Autoimmune Responses in Systemic Vasculitis

Lockwood, C. M.

doi:10.1159/000168035

Cited by 5 publications

(2 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One year after the start of treatment, the average steroid dosage was 10 mg/day in group A patients and 13.7 mg/day in group B patients (P not significant). A high rate of relapse was observed in both groups (10 in group A, 8 in group B). In 26 patients (14 in group A, 12 in group B), the study therapy failed to control the disease activity, and the patients experienced deterioration or relapse, despite therapy.…”

Section: Methodsmentioning

confidence: 80%

Lack of Superiority of Steroids Plus Plasma Exchange to Steroids Alone in the Treatment of Polyarteritis Nodosa and Churg‐Strauss Syndrome

Guillevin

Fain²,

Lhote³

et al. 1992

Arthritis & Rheumatism

153

View full text Add to dashboard Cite

Objective. To define the most effective treatment for polyarteritis nodosa (PAN) and Churg‐Strauss syndrome (CSS). Methods. We conducted a prospective, randomized, multicenter trial in which 78 patients were randomly assigned to receive either prednisone and plasma exchange (group A; n = 36) or prednisone alone (group B; n = 42) as first‐line treatment of PAN and CSS. Patients with hepatitis B virus—related PAN were not included in this study. The end point of the study was control of the disease (recovery and remission) or death. Results. Clinical symptoms and laboratory findings did not differ statistically in the 2 groups at study entry. Initial control of the disease was similar in both groups. The assigned treatment was stopped in 16 patients because of lack of efficacy. Oral cyclophosphamide or dapsone therapy reversed the disease evolution in 7 of these 10 group A patients and in 4 of these 6 group B patients. At 7 years of followup, 56 patients had completely recovered (27 in group A, 29 in group B), 7 patients were in clinical remission, and 15 patients had died (19.2%; 6 group A patients and 9 group B patients). The prednisone—plasma exchange combination was no more beneficial than corticosteroids alone in preventing relapses over the long term. There was no significant difference in the 7‐year cumulative survival rates of the two groups (83% and 79%, respectively). Conclusion. Based on our data, we conclude that combined treatment with prednisone and plasma exchange is not superior to treatment with prednisone alone and must not be systematically employed for initial treatment of PAN and CSS. In most cases, cyclophosphamide as second‐line treatment is effective and well tolerated.

show abstract

Section: Methodsmentioning

confidence: 80%

Lack of Superiority of Steroids Plus Plasma Exchange to Steroids Alone in the Treatment of Polyarteritis Nodosa and Churg‐Strauss Syndrome

Guillevin

Fain²,

Lhote³

et al. 1992

Arthritis & Rheumatism

153

View full text Add to dashboard Cite

show abstract

“…T cell involvement in vascul itis is implied from the infiltration of affected vessels by ac tivated T cells, the correlation of serum IL-2 receptor levels with disease activity, and the effectiveness o f anti-T cell an tibodies in therapy [44]. The presence o f circulating PR-3-specific T cells in ANCA vasculitis has been reported [45].…”

Section: T Cell Involvement In Glomerulonephritis Associated With Sysmentioning

confidence: 99%

T Cell Involvement in Glomerular Injury

Merkel

Marx

Netzer

et al. 1996

Kidney Blood Press Res

View full text Add to dashboard Cite

The mechanisms of glomerular injury are multiple: one aspect is cell-mediated immunity in inflammatory kidney disease. Its fundamental role has been established within the last decade. T cells seem to play a regulatory role in the course of inflammation not only in the proliferative and crescentic disease, but also in nonproliferative glomerulonephritis. T cells become increasingly important in the pathogenesis of both glomerular and interstitial kidney diseases and seem to determine course and prognosis. The recent advances in understanding the mechanisms of T cell-mediated inflammation in kidney disease offer new approaches in therapy.

show abstract