primary and secondary endpoints were all\u2010cause mortality and major adverse cardiovascular events (MACE), respectively. Cox models were adjusted for 10 Steno T1 Risk Engine variables and inflammatory biomarkers. Net reclassification improvement (NRI) and C\u2010statistics were calculated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Among 962 participants (52% male, median age 50, median follow\u2010up 13.1 years), mortality was higher in patients with elevated inflammation: 31% for elevated versus 9% for low suPAR; 30% for elevated versus 11% for low IL\u20106; and 50% for simultaneously elevated suPAR and IL\u20106 versus 5% for low suPAR and IL\u20106. In fully adjusted models, elevated inflammation was associated with mortality (hazard ratios [95% confidence intervals]: suPAR 2.0 [1.4\u20133.0,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.001], IL\u20106 1.8 [1.3\u20132.6;\n                      <jats:italic>p\u00a0<\/jats:italic>\n                      =\u00a00.001], and combined 4.0 [2.3\u20137.2,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.001]) and MACE (suPAR 1.9 [1.4\u20132.6,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.001], IL\u20106 1.4 [1.0\u20131.8,\n                      <jats:italic>p\u00a0<\/jats:italic>\n                      =\u00a00.034], and combined 2.6 [1.7\u20134.1,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.001]). Adding suPAR, IL\u20106, and their combination to the Steno T1 Risk Engine improved NRI for mortality by 61%, 53%, and 84%, respectively, whereas C\u2010statistics improved from 0.808 to 0.829, 0.826, and 0.881, respectively.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>suPAR, IL\u20106, and especially their combination independently predicts all\u2010cause mortality and MACE in T1D without known cardiovascular disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/joim.20108","type":"journal-article","created":{"date-parts":[[2025,7,7]],"date-time":"2025-07-07T03:03:03Z","timestamp":1751857383000},"page":"188-199","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Soluble urokinase plasminogen activator receptor and interleukin\u20106 improves prediction of all\u2010cause mortality and major adverse cardiovascular events in Type 1 diabetes"],"prefix":"10.1111","volume":"298","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0141-7110","authenticated-orcid":false,"given":"Hashmat Sayed Zohori","family":"Bahrami","sequence":"first","affiliation":[{"name":"Department of Clinical and Translational Research Steno Diabetes Center Copenhagen  Herlev Denmark"},{"name":"Department of Cardiology Copenhagen University Hospital, Amager &amp; Hvidovre  Hvidovre Denmark"},{"name":"Department of Clinical Medicine Faculty of Health and Medical Sciences University of Copenhagen  Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter Godsk","family":"J\u00f8rgensen","sequence":"additional","affiliation":[{"name":"Department of Cardiology Copenhagen University Hospital Herlev &amp; Gentofte  Herlev Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jens Dahlgaard","family":"Hove","sequence":"additional","affiliation":[{"name":"Department of Cardiology Copenhagen University Hospital, Amager &amp; Hvidovre  Hvidovre Denmark"},{"name":"Department of Clinical Medicine Faculty of Health and Medical Sciences University of Copenhagen  Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrik","family":"Dixen","sequence":"additional","affiliation":[{"name":"Department of Cardiology Copenhagen University Hospital, Amager &amp; Hvidovre  Hvidovre Denmark"},{"name":"Department of Clinical Medicine Faculty of Health and Medical Sciences University of Copenhagen  Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6613-2469","authenticated-orcid":false,"given":"Line Jee Hartmann","family":"Rasmussen","sequence":"additional","affiliation":[{"name":"Department of Clinical Research Copenhagen University Hospital Amager &amp; Hvidovre  Hvidovre 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