METHODS: Fifteen patients with actinic prurigo participated in the study. A biopsy from the uninvolved and unirradiated skin of the left buttock was performed, and another from the uninvolved skin of the right buttock, 72 hours after exposure to two MEDs of SSR. Immunohistochemistry staining was used to identify Langerhans cells (CD1a) in all samples.
RESULTS: In actinic prurigo patients with normal MED, there was a significant decrease in the number of epidermal Langerhans cells on the buttock skin exposed to two MED of SSR compared with the unirradiated buttock skin (P = .02 and .035 respectively). On the contrary, in patients with low MED there were no significant differences in the number of epidermal Langerhans cells between irradiated and unirradiated skin (P = .39).
CONCLUSIONS: Epidermal Langerhans cells migration after ultraviolet radiation exposure is decreased in actinic prurigo patients with low MED as has been reported in PLE patients, especially, those with low MED or positive UVB provocation tests. Langerhans cells resistance could be part of a common pathogenic mechanism in these two photodermatoses.
方法:15例光化性痒疹患者参与了研究。对左臀部未受累和未照射的皮肤进行了活检,另一个来自右臀部的皮肤,暴露于SSR的两个MED后72小时。免疫组织化学染色用于鉴定所有样品中的朗格汉斯细胞(CD1a)。
结果:在MED正常的光化瘙痒患者中,与未照射的臀部皮肤相比,暴露于两次MED的SSR的臀部皮肤上的表皮朗格汉斯细胞数量显着减少(分别为P=.02和.035)。相反,在MED较低的患者中,照射和未照射的皮肤之间的表皮朗格汉斯细胞数量没有显着差异(P=.39)。
结论:如PLE患者报道的,在低MED的光化性瘙痒患者中,紫外线照射后表皮朗格汉斯细胞迁移减少,尤其是,MED低或UVB激发试验阳性者。朗格汉斯细胞抗性可能是这两种光皮肤病的常见致病机制的一部分。