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)

Forty-one patients with rheumatoid arthritis, including 6 with acute vasculitis, 13 with chronic vasculitis, and 22 without vasculitis, were studied for evidence of intravascular coagulation and fibrinolysis (ICF). The mean plasma fibrinogen levels were elevated in all groups. The fibrinogen, platelet count, and fibrin split products were usually elevated in acute vasculitis. Fewer patients on corticosteroids had abnormal coagulation tests. Active plasmin was detected in 12 patients primarily with chronic vasculitis. Plasminogen activator activity was not diminished in vascular endothelium of normal appearing skin of those patients with or without vasculitis. None of the patients demonstrated decompensated intravascular coagulation and fibrinolysis. The results suggest overcompensated ICF occurring in rheumatoid arthritis, but rheumatoid patients with vasculitis cannot be clearly distinguished from those without vasculitis on the basis of the usual tests performed for coagulation and fibrinolysis abnormalities.
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PMID:Coagulation abnormalities in rheumatoid disease. 99 34

Kawasaki disease (KD) in children takes the form of acute systemic vasculitis, which causes coronary artery dilation and aneurysm formation in 10% to 15% of the patients. We have recently shown that matrix metalloproteinases (MMPs) are intimately involved in coronary arterial wall destruction and the resultant formation of coronary artery lesions (CALs) in this disease. Plasminogen activators (PAs) are known to be a major pathway of MMP activation, and this suggests that their inhibitor, plasminogen activator inhibitor-1 (PAI-1), also plays important roles in the development of CALs in KD. The present study was conducted to test the hypothesis that circulating levels of PAI-I are related to CAL formation in KD. Plasma levels of PAI-1 were measured by enzyme-linked immunoassay in 37 KD patients without CALs (group 1) and 7 KD patients with CALs (group 2). Blood samples were obtained before and after i.v. gammaglobulin therapy (IVGG), and in the convalescent stage. Levels of PAI-1 were significantly higher in KD patients before IVGG than in 18 age-matched healthy control subjects (p < 0.01). More importantly, both pre-IVGG and post-IVGG levels of PAI-1 were significantly higher in group 2 than in group 1 (p < 0.01). Furthermore, PAI-1 levels of 9 patients from group 1 who showed pre-IVGG PAI-1 levels higher than the minimum PAI-1 level in group 2 significantly decreased after IVGG, whereas PAI-1 levels of group 2 patients remained persistently elevated, further suggesting a close association between PAI-1 and CAL development in KD. Thus, PAI-1 may be useful as a predictive marker for CAL development in KD. Studies of the effects of PA inhibition on coronary outcome may provide evidence that PA is a viable therapeutic target for the prevention of KD-related CALs.
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PMID:Plasminogen activator inhibitor-1 in patients with Kawasaki disease: diagnostic value for the prediction of coronary artery lesion and implication for a new mode of therapy. 1262 Nov 3