中华皮肤科杂志 ›› 2012, Vol. 45 ›› Issue (2): 87-90.

• 论著 • 上一篇    下一篇

表皮蛋白质及板层小体对激素依赖性皮炎皮肤屏障变化的影响

起珏1,顾华2,汤諹1,涂颖2,庞勤1,张丽2,何黎2   

  1. 1. 昆明医学院第一附属医院
    2. 昆明医学院第一附属医院皮肤科
  • 收稿日期:2011-04-25 修回日期:2011-07-07 出版日期:2012-02-15 发布日期:2012-01-31
  • 通讯作者: 何黎 E-mail:Heli2662@yahoo.com

Effects of epidermal proteins and lamellar bodies on epidermal barrier in glucocorticoid-dependent dermatitis

  • Received:2011-04-25 Revised:2011-07-07 Online:2012-02-15 Published:2012-01-31

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摘要：

目的 探讨表皮蛋白质、板层小体的变化对激素依赖性皮炎皮肤屏障变化的影响。 方法 无创性皮肤测试比较60例激素依赖性皮炎患者与40例正常人，皮肤经表皮水分流失（TEWL）的差异，13例患者及10例正常人配合皮损取材，行HE染色观察皮损组织病理学变化。免疫组化观察患者表皮K6、K10、K14、K15、兜甲蛋白、丝聚合蛋白、内披蛋白的变化。电镜观察板层小体密度的变化。结果 与正常人比较，患者TEWL增加，差异有统计学意义（P < 0.05），显示皮肤屏障功能受损。患者皮损的组织病理学为非特异性炎症表现，根据临床特点，各类皮损的组织病理学表现存在一定差异。免疫组化示患者表皮K10、K14、丝聚合蛋白、兜甲蛋白、内披蛋白的表达均减少，K15出现异常表达，差异均有统计学意义（P < 0.05），显示表皮增殖、分化受抑制，CE结构受损；电镜下颗粒层内板层小体数量减少，密度降低。结论 与正常人皮肤比较，激素依赖性皮炎患者皮肤屏障结构受到破坏，恢复皮肤屏障对治疗激素依赖性皮炎具有重要意义。

关键词: 皮肤屏障

Abstract:

Objective To explore the effects of epidermal proteins and lamellar bodies on skin barrier in glucocorticoid-dependent dermatitis. Methods Totally, 60 patients with glucocorticoid-dependent dermatitis and 40 normal human controls were eligible for this study. A noninvasive method using TewameterTM was applied to determine transepidermal water loss （TEWL） value in these subjects. Tissue specimens were obtained from the lesions of 13 patients with glucocorticoid-dependent dermatitis and normal skin of 10 human controls. Subsequently, haematoxylin and eosin （HE） staining was performed to observe the histopathological changes, immunohistochemistry to detect the protein expressions of K6, K10, K14, K15, loricrin, filaggrin, involucrin in epidermis, and electron microscopy （EM） to estimate the density of lamellar bodies in tissue specimens. Results Compared with the normal controls, the patients displayed an elevated TEWL value （P < 0.05）, which suggested an impaired epidermal barrier. Histopathology of lesions revealed nonspecific inflammatorychanges with marked differences between different clinical types of glucocorticoid-dependent dermatitis. Immunohistochemistry revealed an attenuated expression of K10, K14, loricrin, filaggrin, involucrin and abnormal expression of K15 in lesional epidermis compared with the normal epidermis （all P < 0.05）, hinting a suppression of epidermal differentiation and proliferation as well as an impairment of cornified envelope structure. The number and density of lamellar bodies were also reduced in lesional epidermis compared with the control epidermis. Conclusions Compared with normal skin, the structure of skin barrier is impaired in lesions of glucocorticoid-dependent dermatitis, to restore skin barrier is essential for the treatment of this entity.

Key words: epidermal barrier