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Eccrine angiomatous hamartoma (nevus) is a rare form of congenital tumorous malformation with proliferation of eccrine secretory coils and ducts, surrounding capillary angiomatous channels and occasionally other minor elements. To date, there have been only about 24 cases reported in the literature. We report an additional case with more detailed description of the microscopic findings, including immunohistochemical observations. The patient was a 28-year-old female who presented with painless, flesh- to reddish brown-colored, violaceous or bluish subcutaneous nodules on the extremities and trunk. The tumors did not show sweating following exertion. The histologic features were comparable to the previously reported cases. The hamartomatous eccrine sweat glands and ducts and a few apocrine glands demonstrated qualitatively diminished antigens commonly found in the eccrine sweat apparatuses, such as carcinoembryonic antigen (CEA) and S-100 protein. The findings of CD34, CD44, human nerve growth factor receptor and Ulex europaeus antigens have not been previously reported. The histologic features suggested a "hamartomatous" growth rather than a true neoplastic process.

Carcinoembryonic antigen was demonstrated in sweat gland adenomas by immunostaining using standard immunoperoxidase techniques. Carcinoembryonic antigen could not be found in adnexal tumors derived from the pilar and sebaceous apparatus. The demonstration of this specific antigen in certain sweat gland tumors may be helpful in the recognition and classification of these kinds of lesions.

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Granulomatous reactions at sites of previous cutaneous herpes zoster lesions occur, but their etiology is not known. Three tissue specimens from 5 cases identified clinically and histologically as post-zosteric granulomatous reactions were studied for the presence of varicella-zoster virus (VZV) deoxyribonucleic acid (DNA) by the polymerase chain reaction using specific primers for VZV. VZV DNA was detected in 1 of 3 cases where the granulomatous reaction occurred immediately in the wake of resolving vesicular herpes zoster lesions. Finding viral DNA in earlier reactions probably represents residue from the active herpetic process. VZV DNA was not identified in granulomatous reactions arising between 1 month and up to 4 years after resolved herpes zoster. The negative result in these cases supports the hypothesis that there is no association between persistence of VZV DNA and granuloma formation. How long VZV DNA is detectable at sites of resolved herpes zoster lesions could be the subject of further studies.

Factor XIIIa (FXIIIa), a blood and intracellularly produced coagulation factor, has been found in a variety of cell types including fibroblast-like mesenchymal cells, and has been shown to stimulate the proliferation of fibroblasts and some neoplastic cells in vitro. We have already shown that the dendritic fibroblasts composing the fibrous papule contain this factor. We hypothesized that histopathologically similar fibrovascular tumors may also express FXIIIa and, in this report, show that the large stellate fibroblasts found in acquired digital fibrokeratomas, angiofibromas (adenoma sebaceum of Pringle), and oral fibroma (oral fibrous hyperplasia) also express FXIIIa. We postulate that FXIIIa, possibly acting as a growth factor, may be a common denominator in the pathogenesis of these tumors. Another possibility is that these tumors may be the consequence of a local overproduction of FXIIIa in response to an, as yet, unidentified stimulus.

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