Hereditary multiple exostoses as a novel cause of bilateral popliteal artery aneurysms in the elderly

• Published in: Cardiovascular pathology Vol. 31; pp. 20 - 25
• Main Authors: Ferrari, Eliza J., Crotty, Rory K., Eikermann-Haerter, Katharina, Stone, James R.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.11.2017
• Subjects: Aged, 80 and over; Aneurysm, False - etiology; Aneurysm, False - pathology; Autopsy; Exostoses, Multiple Hereditary - complications; Hereditary multiple exostoses; Humans; Male; Osteochondroma; Popliteal Artery - pathology; Pseudoaneurysm; Vascular injury; Osteochondroma; Vascular injury; Hereditary multiple exostoses; Autopsy; Pseudoaneurysm
• ISSN: 1054-8807; 1879-1336
• DOI: 10.1016/j.carpath.2017.07.001

Hereditary multiple exostoses (HME) is a genetic condition characterized by the development of multiple osteochondromas during childhood and adolescence. On rare occasions, these bony tumors can be associated with vascular injury, most commonly involving the popliteal artery. Such patients typically present with vascular complications in adolescence and young adulthood. We report an autopsy study of an elderly man who presented with bilateral popliteal artery pseudoaneurysms in the setting of HME at age 81. This is the oldest patient presenting with a vascular complication due to HME reported to date, as well as the only known case of bilateral popliteal pseudoaneurysms caused by HME. This is also the only autopsy study of this vascular complication so far reported. Our case illustrates that vascular complications from HME can occur even in the elderly, and may show bilateral involvement. •Vascular complications due to hereditary multiple exostoses usually present in the second or third decade but may present as late as the ninth decade of life.•Vascular injury due to hereditary multiple exostoses can result in bilateral popliteal artery aneurysms.•Histologically, the vascular injury caused by the osteochondromas in hereditary multiple exostoses consists of vascular wall scarring, fragmentation and loss of elastic lamina, neovascularization, macrophage infiltration, hemosiderin deposition, and organizing luminal thrombus.