Journal of cutaneous pathology
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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). ⋯ 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.