atrophie blanche

a·tro·phie blanche

(a-trō'fē blahnsh'),
Small smooth ivory-white areas on the skin with hyperpigmented borders and telangiectasis, developing into atrophic stellate scars; seen especially on the legs and ankles of middle-aged women, and associated with livedo reticularis and dermal hyalinizing vasculitis.
[Fr.]

livedoid vasculopathy

A thrombogenic vasculopathy caused by fibrin thrombi in the small dermal vessels of the lower legs, especially in older women, which are attributed to decreased fibrinolytic activity in the blood coupled with defective release of intrinsic tissue plasminogen activator from vessel walls. The typical lesions are telangiectatic purpuric papules and plaques which evolve into crusted ulcers that heal into atrophic stellate scars.

Associations
Patients may also have livedo reticularis, scleroderma, systemic lupus erythematosus and cryoglobulinaemia.

atrophie blanche

irregular, slightly depressed areas of white fibrous tissue overlain by very thin, atrophic skin through which one or two dilated capillaries may be visible, within an area of varicose eczema and/or haemosiderosis at the lower one-third of the leg in cases with compromised venous return and resultant long-standing chronic tissue inflammation; prone to trauma and resultant ulceration
References in periodicals archive ?
Cutaneous clues suggestive of thrombosis in SLE patients include atrophie blanche, pseudo-Degos lesions, livedo racemosa, acral nonpalpable purpura or reticulate erythema, cutaneous necrosis, splinter hemorrhage, thrombophlebitis, and nailfold telangiectasias.
Atrophie blanche in a patient with SLE is also strong evidence of thrombotic vasculopathy.
The examination of the leg should include palpation of pulses and a search for the signs of venous hypertension, including varicose veins, hemosiderin pigmentation, varicose eczema, atrophie blanche, and lipodermatosclerosis.
For management of leg ulcers, the leg should be assessed for signs of venous disease, in particular, varicose veins, venous dermatitis, hemosiderin deposition, lipodermatosclerosis and atrophie blanche.
Venous-related skin changes may also develop, including hyperpigmentation in the perimalleolar region secondary to haemosiderin deposition, lipodermatosclerosis with scarring, thickening of the skin secondary to fibrosis in the dermis and subcutaneous fatty tissue, and atrophie blanche characterised by circular whitish and atrophic skin surrounded by dilated capillaries and hyperpigmentation.
Other characteristic skin findings include hyperpigmentation, eczematous dermatitis, atrophie blanche, and lipodermatosclerosis.
Clinical findings in the study included edema (32% of limbs), hyperpigmentation (24%), lipodermatosclerosis (13%), dermatitis (7%), atrophie blanche (4%), and lyrnphedema (1%).