Reply to: Direct Immunofluorescence Findings in Discoid Lupus Erythematosus and Bullous Pemphigoid.

sia of the ductal cells is a reactive process to some as yet unknown stimulus. Exposure to heat could be one of them, as in 2 cases the lesions became inflamed after heat exposure.3,4 Scarring was present in another case,6 but in our patient, there was no obvious trigger, neither significant periglandular inflammation. The process could have its onset in the dermal duct and spread to the acrosyringium, as the cells of the latter seem to derive from dermal duct cells.8 The reason why not all cases have manifested clinically with papular lesions is unclear. It may be speculated that when the ductal hyperplasia is not pronounced, the process passes clinically unnoticed, but when the hyperplasia becomes sufficiently important, namely, involving the acrosyringium, papular lesions could develop, possibly due to partial obstruction of the sweat ducts, justifying the term “papular” eccrine duct hyperplasia. It can also be hypothesized that the process could be self-regressing if the triggering stimulus disappears. In conclusion, clear-cell hyperplasia of eccrine ducts is a very rare but distinctive pathologic change of eccrine sweat glands usually observed in diabetic women, although this condition can also be encountered in men and is not necessarily associated with diabetes. The sweat duct clear-cell proliferation may be an incidental pathologic finding or manifest clinically with miliaria-like papular lesions, presumably when the hyperplastic changes are sufficiently severe and involve the acrosyringia. The observation of additional cases will hopefully shed more light on this puzzling eccrine sweat gland disorder.