Case Reports
Case 1
A 49-year-old homosexual man known to be HIV-infected since 1986 (CDC-C) suddenly developed intermittent claudication within a walking distance of 100 m. His medical history associated nephrocalcinosis under indinavir and ophthalmic shingles.
His weight was 58 kg and height 1.60 m; blood pressure was 130/80 mmHg and he was an active smoker (45 pack-years). Results of laboratory analyses were: hypertriglyceridemia (4.23 mmol/L), normal total cholesterol (TC; 5.40 mmol/L) and low HDL cholesterol (0.78 mmol/L) giving an increased TC/HDL ratio (6.92). Antiretroviral treatment associated stavudine, lamivudine, and indinavir. HIV viral load was undetectable (palmar arteries showing alternating alternance of normal and necrotic-inflammatory aspects of the wall— hematein-eosin-saffron (HES) stain. In some segments, the entire thickness of the arterial wall contained diffuse acidophilic necrosis, and fibrinous thrombi were visible in the lumen (a original magnification ?100); in others, numerous neutrophils had infiltrated the media (b ?200) or populated the entire wall thickness (c ?50). In adjacent veins (d ?200) and capillaries (e ?200), leukocytoclasia and fibrinoid necrosis were sometimes observed. Specific stains were negative for bacteria and fungi. No viral inclusions were detected and In Situ hybridization for varicella zoster virus and cytomegalovirus were negative. Muscles were necrotic. The vascular lesions were difficult to classify, because of the diversity of types and calibers of affected vessels, the types and locations of the cellular infiltrates, and it was unknown whether the vascular necrotic-inflammatory changes were primary or secondary
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