ISSN:1040-8711    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Aspects of pathogenesis of primary systemic vasculitis are highlighted in this review. The cause of these entities is still obscure, although new information on the possible role of infections has emerged. Success of antimicrobial treatment to ameliorate systemic vasculitis, for which proof was recently provided, adds to the new information. Apart from new data that point to a precipitating role for environmental toxins the background for development of these diseases is most likely genetic predisposition. Reports on hereditary α1-antitrypsin deficiency, the link between systemic vasculitis and human leukocyte antigen molecules, and an animal model of spontaneous granulomatous arteritis in mice with a hereditary deficit in Fas-mediated apoptosis, are some of the new data that strongly favor genetic predisposition. Progress has been made in the process of identification of the agonists and antagonists in the front line of vasculitic inflammation. The interaction of blood cells (eg, neutrophils and monocytes) with vascular endothelium has become more evident as have the signals for the release of harmful proteolytic enzymes. Antineutrophil cytoplasmic antibodies, which are important markers of disease, may be actively involved in these processes.

ISSN:1040-8711    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:1040-8711    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

A combination of risk factors are involved in susceptibility to a primary or secondary form of vasculitis. Most forms of vasculitis are probably genetically based but environmentally triggered. This review discusses currently available evidence for a pathophysiologic role of one possible environmental trigger, silica. Since 1960, several patients with pulmonary silicosis have been described that developed pauci-immune necrotizing crescentic glomerulonephritis, ie, with either completely negative immunofluorescence findings or nonspecific granular IgM or C3 deposits along the capillary wall. Recently it was reported that these patients have antineutrophil cytoplasmic antibodies (ANCAs) that are in most cases directed to myeloperoxidase. Further, patients with pulmonary silicosis may develop microscopic polyangiitis, the syndrome of lung hemorrhage and nephritis, or Wegener's granulomatosis. To further substantiate the relation between silicon exposure and renal failure or vasculitis, several case-control studies have been reported. Exposure to silicon-containing compounds was found to be related to chronic renal failure (odds ratio, 1.7:2.5) or vasculitis (odds ratio, 6.5:14.0). The mechanisms by which silica may induce ANCA-associated glomerulonephritis or vasculitis are not well known. Silicon-containing compounds have a pronounced adjuvant effect on immune responses, and silica particles are potent stimulators of lymphocytes and monocytes or macrophages. Further, silica may induce apoptosis of monocytes or macrophages and possibly neutrophils. In conclusion, at present there is ample evidence that occupational exposure to silicon-containing compounds is related to the development of ANCA-associated glomerulonephritis and vasculitis, and silica is one of the first well-documented environmental triggers in these diseases.

ISSN:1040-8711    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

During the past few years remarkable progress has been achieved in the understanding of the pathogenic mechanisms leading to vascular inflammation and injury in giant cell (temporal) arteritis. T lymphocytes are activated by specific recognition of a putative antigen residing in the arterial wall and, subsequently, activate macrophages that undergo a functional differentiation and contribute to vessel damage through various pathways. Vascular response to inflammation amplifies the inflammatory response through neovascularization and adhesion molecule expression. We are beginning to appreciate that products released by infiltrating inflammatory cells may play an important role in vessel occlusion and resulting ischemic complications. Concomitantly, synovitis underlying polymyalgia rheumatica musculoskeletal symptoms has been immunopathologically characterized and the nature of its relationship to giant cell arteritis is discussed. Although some components of the disease are highly corticosteroid responsive, other underlying pathogenic mechanisms may remain active. Long-term outcome is heterogeneous in patients with giant cell arteritis. Much less is known about the pathogenesis of Takayasu's arteritis. Recent work supports its association with HLA class I antigens, which may differ in different geographic areas or ethnic groups. Because Takayasu's disease expression may vary in different ethnic settings, this possibility has led to the proposal of new diagnostic criteria. Finally, the role of new imaging techniques in diagnosis and assessment of disease activity is discussed.

ISSN:1040-8711    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Kawasaki disease is an acute systemic vasculitis of childhood. Children are predominantly affected at less than 5 years of age, and coronary artery involvement is responsible for most of the morbidity and mortality of the disease. Since the institution of intravenous immune globulin in the treatment of the disease, outcome has significantly improved. Although multiple infectious agents and toxins have been implicated in the etiology of the disease, none has been identified. Activation of the immune system is known to occur in the acute stage of the disease and plays an important role in the pathogenesis of the disease.

ISSN:1040-8711    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Infection continues to be a major cause of morbidity and mortality in patients with systemic vasculitis. The recognition and treatment of infections in these patients is a particularly difficult task because the spectrum of potential pathogens is broad and the clinical manifestations of infection often mimic those of the underlying disease. This article provides 1) a general overview of the immunosuppressive properties of agents commonly used in the treatment of systemic vasculitis, and 2) a framework for the diagnostic evaluation and treatment of various infectious syndromes in patients with systemic vasculitis.

ISSN:1040-8711    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Newer agents of particular interest to rheumatologists are increasingly associated with vasculitis. There is now good evidence that treatment with hematopoietic growth factors, including granulocyte colony-stimulating factor and granulocyte- macrophage colony-stimulating factor, can cause or mimic vasculitides such as Sweet's syndrome and pyoderma gangrenosum. Similarly, there is strong evidence that clinical use of interferons is associated with a variety of autoimmune phenomenon rarely including vasculitis. The increased availability of testing for antineutrophil cytoplasmic antibody (ANCA) has widened the clinical spectrum of systemic vasculitides. There are now many reports that treatment with either hydralazine or propylthiouracil is associated with ANCA-positive vasculitis. A small number of case reports also implicate penicillamine and minocycline as agents capable of inducing an ANCA-associated vasculitis. Clinicians should be aware of the potential of certain drugs to cause vasculitis and especially cautious in using these agents in patients with known vasculitis.

ISSN:1040-8711    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Bacterial infections can clinically mimic a primary vasculitic syndrome and can directly cause a vasculitis that may respond to prompt recognition and treatment of the infection. Increasing direct and indirect evidence is establishing links between certain infections and vasculopathies, including aortitis, atherosclerosis, and Wegener's granulomatosis. The literature on the hepatitis viruses, particularly hepatitis C, and various vasculitic syndromes continues to grow. The spectrum of clinical syndromes, including “essential” cryoglobulinemia (elicited by the hepatitis viruses) and HIV, continues to broaden. Clinical trials have begun to demonstrate the therapeutic value of antiviral therapy in patients with these conditions.

ISSN:1040-8711    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Vasculitis is an uncommon but important manifestation of autoimmune rheumatic diseases. Although the blood vessels of any organ can be involved, cutaneous involvement of arterioles and venules is the most common. Autoimmune rheumatic diseases may present as systemic vasculitis, and systemic vasculitis may simulate autoimmune rheumatic diseases. A crucial event in the initiation, localization, and propagation of vascular injury involves activation of the vascular endothelium by a variety of stimuli, including cytokines, complement split products, and cognate interactions between endothelial and T cells. Endothelial cell permissiveness to the deposition of circulating immune complexes or in situ formation of immune complexes in the vessel wall is also important. Vascular injury may be mediated by local or systemic activation of the complement system as well as autoantibody or T-cell-dependent mechanisms. This review focuses on the clinical features and pathogenic mechanisms involved in vasculitis complicating autoimmune rheumatic diseases.

ISSN:1040-8711    

出版商:OVID    

年代:1998

数据来源: OVID