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Three common themes are as follows: excess chromophore allowing visible light energy to cause photodynamic damage, reduced <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> repair capacity to <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> damage, and enhanced sensitivity to light\u2010induced allergens mediated immunologically. Although the cause of each condition may be known, the precise pathogenesis underlying the photosensitivity has taken longer to understand. By focussing on three clinical disorders under each of these themes, we have explored the following: why erythropoietic protoporphyria differs so markedly from the other cutaneous porphyrias; how a <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> repair defect was eventually revealed to be the underlying cause of the vitamin B3 deficiency disorder of pellagra; an immunological explanation for the over reactivity to photoallergens in chronic actinic dermatitis.<\/jats:p>","DOI":"10.1111\/exd.12467","type":"journal-article","created":{"date-parts":[[2014,6,9]],"date-time":"2014-06-09T11:03:47Z","timestamp":1402311827000},"page":"543-546","source":"Crossref","is-referenced-by-count":15,"title":["Evidence and conjecture about mechanisms of cutaneous disease in photodermatology"],"prefix":"10.1111","volume":"23","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6748-0916","authenticated-orcid":false,"given":"Rebecca 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