Discussed online (synchronous) in April 2011.
The term anetoderma (Gk anetos slack) refers to a circumscribed area of macular atrophy of the skin associated with a loss of dermal substance on palpation and a loss of elastic tissue on histopathological examination.
Primary anetoderma implies that there is no associated, localized, underlying cutaneous disease, whereas true secondary anetoderma can be attributed to some associated condition though the atrophic areas do not always develop at the sites of the known inflammatory lesions.
Primary anetoderma has been divided into the Jadassohn–Pellizari type, in which the lesions are preceded by erythema, and the Schweninger–Buzzi type, in which there is no preceding erythema. The two types of primary anetoderma can coexist in the same patient, and the prognosis and histopathology are identical in both. Thus this differentiation is of historical interest only.
Primary anetoderma is strongly associated with antiphospholipid antibodies with or without a prothrombotic state.
A middle-aged woman presented with skin coloured to pink sac-like protrusions 1–2 cm in diameter, mainly on upper arms and back that have developed over many years and remained unchanged. The lesion surface was thinned and on palpation the examining finger sank into a pit (buttonhole sign). The protrusion reappeared as soon as the pressure from the finger was removed. Coalescence of smaller lesions gave rise to larger protrusions. The lesions arose on clinically normal skin. Few lesions were depressed. There was no history of underlying associated skin disease. Histopathology was consistent with anetoderma. Diagnosis of primary anetoderma was made. The key defect in anetoderma is damage to the dermal elastic fibres (focal elastolysis). Antiphospholipid antibodies have not been detected in the patient. No regularly effective treatment has been found.