Wallace M L, Grichnik J M, Prieto V G, Shea C R
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA.
J Cutan Pathol. 1998 Aug;25(7):375-9. doi: 10.1111/j.1600-0560.1998.tb01761.x.
The etiology and pathogenesis of idiopathic guttate hypomelanosis (IGH) are largely unknown. To investigate whether the pathologic alteration in IGH involves changes in melanocytic differentiation, cell number, or both, we studied nine lesions of IGH by immunoperoxidase, using monoclonal antibodies against the KIT receptor and a panel of melanocyte differentiation antigens (tyrosinase-related protein-1, tyrosinase, and gp100/pme117). In each case, compared with grossly normal non-lesional skin, IGH lesions showed markedly reduced numbers both of KIT+ cells and of cells expressing melanocyte differentiation antigens (p < 0.0001). Double immunofluorescence labeling of lesions revealed only scattered cells with a less-differentiated phenotype, i.e. cells positive for KIT but having low or undetectable TRP-1. These results indicate that the pathogenesis of IGH involves an absolute decrease in the number of melanocytes; a block in melanocyte differentiation does not appear to be a major component of the process.
特发性点滴状色素减退症（IGH）的病因和发病机制在很大程度上尚不清楚。为了研究IGH的病理改变是否涉及黑素细胞分化、细胞数量的变化或两者兼有，我们使用针对KIT受体的单克隆抗体和一组黑素细胞分化抗原（酪氨酸酶相关蛋白-1、酪氨酸酶和gp100/pme117），通过免疫过氧化物酶法研究了9例IGH皮损。在每例中，与外观正常的非皮损皮肤相比，IGH皮损中KIT+细胞和表达黑素细胞分化抗原的细胞数量均显著减少（p<0.0001）。皮损的双重免疫荧光标记显示只有散在的具有低分化表型的细胞，即KIT阳性但TRP-1低表达或未检测到的细胞。这些结果表明，IGH的发病机制涉及黑素细胞数量的绝对减少；黑素细胞分化受阻似乎不是该过程的主要组成部分。
