{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T18:45:26Z","timestamp":1777661126729,"version":"3.51.4"},"reference-count":28,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2024,2,27]],"date-time":"2024-02-27T00:00:00Z","timestamp":1708992000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,7,16]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>It is increasingly clear that triglyceride-rich lipoproteins are proinflammatory and cause low-grade systemic inflammation. However, it is currently unknown whether elevated plasma triglycerides are causally related to the development of psoriasis, a skin disorder driven by chronic inflammation.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objectives<\/jats:title>\n                  <jats:p>To determine if elevated plasma triglycerides are associated with increased risk of psoriasis in observational and Mendelian randomization analysis.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Consecutive individuals from the Copenhagen General Population Study were included. We used plasma triglycerides (n = 108 043) and a weighted triglyceride allele score (n = 92 579) on nine known triglyceride-altering genetic variants. Genetic results were replicated in 337 159 individuals from the UK Biobank. Psoriasis was defined using the International Classification of Diseases, version 10 (ICD-10) code for hospital contact in the main analyses, and prescription of topical antipsoriatics for mild psoriasis in the sensitivity analysis.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>During a follow-up of median (range) 9.3 (0.1\u201315.1) years from 2003 to 2015 through 2018, 855 (1%) individuals were diagnosed with psoriasis by ICD-10 in the observational analysis and 772 (1%) in the Mendelian randomization analysis. In the observational analysis, the multivariable adjusted hazard ratio for psoriasis by ICD-10 was 1.26 [95% confidence interval (CI) 1.15\u20131.39] per doubling in plasma triglycerides with a corresponding causal odds ratio of incident psoriasis of 2.10 (95% CI 1.30\u20133.38). Causality was confirmed from data from the UK Biobank. Results were similar but slightly attenuated when we used topical antipsoriatic prescriptions for mild psoriasis.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Elevated plasma triglycerides are associated with an increased risk of psoriasis in observational and Mendelian randomization analysis.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/bjd\/ljae089","type":"journal-article","created":{"date-parts":[[2024,2,27]],"date-time":"2024-02-27T15:50:41Z","timestamp":1709049041000},"page":"209-215","source":"Crossref","is-referenced-by-count":22,"title":["Elevated plasma triglycerides increase the risk of psoriasis: a cohort and Mendelian randomization study"],"prefix":"10.1093","volume":"191","author":[{"given":"Anders M","family":"Greve","sequence":"first","affiliation":[{"name":"Department of Clinical Biochemistry, Rigshospitalet"},{"name":"Department of Clinical Biochemistry"},{"name":"The Copenhagen General Population\u00a0Study, Herlev and Gentofte Hospital"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anders B","family":"Wulff","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry"},{"name":"The Copenhagen General Population\u00a0Study, Herlev and Gentofte Hospital"},{"name":"Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen , Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stig E","family":"Bojesen","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry"},{"name":"The Copenhagen General Population\u00a0Study, Herlev and Gentofte Hospital"},{"name":"Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen , Denmark"},{"name":"The Copenhagen City Heart Study, Bispebjerg and Frederiksberg Hospital; Copenhagen\u00a0University Hospital , Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1954-7220","authenticated-orcid":false,"given":"B\u00f8rge G","family":"Nordestgaard","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry"},{"name":"The Copenhagen General Population\u00a0Study, Herlev and Gentofte Hospital"},{"name":"Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen , Denmark"},{"name":"The Copenhagen City Heart Study, Bispebjerg and Frederiksberg Hospital; Copenhagen\u00a0University Hospital , Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2024,2,27]]},"reference":[{"key":"2024071611290655000_ljae089-B1","doi-asserted-by":"crossref","first-page":"1945","DOI":"10.1001\/jama.2020.4006","article-title":"Pathophysiology, clinical presentation, and treatment of psoriasis: a review","volume":"323","author":"Armstrong","year":"2020","journal-title":"JAMA"},{"key":"2024071611290655000_ljae089-B2","doi-asserted-by":"crossref","first-page":"1475","DOI":"10.3390\/ijms20061475","article-title":"Psoriasis pathogenesis and treatment","volume":"20","author":"Rendon","year":"2019","journal-title":"Int J Mol Sci"},{"key":"2024071611290655000_ljae089-B3","doi-asserted-by":"crossref","first-page":"15382","DOI":"10.1038\/ncomms15382","article-title":"Large scale meta-analysis characterizes genetic architecture for common psoriasis associated variants","volume":"8","author":"Tsoi","year":"2017","journal-title":"Nat Commun"},{"key":"2024071611290655000_ljae089-B4","doi-asserted-by":"crossref","first-page":"486","DOI":"10.1111\/bjd.12101","article-title":"The association between psoriasis and dyslipidaemia: a systematic review","volume":"168","author":"Ma","year":"2013","journal-title":"Br J Dermatol"},{"key":"2024071611290655000_ljae089-B5","doi-asserted-by":"crossref","first-page":"1298","DOI":"10.1161\/CIRCULATIONAHA.113.003008","article-title":"Elevated remnant cholesterol causes both low-grade inflammation and ischemic heart disease, whereas elevated low-density lipoprotein cholesterol causes ischemic heart disease without inflammation","volume":"128","author":"Varbo","year":"2013","journal-title":"Circulation"},{"key":"2024071611290655000_ljae089-B6","doi-asserted-by":"crossref","first-page":"191","DOI":"10.1007\/BF00604821","article-title":"Demonstration of beta-lipoproteins in the psoriatic skin by immunofluorescent technique","volume":"249","author":"Ishikawa","year":"1974","journal-title":"Arch Dermatol Forsch"},{"key":"2024071611290655000_ljae089-B7","doi-asserted-by":"crossref","first-page":"547","DOI":"10.1161\/CIRCRESAHA.115.306249","article-title":"Triglyceride-rich lipoproteins and atherosclerotic cardiovascular disease: new insights from epidemiology, genetics, and biology","volume":"118","author":"Nordestgaard","year":"2016","journal-title":"Circ Res"},{"key":"2024071611290655000_ljae089-B8","doi-asserted-by":"crossref","first-page":"626","DOI":"10.1016\/S0140-6736(14)61177-6","article-title":"Triglycerides and cardiovascular disease","volume":"384","author":"Nordestgaard","year":"2014","journal-title":"Lancet"},{"key":"2024071611290655000_ljae089-B9","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1093\/ije\/dyg070","article-title":"\u2018Mendelian randomization\u2019: can genetic epidemiology contribute to understanding environmental determinants of disease?","volume":"32","author":"Smith","year":"2003","journal-title":"Int J Epidemiol"},{"key":"2024071611290655000_ljae089-B10","first-page":"1192","article-title":"From genome-wide association studies to Mendelian randomization: novel opportunities for understanding cardiovascular disease causality, pathogenesis, prevention, and treatment","volume":"114","author":"Benn","year":"2018","journal-title":"Cardiovasc Res"},{"key":"2024071611290655000_ljae089-B11","doi-asserted-by":"crossref","first-page":"32","DOI":"10.1056\/NEJMoa1308027","article-title":"Loss-of-function mutations in APOC3 and risk of ischemic vascular disease","volume":"371","author":"J\u00f8rgensen","year":"2014","journal-title":"N Engl J Med"},{"key":"2024071611290655000_ljae089-B12","doi-asserted-by":"crossref","first-page":"2901","DOI":"10.1161\/01.CIR.99.22.2901","article-title":"Lipoprotein lipase mutations, plasma lipids and lipoproteins, and risk of ischemic heart disease. 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