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  • 1
    Electronic Resource
    Electronic Resource
    Mechanisms of endothelial cell injury in vasculitis (1994)
    Springer
    Springer seminars in immunopathology 16 (1994), S. 23-37 
    Details
    ISSN: 1432-2196
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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 [44]. 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. [52] 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 [76, 80, 87]. In vivo, IVIG may also provide the immunoregulatory elements needed for the idiotype network and control of the autoimmune repertoire. Mathieson et al. [68] 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 [63] and reduced the inflammation and proteinuria in animal models of anti-glomerular basement membrane disease [60]. 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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00196711
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  • 2
    Electronic Resource
    Electronic Resource
    Soluble circulating cell adhesion molecules in haemolytic uraemic syndrome (1995)
    Springer
    Pediatric nephrology 9 (1995), S. 574-578 
    Details
    ISSN: 1432-198X
    Keywords: Haemolytic uraemic syndrome ; Endothelium ; Soluble vascular cell adhesion molecule-1 ; Soluble intercellular adhesion molecule-1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Plasma concentrations of soluble vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sE-selectin) and intercellular adhesion molecule-1 (sICAM-1) were measured by enzyme-linked immunosorbent assay in four groups of children. Group 1 consisted of 20 patients with acute diarrhoea-associated haemolytic uraemic syndrome (D+HUS), the aetiology of HUS being verocytotoxin-producingEscherichia coli infection in each case. Controls consisted of 11 patients who had previously had D+HUS (group 2), 12 with chronic renal failure (group 3) and 8 healthy controls (group 4). When compared with healthy controls, the acute D+HUS group had higher sVCAM-1 (median 1,875 ng/ml, range 1,200–6,450 ng/ml vs. 1,200 ng/ml, range 975–2,125 ng/ml), von Willebrand factor antigen, (1.9 U/ml, range 0.85–5.1 U/ml vs. 0.55 U/ml, range 0.3–1.57 U/ml), white cell count (WBC, 14.5×109/l, range 7.8–43.1 109/l vs. 8.9 109/l, range 5.7–10.8 109/l) and neutrophil count (PMN, 10.1×109/l, range 4.3–26.5 109/l vs. 4.3 109/l, range 3.7–6.6 109/l), allP〈0.005, and sICAM-1 was reduced (230 ng/ml, range 130–340 ng/ml vs. 400 ng/ml, range 260–690 ng/ml),P〈0.05. Within the acute D+HUS group there was a significant correlation between sICAM-1 and PMN (r=0.56,P〈0.01). There was no correlation between any adhesion molecule and plasma creatinine or von Willebrand factor. Comparing the acute HUS group with children with chronic renal failure, WBC (P〈0.001), PMN (P〈0.01) and sVCAM-1 (P〈0.01) were significantly elevated, but there was no difference between the von Willebrand factor (P=0.08) or the sICAM-1 (P〉0.1). sVCAM-1 is elevated and sICAM-1 decreased in acute D+HUS. This pattern of altered adhesion molecule concentration is unlike that in adults with vasculitis and suggests that different endothelial regulatory factors are at play.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00860938
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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