Lower limb giant cell arteritis and temporal arteritis: followup of 8 cases.

Among 8 patients with giant cell arteritis (GCA) (6 women, 2 men) whose clinical presentations were compatible with temporal arteritis (TA), 6 were followed for 37-105 (mean 74.9) months, one died shortly after treatment onset, and the last was asymptomatic (10 mg steroids/day) when lost to followup at 29 months. All 8 patients had bilateral leg claudication of recent onset; for 6 patients, this was the first symptom. All leg angiograms showed multiple, bilateral, long and smooth stenoses, thromboses, or both. Biopsies of diseased leg arteries from 4 patients provided histological proof of GCA; another case was histologically proven post mortem. Among the 5 patients who met at least 3 American College of Rheumatology criteria of GCA or TA, 3 without histologically documented leg GCA also had biopsy proven temporal GCA (n = 1), or headaches and claudication and angiographic inflammatory arteritis of the arms (n = 2). All patients received steroids; 3 had bypasses, one with endarterectomy. Five are asymptomatic after 24-100 months of steroids (mean 50.6). Revascularization was not successful; one amputation was necessary. Large artery involvement in GCA can affect the legs. Bilateral and rapidly progressive intermittent claudication of recent onset is the most common symptom, even in the absence of headaches or the presence of a silent inflammatory syndrome. Early diagnosis allows rapid initiation of steroid therapy, which is usually able to generate a sufficiently good response to avoid vascular surgery.

[Are antiphospholipid antibodies thrombogenic in the course of human immunodeficiency virus infection?]. / Les anticorps antiphospholipides au cours de l'infection par le virus de l'immunodéficience humaine sont-ils thrombogènes?

Lupus-like anticoagulant is commonly encountered in human immunodeficiency virus infection although thromboembolic manifestations are rare in HIV patients. We report the case of an HIV patient who developed gangrene of both forefeet associated with anticardiolipin antibodies. A 42-year-old woman had a 12-year history of HIV infection (stage B2). She presented with painful gangrene involving the forefeet of 4-day duration. Doppler ultrasonography, electromyography and nailfold capillaroscopy were normal. Skin biopsy revealed intracapillary thrombi and severe necrosis within the hypodermis; there was no evidence of vasculitis. Laboratory findings showed a marked inflammatory syndrome and the presence of anticardiolipin antibodies (IgG: 22 GPL U/ml). Several cutaneous manifestations are known to be associated with antiphospholipid syndrome, such as livedo reticularis, ulcers and gangrene of the extremities. Skin biopsy often shows noninflammatory thrombosis of small vessels within the dermis. Microcirculation damages have also been described in HIV infection, mainly vasculitis. In the present case report, the absence of both vasculitis and other causes suggest that anticardiolipin could be the culprit. But, it is possible that painful gangrene of the forefeet was secondary to HIV infection.