The exact cause of<unk>  is unknown. Venous disease, such as venous incompetence, venous hypertension, and body mass (obesity) may be relevant to the underlying pathogenesis. Increased blood pressure in the veins (venous hypertension) can cause diffusion of substances, including fibrin, out of capillaries. Fibrotic tissue may predispose the tissue to ulceration. Recurrent ulceration and fat necrosis is associated with<unk> . In advanced<unk>  the proximal leg swells from chronic venous obstruction and the lower leg shrinks from chronic ulceration and fat necrosis resulting in the inverted coke bottle appearance of the lower leg.<unk>  is most commonly diagnosed in middle-aged women. The origin of<unk>  is probably multifactorial, involving tissue hypoxia, leakage of proteins into the interstitium, and leukocyte activation. Studies of patients with<unk>  have demonstrated significantly decreased concentrations of cutaneous oxygen associated with decreased capillary density. Capillaries are virtually absent in areas of fibrotic scars, leading to a condition known as atrophie blanche or livedoid vasculopathy.
Lipodermatosclerosis
Hypodermyasis
Phakomatosis
Calcinosis cutis
Nevus anemicus
Generalized lentiginosis
Universal angiomatosis
Facial infiltrating lipomatosis