Anetoderma can be diagnosed clinically. But if the diagnosis proves to be difficult, a
skin biopsy—ideally a
punch biopsy—can be carried out to include the mid dermis. Under a
microscope, the
epidermis of anetoderma exhibits a nearly total loss of
elastic fibers in the reticular and papillary dermal layers. A dermal periadnexal and perivascular infiltrate containing
histiocytes and
plasma cells can also be seen in the
histopathology of the lesion. In lesional skin, elastophagocytosis and tiny fragmented elastic fibrils can be seen in addition to the histopathology on
electron microscopy.
Desmosine has been used to quantify the amount of
elastin in lesional skin, which is considerably lower in anetoderma, since it is a major
amino acid in elastin.
Classification There are five subtypes of anetoderma: drug-induced anetoderma, familial anetoderma, prematurity-associated anetoderma, primary (idiopathic) anetoderma, and secondary anetoderma from a previous dermatosis. The Jadassohn-Pellizzari type and the Schweninger-Buzzi type are the historical subtypes of the primary type, which is found in areas of previously normal skin. While the Schweninger-Buzzi type of anetoderma develops in skin that appears normal with no predisposition skin changes, the Jadassohn-Pellizzari type occurs following the occurrence of inflammatory or urticarial lesions. These terms are now obsolete because the two primary types are identical histologically as well as having a similar disease course. ==See also==