We frequently encounter characteristic color variation including hypopigmentation,\nhyperpigmentation, and erythema in extramammary Paget�s disease\n(EMPD) lesions. Owing to unclear hypopigmentation, the lesional border\nof EMPD can be poorly defined and it is likely insufficient to perform its\ncomplete resection. Although the existence of Toker�s cells and lack of lesional\nbFGF production have been reported to cause hypopigmentation inside of\nEMPD lesions, exact mechanisms of hypopigmentation in EMPD are not fully\nexplored. We experienced three EMPD patients with obviously hypopigmented\nEMPD macules and histopathologically confirmed a reduced number\nof melanocytes on the hypopigmented macules and their loss on the erythematous\nplaques or nodules. An ultrastructural analysis on the hypopigmented\nlesions revealed disturbance of melanosome maturation and melanosome\ntransfer to the adherent Pagets� cell on the basal layer. No Paget�s cells even\nadhered to remaining melanocytes with dendrites contained matured melanosome\nand a few number of matured melanosome complexes were observed\nin basal keratinocytes. In the present study, we hypothesize that severe disturbance\nof not only melanogenesis but also melanosome transfer to surrounding\nPaget�s cells and basal keratinocytes may cause characteristic hypopigmentation\nin EMPD. Future bioanalysis would reveal molecular mechanisms\nfor hypopigmentation in EMPD.
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