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Results for “Systemic Vasculitis”

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At least 469 records · Page 26Linked to original sources
PubMed1987

Prospective study of radioimmunoassay for antibodies against neutrophil cytoplasm in diagnosis of systemic vasculitis.

The diagnosis and management of Wegener's granulomatosis and microscopic polyarteritis are complicated by the lack of specific diagnostic tests. The diagnostic performance of a solid-phase radioimmunoassay, which detects the autoantibodies against neutrophil cytoplasm present in these disorders, was assessed in a prospective study of patients with suspected vasculitis and/or rapidly progressive nephritis. The assay had a sensitivity and specificity of 96% when carried out in combination with a specific inhibition stage and indirect immunofluorescence staining of alcohol-fixed normal neutrophils.

Autoantibodies↗
PubMed2005

[Spermatic cord mass as a manifestation of systemic vasculitis: a case report and review of the literature].

We report a case of necrotizing granulomatous vasculitis in the spermatic cord in a 35-year-old man with an antecedent of brain stroke 3 years before. The clinical manifestation was as a painless left scrotal mass. The diagnosis was established by histological examination of the spermatic cord. We discuss the physical findings, radiological features and pathological findings, reviewing the literature for previous similar cases.

Adult↗
PubMed1993

[Role of the titration of anti-neutrophil cytoplasmic antibodies in therapeutic follow-up of patients with systemic vasculitis].

We studied clinical and biological data of 18 patients presenting ANCA associated diseases for 16 months at least. Five relapses were preceded by ANCA elevation, 1 relapse was not. Four transient elevations were noted without any clinical event. We think ANCA level elevation by itself is not enough for deciding therapy intensification, clinical data are necessary for doing so.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2002

Neurologic manifestations of systemic vasculitis.

The clinical features, diagnosis, and treatment of polyarteritis nodosa, Kawasaki disease, hypersensitivity angiitides (including drug-related vasculitis, serum sickness, Henoch-Schönlein purpura, hypocomplementemic vasculitis and cryoglobulinemia), Wegner's granulomatosis, temporal arteritis and Takayasu's arteritis are reviewed from a neurological perspective.

Arteritis↗
PubMed2001

Leukocyte-endothelial interactions in antineutrophil cytoplasmic antibody-associated systemic vasculitis.

The etiology of ANCA-associated vasculitis is unknown. Currently, it is believed that disease may be triggered by infection with the release of proinflammatory cytokines in genetically susceptible individuals. Priming of PMNs and endothelial cells by these cytokines allows ANCAs to activate PMNs, with damage localized to the endothelium, resulting in early lesions. Damage and activation of endothelial cells produces proinflammatory chemokines and cytokines with influxes of monocytes and T cells that intensify endothelial damage. In the kidney, these changes eventually lead to crescent formation. Antigen-specific memory T cells persist after disease remission with the potential of reactivation and disease relapse. Although our understanding of the pathophysiologic mechanisms of ANCA-associated vasculitis is far greater now than when ANCAs were first identified in 1982, more experimental work in combination with clinical observations is required to further elucidate these mechanisms.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1994

Isotype and affinity of anti-myeloperoxidase autoantibodies in systemic vasculitis.

The role of immunoglobulin (Ig) isotype and affinity of antimyeloperoxidase (MPO) antibodies in the clinical expression of vasculitis (organ involvement, severity and evolution) remains incompletely defined. We have determined the anti-MPO antibody isotypes, as well as the apparent affinity constant (aK) of anti-MPO IgG by using fluid phase MPO inhibition of IgG binding in an MPO specific ELISA. Twenty-eight patients with anti-MPO antibodies and necrotic and crescentic glomerulonephritis, either isolated or associated to various other organ localizations, were analyzed. Serum samples were obtained before treatment and during follow-up. No association was observed between the isotype, the level or apparent affinity of anti-MPO antibodies and the clinical symptoms, severity, and organ distribution of vasculitis, including alveolar hemorrhage. No significant correlation was found between the apparent affinity and the level of anti-MPO IgG. However, the presence of anti-MPO IgM was clearly associated with low affinity anti-MPO IgG and vice versa. Furthermore, in a longitudinal study, high levels of anti-MPO IgM, when present, were observed early in the course of the disease and in some cases preceded the reappearance of anti-MPO IgG during relapses. High affinity anti-MPO IgG were usually present before treatment. Immunosuppressive therapy resulted in decreased apparent affinity and level of anti-MPO IgG. Importantly, anti-MPO IgG level increased during relapses but the affinity of these IgG autoantibodies remained low.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗