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苔藓样淀粉样变和斑状淀粉样变中的两种不同致病途径。

Two different pathogenetic pathways in lichen amyloidosus and macular amyloidosis.

作者信息

Westermark P, Norén P

出版信息

Arch Dermatol Res. 1986;278(3):206-13. doi: 10.1007/BF00412925.

Abstract

In lichen amyloidosus (LA) and macular amyloidosis (MA), small amyloid deposits occur in the upper papillary dermis. Previous electron-microscopic studies have indicated an epidermal origin of the amyloid, where degenerating keratinocytes drop into the dermis and undergo transformation to amyloid. While this mechanism seems possible at least in MA, we suggest an alternative pathogenetic pathway in LA, in which amyloid fibrils seem to form on the dermal surface of living basal keratinocytes. It is possible that the different morphology of the amyloid in LA and MA is explained by partially different pathogenetic mechanisms although the amyloid in both conditions may be chemically closely related.

摘要

在苔藓样淀粉样变(LA)和斑状淀粉样变(MA)中,小的淀粉样沉积物出现在乳头层上部真皮。先前的电子显微镜研究表明淀粉样蛋白起源于表皮,退变的角质形成细胞落入真皮并转化为淀粉样蛋白。虽然这种机制至少在MA中似乎是可能的,但我们提出LA中存在另一种致病途径,其中淀粉样原纤维似乎在活的基底角质形成细胞的真皮表面形成。尽管两种情况下的淀粉样蛋白在化学上可能密切相关,但LA和MA中淀粉样蛋白的不同形态可能由部分不同的致病机制所解释。

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