Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Poly arteritis nodosa (PAN) is a systemic vasculitis with a male: female ratio of 2:1 and a peak incidence in the fifth decade. Small to medium-sized arteries are involved by focal transmural inflammatory necrosis. Aneurysms with inflammatory destruction of the media also occur. The most frequently involved organs are the kidney, heart, lung, liver, and gastrointestinal tract. There are few reported cases of ischemic necrosis of the intestine and even fewer survivors. A 22-year-old woman was transferred to St. Thomas Hospital (Nashville, TN) after resection of 80 per cent of the small bowel for ischemic necrosis. She had a history of juvenile onset diabetes mellitus, recurrent abdominal pain, and splinter hemorrhages. Emergency aortogram and selective mesenteric arteriogram were performed. The celiac artery was not visualized and small aneurysms were present in the mesenteric and renal arteries. The patient was successfully resuscitated from a cardiac arrest in x ray from a cardiac tamponade. Laparotomy was performed to determine the viability of the bowel. The celiac, hepatic, and splenic arteries were found to be chronically occluded. Pathology of these arteries revealed a nonspecific arteritis. At a third operation, several more inches of small bowel were removed. Characteristic changes of PAN were present on all small bowel specimens. She was treated with high-dose cyclophosphamide and steroids for 6 months and has continued on low-dose cyclophosphamide. She is now 36 months from her original operation and is doing well on oral nutrition. Intestinal hemorrhage from aneurysm rupture or gangrene with perforation are gastrointestinal complications of PAN that the surgeon may be called upon to treat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Surviving gastrointestinal infarction due to polyarteritis nodosa: a rare event. 134 8

Rat kidneys were perfused with anti-intercellular adhesion molecule-1 (anti-ICAM-1) monoclonal antibody prior to allotransplantation. In the two strain combinations examined, LEF-to-WKAH transplants resulted in accelerated graft loss, and no prolongation of graft survival. The accelerated graft loss was the result of frequent occurrence of necrotizing arteritis within the grafts. In contrast, TO-to-WKAH transplants resulted in no change in graft survival and no arteritis. Necrotizing vasculitis in the LEJ-to-WKAH grafts was characterized by fibrinoid necrosis, collection of cellular infiltrates and serum macromolecular protein entrapment. The F(ab1)2 form of anti-ICAM-1 antibody partially preserved the antibody's capacity to accelerate graft loss. Therefore, although endothelial injury by Fc-mediated cytotoxicity may be involved in vascular damage, other mechanisms also come into play. The amount and distribution pattern of ICAM-1 antigen were identical in both TO and LEJ strains. Intravenous anti-ICAM-1 antibody administration combined with lipopolysaccharide, Poly(I)-Poly(C), warm ischemia to the kidney, or subcutaneous immunization with allogeneic spleen cells, but without renal transplantation, did not generate necrotizing vasculitis or proteinuria. These observations plus our previous data on the rat liver transplantation model clearly show that graft perfusion with anti-ICAM-1 monoclonal antibody invokes extensive vascular damage within allografts by Fc-mediated and Fc-independent mechanisms, depending on the donor-to-host combination.
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PMID:Strain combination-dependent genesis of necrotizing arteritis in anti-ICAM-1 antibody-perfused renal allografts in the rat. 778 89