Friday 21 December 2012
They usually present as solitary nodules 2–3 cm in diameter, but larger variants occur. They predominate in females. There is no site predilection. They can occur at all ages, including infancy.
Local recurrence can occur, particularly if the lesion is incompletely excised. The malignant variant, hidradenocarcinoma, is exceedingly rare. It may arise ab initio or by transformation of a benign lesion.
Hidradenomas are usually circumscribed non-encapsulated multilobular tumors, centered on the dermis but sometimes extending into the subcutis. Epidermal connections are present in up to one-quarter of cases.
Mucinous syringometaplasia has been described in one case, overlying a clear cell variant of hidradenoma.
Hidradenomas may be solid or cystic in varying proportions. Uncommonly they are pedunculated.
The closely arranged tumor cells, which may be round, fusiform, or polygonal in shape, are biphasic in cytoplasmic architecture, with one type having clear and the other eosinophilic cytoplasm.
There are variable proportions of each cell type in different tumors, but clear cells predominate in less than one-third.
Sometimes, only a few clear cells can be seen. They contain glycogen and some PAS-positive diastase-resistant material, but no lipid. The nuclei of the clear cells tend to be smaller than those in the eosinophilic cells. The nuclei of the non-clear cells are often elongated and about one-third of these cells often contain nuclear grooves.
Focal goblet-cell metaplasia is sometimes seen.
A diffuse proliferation of mucinous epithelium (mucinous hidradenoma) is rare.
Mitoses are variable in number; their presence does not necessarily indicate malignancy.
However, in one study mitoses and atypical nuclear changes were associated with an increased local recurrence rate, and even subsequent malignant transformation.
Other cellular variations include an oncocytic variant, an epidermoid variant with large polyhedral cells having a squamous appearance, and a pigmented variant with some melanocytes and melanin pigment in cells and macrophages.
A racemiform and reticulated pattern of growth has been recorded.
Duct-like structures are often present in the tumor. Some resemble eccrine or apocrine ducts, whereas others consist of several layers of concentric squamous cells with slit-like lumina. The stroma between the lobules varies from thin, delicate, vascularized cords of fibrous tissue to abundant focally hyalinized collagen. A myxoid or chondroid stroma is rarely present.
Immunohistochemistry demonstrates low molecular weight cytokeratin (CAM5.2) in most tumors. Some also express CEA and EMA.
There is some variability in the expression of the various keratin subtypes in different parts of the tumor.
Smooth muscle actin and S100 protein were co-expressed in one case.
The malignant variant has an infiltrative growth pattern, frequent mitoses (although some overlap exists in the mitotic rate between benign and malignant variants), and sometimes angiolymphatic invasion.
The cells composing the tumor are connected by desmosomes.
The clear cells have abundant glycogen and few tonofilaments, whereas the other cell type has abundant tonofilaments and small amounts of glycogen.
Most of the cases reported previously as eccrine hidradenoma and eccrine acrospiroma have been reclassified as apocrine hidradenoma on the basis of their presumed apocrine histogenesis.
A skin-type hidradenoma associated with a t(11;19) translocation has been reported in the breast parenchyma. An identical translocation has also been reported in a cutaneous (clear cell) hidradenoma. The fusion genes are the mucoepidermoid carcinoma-translocated 1 (MECT1) gene on chromosome 19p13 and the mastermind-like family (MAML2) gene on chromosome 11q21.