sQUIZ your knowledge: A pigmented tumour on the cheek

Acroangiodermatitis (AAD) (also known as PseudoKaposi’s sarcoma) is a vasoproliferative disorder that clinically and histologically resembles Kaposi’s sarcoma (KS), which occurs within a context of different vascular disturbances, including chronic venous insufficiency (acroangiodermatitis of Mali) and arteriovenous fistules (Stewart-Bluefarb syndrome) [1, 2]. The pathogenesis of AAD is still not completely understood. However, it is likely that an increased venous and capillary pressure along with hypoxia could induce an angiogenic response [1]. Apart from Kaposi’s sarcoma (KS), lichen planus, angiokeratomas, pigmented purpuric dermatitis and lichen aureus should also be considered as differential diagnoses. Unlike AAD, the histological examination of KS reveals the presence of spindle cells and irregular lymphatic-like vascular channels. The promontory sign (pre-existing vessels protruding into newly formed vessels) can also be observed in KS but not in AAD. Finally, immunohistochemistry, with markers such as HHV-8 (human herpes virus 8) and CD34, is also useful in distinguishing between both disorders [3]. The dermoscopic features of AAD have only been described in three previous cases. [2, 4]. The venous lakes probably correlate with lobular vascular proliferation. The white structureless area presumably reflects fibroblastic proliferation, which is more intense in AAD than KS, serving as a clue to distinguish between the two conditions. The associated stasis dermatitis manifests dermoscopically as a peripheral, punctuated, coppery pigmentation, emphasizing the role of venous insufficiency in the aetiopathogenesis of AAD.