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Abstract：
BACKGROUND: Actinic prurigo is a chronic photodermatosis of unclear pathogenesis. Epidermal Langerhans cell resistance to migration after ultraviolet radiation exposure has been proposed as a possible mechanism, as occurs in polymorphic light eruption patients. The purpose of this study was to evaluate the effect of solar-simulated radiation (SSR) on epidermal Langerhans cells in the uninvolved skin of actinic prurigo patients.
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.
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.
摘要：
背景：光化瘙痒是一种发病机制不明确的慢性光性皮肤病。表皮朗格汉斯细胞在紫外线照射后对迁移的抗性已被认为是一种可能的机制。如多形性光疹患者。这项研究的目的是评估太阳模拟辐射（SSR）对光化瘙痒患者未受累皮肤中表皮朗格汉斯细胞的影响。
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。
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。
