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  Vol. 298 No. 23, December 19, 2007 TABLE OF CONTENTS
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Treatment of ANCA-Associated Vasculitis

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

To the Editor: Dr Bosch and colleagues1 considered the treatment of ANCA-associated vasculitis, discussing the relationship of its pathophysiology to current immunotherapy. The authors point out that although ANCA may be important in orchestrating neutrophil-mediated damage to the vascular endothelium, ANCA production is a T-cell driven process and novel forms of immunotherapy target this population of lymphocytes.

Cyclophosphamide has transformed the prognosis of these disorders from universally fatal to survival rates as high as 90%.2 However, considerable morbidity and failure to control disease can occur in 10% of affected individuals treated with this drug, so better forms of immunotherapy are required. In life-threatening or refractory forms of the disease, plasma exchange may be used in addition to conventional immunosuppression.

One novel therapy for refractory disease not discussed in the article by Bosch et al is the combination of monoclonal antibodies to CD52 (panlymphocyte marker) and CD4 (a subpopulation of T . . . [Full Text of this Article]

Matt P. Wise, DPhil
mattwise@doctors.org.uk

Paul Frost, FRCP
Department of Adult Critical Care
University Hospital of Wales
Cardiff, United Kingdom


RELATED LETTERS

Treatment of ANCA-Associated Vasculitis
Alfredo N. C. Santana, Telma Antunes, and Carmen S. V. Barbas
JAMA. 2007;298(23):2739.
EXTRACT | FULL TEXT  

Treatment of ANCA-Associated Vasculitis—Reply
Xavier Bosch, Antonio Guilabert, Gerard Espinosa, and Eduard Mirapeix
JAMA. 2007;298(23):2740.
EXTRACT | FULL TEXT  

RELATED ARTICLE

Treatment of Antineutrophil Cytoplasmic Antibody–Associated Vasculitis: A Systematic Review
Xavier Bosch, Antonio Guilabert, Gerard Espinosa, and Eduard Mirapeix
JAMA. 2007;298(6):655-669.
ABSTRACT | FULL TEXT  






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