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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aetiology of the primary systemic vasculitides remains obscure. Recent years have seen significant advances in our understanding of inflammation and in particular the role of and interaction between the vascular endothelium, mediators and immune effector cells. This has helped to further elucidate those specific processes relevant to vasculitis which result in endothelial cell damage. In Wegener's granulomatosis and microscopic polyarteritis the evidence favours an autoimmune inflammatory response characterised by specific mediators in which the endothelium is both target and active participant. Current treatment of these disorders with combinations of corticosteroids and cytotoxics is highly effective in inducing remission. However, long-term use of this therapy is potentially toxic and there remains also a significant risk of relapse. It is hoped that increased understanding of the pathogenesis of systemic vasculitis will enable more specific, less toxic and more effective therapies to be defined. Jayne et al. have suggested a beneficial effect of intravenous pooled normal human immunoglobulin (IVIG) in patients with ANCA-positive vasculitis. In vitro studies have shown that IVIG contains antiidiotypic antibodies to ANCA and AECA, capable of inhibiting the binding of these autoantibodies to their autoantigens. In vivo, IVIG may also provide the immunoregulatory elements needed for the idiotype network and control of the autoimmune repertoire. Mathieson et al. successfully used monoclonal antibodies to T cells (Campath-H directed against CDw52) in a patient with ANCA-negative dermal lymphocytic vasculitis. Monoclonal antibodies to CAMs have been used in human renal transplant rejection and reduced the inflammation and proteinuria in animal models of anti-glomerular basement membrane disease. In vasculitis, the therapeutic use of specific anti-CAM antibodies may result from further definition of the role of CAMs. Increased understanding of the pathogenesis of systemic vasculitis is likely to provide the basis for the use of more specific immunotherapies in the future.
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PMID:Mechanisms of endothelial cell injury in vasculitis. 799 43

The cause or mechanism of the female predisposition in systemic lupus erythematosus and progressive systemic sclerosis is largely unknown. Accumulating evidence shows that dysfunction or activation of endothelial cells plays an important role in these conditions. In this study, we investigated the influence of various steroid hormones on the IL-1beta (50 U/mL)/TNF-alpha (50 U/mL) stimulated human dermal microvascular endothelial cell line (HMEC-1) and human umbilical vein endothelial cells (HUVEC). Dexamethasone showed significant inhibition of cytokine-induced ICAM-1 expression in HMEC-1, and E-selectin, VCAM-1 and ICAM-1 expressions in HUVEC. Androgens, especially dihydrotestosterone had a small, but statistically significant suppressive effect in HMEC-1 only. Estrogen exhibited no regulatory function in either cell line. No obvious expression of estrogen and androgen receptors could be demonstrated in either cell by immunostaining. Our study provided some pharmacological evidence that the superior anti-inflammatory effect of glucocorticoids on vasculitis was partly due to their inhibition of the CAM expression in endothelial cells. More studies are needed to determine if androgens could have a protective effect in vasculitis or vasculopathy associated with connective tissue diseases.
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PMID:Effects of dexamethasone and sex hormones on cytokine-induced cellular adhesion molecule expression in human endothelial cells. 1237 Jan 31

A 75-year-old man with interstitial pneumonia due to ANCA-related vasculitis requiring immunosuppressive treatment was admitted to our hospital because of fever and rapidly progressive dyspnea. Chest CT showed diffuse ground-glass opacity with infiltration shadow in the bilateral lungs. We established a definitive diagnosis by isolating Mycobacterium massiliense on culture examination of acid-fast bacilli from peripheral blood and sputum. We began to administer CAM, LVFX, AMK, IPM/CS to this patient two weeks after admission. However, he died of respiratory failure and septic shock. There are few case reports of pulmonary lesion with septicemia due to Mycobacterium massiliense.
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PMID:Pulmonary Mycobacterium massiliense disease with septicemia during immunosuppressive treatment. 2153 36