多形性日光疹。一例病例报告及硬化机制探讨。
Polymorphous light eruption. A case report and consideration of the hardening mechanism.
作者信息
Watanabe M, Yamanouchi H, Ogawa F, Katayama I
机构信息
Department of Dermatology, Nagasaki University School of Medicine, Nagasaki, Japan.
出版信息
Dermatology. 1999;199(2):158-61. doi: 10.1159/000018226.
BACKGROUND
Polymorphous light eruption (PLE) is a common form of photodermatosis. The pathogenesis of the disease and the mechanism of the hardening phenomenon, however, have not been clarified.
OBSERVATION
We report a 62-year-old Japanese woman with PLE. Provocation and hardening induction testing revealed that hardening was induced at the sites irradiated by a sufficient dose of UV for reproduction of the lesion. Topical steroid could prevent a positive reaction but not the hardening induction. The expression of adhesion molecules and CD1a was decreased at the hardening site.
CONCLUSION
From these results, the hardening phenomenon in our case might be due to immunosuppression by UV exposure supported by the down-regulation of cell adhesion molecule expression and partially due to the depletion of endogenous antigens which cause a delayed-type hypersensitivity reaction.
背景
多形性日光疹（PLE）是光皮肤病的一种常见形式。然而，该疾病的发病机制以及硬化现象的机制尚未阐明。
观察
我们报告了一名62岁患多形性日光疹的日本女性。激发和硬化诱导试验显示，在以足以再现皮损的紫外线剂量照射的部位诱导出了硬化。局部使用类固醇可预防阳性反应，但不能预防硬化诱导。硬化部位的黏附分子和CD1a表达降低。
结论
根据这些结果，我们病例中的硬化现象可能是由于紫外线暴露导致的免疫抑制，这由细胞黏附分子表达下调所支持，部分原因是引起迟发型超敏反应的内源性抗原耗竭。
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