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Cystic adventitial disease of the popliteal artery: is there a consensus in management
Cystic adventitial disease (CAD) is a rare cause of claudication in young to middle-aged individuals. The disease most commonly affects males, presenting as cramps in the lower legs followed by symptoms of intermittent claudication. The cause is the presence of a gelatinous cyst found between the adventitial layer and media, causing complete occlusion or stenosis of the affected vessel.1 The popliteal artery is the most commonly affected, although cases have been documented involving the iliac vessels, great saphenous veins (GSVs) and arterial vessels surrounding the elbow and wrist joints.2–5 Debate persists regarding the pathogenesis of CAD. Among the theories postulated, the four prominent ones are trauma, systemic degeneration, ganglion and developmental theory.6 The trauma theory proposes repetitive trauma as the cause of adventitial degeneration. The systemic degeneration hypothesis postulates that connective tissue disorder is the cause of cyst formation in the adventia. According to the ganglion theory, synovial casts migrate along vessels and implant into the adventia. And finally, the developmental or the embryonal theory states that cystic degeneration is due to erroneous migration of mesenchymal cells from surrounding joints. These cells end up in the adventia and over time secrete mucin, resulting in obstruction of the vessel.
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