Vandermaesen J, Roelandts R, Degreef H
J Am Acad Dermatol. 1986 Oct;15(4 Pt 1):685-92. doi: 10.1016/s0190-9622(86)70224-7.
In this article are reviewed the various hypotheses concerning the etiology of the persistent light reaction and photosensitivity dermatitis, which occurs among older people and is characterized by an extreme photosensitivity that sometimes evolves into a pseudolymphoma, that is, actinic reticuloid. An etiologic agent can sometimes be demonstrated, but the precise pathogenetic mechanism is unknown. Clinical experience and experimental research indicate that the cause is most probably multifactoral: contact allergenic, photoallergenic, phototoxic, immunologic, and metabolic factors are involved, but their precise roles in the origin of the extreme photosensitivity are still unclear. Localized persistent light reactivity could result from the continued effects of the original photoallergen, but generalized photosensitivity is more difficult to account for. Among the many different hypotheses, two are of special interest: autosensitization of skin proteins with endogenous photosensitizers and cellular hypersensitivity to light, as is manifested by fibroblast cultures of actinic reticuloid patients.
本文综述了关于持续性光反应和光敏性皮炎病因的各种假说。持续性光反应和光敏性皮炎发生于老年人,其特征为极度光敏性,有时会发展为假性淋巴瘤,即光化性类网状细胞增多症。有时可以证实存在病因,但确切的发病机制尚不清楚。临床经验和实验研究表明,病因很可能是多因素的:涉及接触性变应原、光变应原、光毒性、免疫和代谢因素,但它们在极度光敏性起源中的确切作用仍不清楚。局限性持续性光反应可能是由原始光变应原的持续作用引起的,但全身性光敏性则更难解释。在众多不同的假说中,有两个特别值得关注:皮肤蛋白与内源性光敏剂的自身致敏作用,以及光化性类网状细胞增多症患者成纤维细胞培养所显示的细胞对光的超敏反应。