{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T19:10:09Z","timestamp":1793387409059,"version":"4.5.0"},"reference-count":64,"publisher":"American Medical Association (AMA)","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Dermatol"],"published-print":{"date-parts":[[2025,11,1]]},"abstract":"<jats:sec id=\"ab-doi250041-4\">\n                    <jats:title>Importance<\/jats:title>\n                    <jats:p>The cardiovascular impact of biologics used in psoriasis is not fully understood. Several studies have suggested that the inhibition of the T-helper 17 cell pathway could lead to the destabilization of atherosclerotic plaques, leading to major adverse cardiovascular events (MACEs).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-doi250041-5\">\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To assess whether the initiation of interleukin (IL)-17(R)A inhibitors triggers MACEs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-doi250041-6\">\n                    <jats:title>Design, Setting, and Participants<\/jats:title>\n                    <jats:p>In this case\u2013time-control study using the French National Health Insurance database, all individuals who received IL-17(R)A inhibitors (secukinumab, ixekizumab, and brodalumab) from 2016 to 2021, were included and classified according to their cardiovascular risk level. The risk period was defined as the 6 months before the MACE, and the reference period as the 6 months before the risk period. The same design for patients who received tumor necrosis factor (TNF)\u2013\u03b1 inhibitors (adalimumab or etanercept) for similar indications (psoriasis, psoriatic arthritis, ankylosing spondylitis, or juvenile arthritis), as an active comparator. The data analysis was conducted between April 2023 and August 2024.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-doi250041-7\">\n                    <jats:title>Exposure<\/jats:title>\n                    <jats:p>The initiation of the biologic was screened in both periods.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-doi250041-8\">\n                    <jats:title>Main Outcomes and Measures<\/jats:title>\n                    <jats:p>The odds ratios (ORs) for the risk of MACEs were assessed following the initiation of IL-17(R)A inhibitors and TNF-\u03b1 inhibitors independently. Subsequently, the OR for the risk of MACE associated with IL-17(R)A inhibitors was estimated using TNF-\u03b1 inhibitors as the comparator.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-doi250041-9\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Among the 34\u202f241 individuals who received an IL-17(R)A inhibitor, 381 MACEs were analyzed, including 176 acute coronary syndromes and 84 ischemic strokes in the main analysis. Initiation of IL-17(R)A inhibitors was not significantly associated with MACEs (OR, 1.25 [95% CI, 0.75-2.08] vs TNF-\u03b1 inhibitor initiation and MACEs: OR, 0.90 [95% CI, 0.65-1.24]). Overall, the initiation of an IL-17(R)A inhibitor was not significantly associated with MACEs in the following 6 months, using TNF-\u03b1 inhibitor as a comparator (OR, 1.40 [95% CI, 0.77-2.54]), regardless of the individual cardiovascular risk (\n                      <jats:italic>P<\/jats:italic>\n                      for homogeneity\u2009=\u2009.29). The definition of MACE was broadened in a first sensitivity analysis, and the risk period was shortened to 3 months in a second sensitivity analysis. The results did not change.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-doi250041-10\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>In this case\u2013time-control study based on a national insurance database, there was no evidence of a significant association between MACEs and the initiation of IL-17(R)A inhibitors, regardless of the individual cardiovascular risk of the patient. However, a modest risk increase cannot be entirely excluded.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1001\/jamadermatol.2025.2972","type":"journal-article","created":{"date-parts":[[2025,9,3]],"date-time":"2025-09-03T15:00:28Z","timestamp":1756911628000},"page":"1107","source":"Crossref","is-referenced-by-count":6,"title":["Interleukin-17 Inhibitors and Early Major Adverse Cardiovascular Events"],"prefix":"10.1001","volume":"161","author":[{"given":"Maxime","family":"Raby","sequence":"first","affiliation":[{"name":"Univ Rennes, CHU Rennes, Inserm, EHESP, Irset (Institut de Recherche en 13 Sant\u00e9, Environnement et Travail)\u2014UMR_S 1085, Rennes, France"},{"name":"Department of Dermatology, Universit\u00e9 de Rennes, CHU Rennes, Rennes, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frederic","family":"Balusson","sequence":"additional","affiliation":[{"name":"Univ Rennes, CHU Rennes, Inserm, EHESP, Irset (Institut de Recherche en 13 Sant\u00e9, Environnement et Travail)\u2014UMR_S 1085, Rennes, France"},{"name":"Pharmacovigilance, Pharmacoepidemiology and Drug Information Center, Department of Clinical Pharmacology, Rennes Hospital, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emmanuel","family":"Oger","sequence":"additional","affiliation":[{"name":"Univ Rennes, CHU Rennes, Inserm, EHESP, Irset (Institut de Recherche en 13 Sant\u00e9, Environnement et Travail)\u2014UMR_S 1085, Rennes, France"},{"name":"Pharmacovigilance, Pharmacoepidemiology and Drug Information Center, Department of Clinical Pharmacology, Rennes Hospital, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marion","family":"Gundelwein","sequence":"additional","affiliation":[{"name":"Univ Rennes, CHU Rennes, Inserm, EHESP, Irset (Institut de Recherche en 13 Sant\u00e9, Environnement et Travail)\u2014UMR_S 1085, Rennes, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alain","family":"Dupuy","sequence":"additional","affiliation":[{"name":"Univ Rennes, CHU Rennes, Inserm, EHESP, Irset (Institut de Recherche en 13 Sant\u00e9, Environnement et Travail)\u2014UMR_S 1085, Rennes, France"},{"name":"Department of Dermatology, Universit\u00e9 de Rennes, CHU Rennes, Rennes, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florence","family":"Poizeau","sequence":"additional","affiliation":[{"name":"Univ Rennes, CHU Rennes, Inserm, EHESP, Irset (Institut de Recherche en 13 Sant\u00e9, Environnement et Travail)\u2014UMR_S 1085, Rennes, France"},{"name":"Department of Dermatology, Universit\u00e9 de Rennes, CHU Rennes, Rennes, France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"10","reference":[{"issue":"16","key":"doi250041r1","doi-asserted-by":"publisher","first-page":"2054","DOI":"10.1093\/eurheartj\/ehr285","article-title":"Psoriasis and risk of 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