1994
DOI: 10.1097/00002281-199401000-00002
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Changing concepts in pathophysiology of the vasculitides

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Cited by 12 publications
(3 citation statements)
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“…Similarly, focal cerebral ischaemia in rats increases TNF-ct production by ischaemic neurones [16] supporting a role for ET-1 in stroke. As might be expected there is also a strong cytokine activation in human vasculitis [17,18], and interestingly in congestive heart failure [19] (in which human state ET-1 receptor antagonists are beneficial [4]), and possibly hypercholesterolaemia [20]. Clearly there are substantial increases in the production and circulating level of TNF-o~ in systemic inflammatory response (septic shock syndrome) and related pathological states [21], and here animal studies indicate that endothelin production is increased for endothelin receptor antagonists potentiate endotoxaemia-associated hypotension [22].…”
Section: Td Warner and P Klemmsupporting
confidence: 56%
“…Similarly, focal cerebral ischaemia in rats increases TNF-ct production by ischaemic neurones [16] supporting a role for ET-1 in stroke. As might be expected there is also a strong cytokine activation in human vasculitis [17,18], and interestingly in congestive heart failure [19] (in which human state ET-1 receptor antagonists are beneficial [4]), and possibly hypercholesterolaemia [20]. Clearly there are substantial increases in the production and circulating level of TNF-o~ in systemic inflammatory response (septic shock syndrome) and related pathological states [21], and here animal studies indicate that endothelin production is increased for endothelin receptor antagonists potentiate endotoxaemia-associated hypotension [22].…”
Section: Td Warner and P Klemmsupporting
confidence: 56%
“…The endothelium normally functions to thwart cell extravasation, but at inflammatory sites this living barrier undergoes remarkable phenotypic changes such as expression of adhesion molecules, which facilitate the passage of mononuclear cells. Diverse studies in patients with SLE have confirmed the permissive role of vascular adhesion molecules in the pathogenesis of vasculitis and glomerulonephritis [1][2][3][4][5][6]. Widespread activation of the endothelium has been suggested by the observation that even in nonlesional, nonsun-exposed (buttock) skin from patients with active SLE, endothelial expression of adhesion molecules as well as inducible nitric oxide synthase (iNOS, NOS2) is up-regulated [7,8].…”
mentioning
confidence: 99%
“…4 By attaching to the site of localization of the immune complexes, inflammation, hemorrhage, and palpable purpuric lesions result. 5 Lesions are most commonly located on the lower extremities, forearms, and hands. In addition, painless gastrointestinal hemorrhage has been associated with leukocytoclastic vasculitis.…”
Section: Discussionmentioning
confidence: 99%