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Benign tumors
Published in Archana Singal, Shekhar Neema, Piyush Kumar, Nail Disorders, 2019
Histopathology exhibits regularly built capillary vessels with thick walls, edematous stroma, and loosely structured lobuli in the papillary and reticular dermis. The epidermis may be acanthotic and hyperkeratotic. Extravasated erythrocytes lead to massive hemosiderin deposits, both within macrophages (siderophages) as well as in the interstitium. With time, the dermis becomes more fibrotic and finally sclerotic. Chronic spongiotic dermatitis (stasis eczema) may develop, particularly in acroangiodermatitis.
Vascular tumors
Published in Eckart Haneke, Histopathology of the NailOnychopathology, 2017
This reactive condition may develop posttraumatically or due to autonomic nerve damage as the result of luxury blood supply with relatively high pressure4 or as a chronic stasis dermatitis associated with venous insufficiency.5 Clinically, it usually results in a pseudo-Kaposi-like appearance with dark red to almost blackish papules and plaques that may also develop keloid-like areas. Acroangiodermatitis of Mali6 and Stewart-Bluefarb syndrome7 are variants. The toes and perionychium may be involved; however, the nails are rarely directly affected, but may show a purple hue or be leukonychotic. One 52-year-old woman with terminal renal insufficiency developed a pincer nail due to a pseudo-Kaposi sarcoma thought to be due to an arteriovenous fistula placed to perform hemodialysis.8 Doppler ultrasound can diagnose an acral hyperstomy syndrome.9 The clinical differential diagnoses are Kaposi's sarcoma, stasis dermatitis, lichen purpuricus, purpura pigmentosa, lichen aureus, vasculitis, lichen simplex chronicus, actinic keratosis, basal cell carcinoma, bleeding melanoma, hemangioma, lymphangioma, and lymphangiosarcoma.10,11
Stasis Dermatitis
Published in Donald Rudikoff, Steven R. Cohen, Noah Scheinfeld, Atopic Dermatitis and Eczematous Disorders, 2014
A skin biopsy of stasis dermatitis shows acute or subacute spongiotic dermatitis, which is frequently indistinguishable from other forms of eczematous dermatitis (except for the accompanying histological indications of venous insufficiency). Acute lesions may exhibit a superficial perivascular lymphocytic infiltrate, epidermal spongiosis, serous exudate, scaling, and crust. Chronic lesions may show signs of lichenification, such as epidermal acanthosis with hyperkeratosis. The dermis is characterized by deep dermal aggregates of siderophages due to uptake of hemosiderin from degraded erythrocytes that have leaked into the perivascular space. Dermal capillaries are frequently dilated and, along with dermal fibrosis, a biopsy may show intimal thickening of small arterioles and venules (Lever and Schaumburg-Lever 1990). In cases of long duration, there may be proliferation of small capillaries and venules along with fibrosis, which is known as pseudo-Kaposi sarcoma or acroangiodermatitis. Biopsy in patients with acroangiodermatitis is valuable in ruling out classic Kaposi sarcoma, which also occurs on the lower legs of elderly patients.
Diffuse dermal angiomatosis localized to abdominal striae
Published in Baylor University Medical Center Proceedings, 2020
Madeline R. Frizzell, Sheevam Shah, Palak Parekh
DDA, first described by Krell et al in 1994, is a distinct variant of reactive angioendotheliomatosis. The lesions typically present as livedoid, erythematous to violaceous plaques that may contain a central ulcer or erosion.1 On histopathology, DDA is characterized by diffuse proliferation of endothelial cells arranged between collagen bundles, which form small vascular channels with scattered extravasated erythrocytes.4 The cells may have a spindle-shaped appearance with vacuolated cytoplasm. Clinically, the differential diagnosis may include vasculitis, acroangiodermatitis, and vascular tumors. Histologically, differentials include Kaposi sarcoma and well-differentiated angiosarcoma. DDA is thought to be caused by ischemia or inflammation that creates local hypoxia, leading to an increase in vascular endothelial growth factor. This, in turn, causes endothelial proliferation and neovascularization.2,3 The resolution of cutaneous lesions after revascularization of the blocked vessel supports this theory.
Diffuse dermal angiomatosis of the breast
Published in Baylor University Medical Center Proceedings, 2020
Nicholas Nguyen, Annika S. Silfvast-Kaiser, Jillian Frieder, Marcus Zaayman, Alan Menter
DDA is a unique variant of RAE commonly reported on the lower extremities and, more recently, in women with large, pendulous breasts.1,2 DDAB tends to affect individuals aged 40 to 60 years who have multiple risk factors for atherosclerosis (i.e., hypertension, hyperlipidemia, diabetes mellitus, chronic smoking history, previous heart disease, and stroke).10,13 The differential diagnosis includes acroangiodermatitis, Kaposi sarcoma, and low-grade angiosarcoma. Histologically, a proliferation of endothelial cells and microscopic capillaries in the dermis is seen, in contrast to the intraluminal proliferation of endothelial cells seen in classic RAE.2,14 CD31, CD34, and ERG stains are positive, underscoring benign dermal endothelial cell proliferation. Human herpesvirus 8 testing is negative.3,9,14–16 Although the pathogenesis of DDA remains unclear, it is postulated that angiogenesis is due to up-regulation of vascular endothelial growth factor, secondary to chronic ischemia and hypoxia.4