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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

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