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小汗腺无汗机制。一、高度阻断。

Mechanisms of eccrine anidrosis. I. High level blockade.

出版信息

J Invest Dermatol. 1966 Aug;47(1):1-9. doi: 10.1038/jid.1966.93.

Abstract

The cause of anidrosis of the chronic dermatoses, hydration, and that produced experimentally by protein precipitants is superficial obstruction of the eccrine duct. In each instance, return of sweating in the anidrotic area is effected simply by removal of the stratum corneum with Scotch Tape stripping. The histologic picture common to this type of anidrosis is ductal dilatation following an adequate sweat stress. The presence of an obstruction, whether functional or anatomic, is confirmed by the inability to achieve a methylene blue pore pattern. Parakeratotic plugging of the eccrine ostia is primarily responsible for the obstruction in the spontaneous dermatoses, while actual intraluminal casts are produced chemically by the protein denaturants, high within the stratum corneum portion of the eccrine duct. The PAS positive, diastase resistant casts regularly found in blocked ducts are secondary to the obstruction and are not a primary cause. No adequate explanation has been found for the persistent anidrosis after occlusion of the skin with impermeable plastic dressings.

摘要

慢性皮肤病、脱水以及蛋白质沉淀剂引起的无汗症的原因是小汗腺导管的表面阻塞。在每种情况下,通过使用 Scotch 胶带剥离去除角质层,无汗区域的出汗都会恢复。这种类型的无汗症的组织学特征是在足够的汗液压力下导管扩张。无论功能障碍还是解剖结构异常,只要无法实现亚甲蓝毛孔模式,就可以确认存在阻塞。无汗性皮肤病的阻塞主要是由于小汗腺口的角化栓阻塞,而蛋白质变性剂在角质层内的小汗腺管腔内产生实际的腔内铸型。在阻塞的导管中经常发现的 PAS 阳性、耐淀粉酶铸型是阻塞的继发表现,而不是主要原因。对于用不透气的塑料敷料封闭皮肤后持续无汗,尚未找到充分的解释。

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