{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,8,22]],"date-time":"2025-08-22T17:10:07Z","timestamp":1755882607051,"version":"3.44.0"},"reference-count":16,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2025,4,2]],"date-time":"2025-04-02T00:00:00Z","timestamp":1743552000000},"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":[[2025,8,22]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Chronic actinic dermatitis (CAD) is an inflammatory, immune-mediated photodermatosis characterized by erythematous, pruritic, lichenified plaques affecting photo-exposed areas of the body. The pathogenesis of CAD remains unknown, with many postulated theories in the literature. The predominant hypothesis suggests a delayed type IV hypersensitivity reaction caused by photosensitive skin antigens, similar in disease process to allergic contact dermatitis. Despite current evidence suggesting no familial inheritance, we present, to our knowledge, the first reported cases of CAD affecting three members of the same family, with increasing severity in each subsequent generation (i.e. two generations), strengthening the case for potential genetic predisposition.<\/jats:p>","DOI":"10.1093\/ced\/llaf154","type":"journal-article","created":{"date-parts":[[2025,4,2]],"date-time":"2025-04-02T04:35:24Z","timestamp":1743568524000},"page":"1838-1842","source":"Crossref","is-referenced-by-count":0,"title":["Chronic actinic dermatitis: a familial link?"],"prefix":"10.1093","volume":"50","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8310-5750","authenticated-orcid":false,"given":"Usamah M","family":"Afzal","sequence":"first","affiliation":[{"name":"Harrogate and District Foundation Trust , Harrogate 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