Cystic adventitial disease is an uncommon cause of lower extremity claudication resulting from accumulation of mucinous fluid in an arterial subadventitial layer, typically of the popliteal artery. A popliteal bruit and/or reduced distal pulses with knee flexion may be seen on examination. Alternatively, popliteal artery entrapment syndrome triggers claudication via an aberrant arterial pathway or muscular hypertrophy. Decreased distal pressures with plantar or dorsiflexion is a key finding. This report details the case of a middle-aged male with cystic adventitial disease whose diagnosis was complicated by concurrent features of popliteal artery entrapment syndrome. Treatment consisted of venous interposition grafting, which yielded excellent results.
Present literature demonstrates an equivocal relationship between testosterone and thrombogenicity. Herein, we describe a case in which a patient used an unspecified amount and duration of exogenous testosterone injections, subsequently developing thrombotic events in his: right radial artery, right iliac artery, superficial femoral artery, splenic artery and a bilateral lower lobe pulmonary embolism. As a result, clinicians should consider exogenous testosterone use as a potential risk factor when the etiology of a patient's thrombotic events are not clear. We also completed a literature review of the molecular mechanisms in which testosterone can increase the clot burden through an increases human platelet thromboxane A2 receptor density and an increase in erythropoiesis.
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