A positive serum basophil histamine release assay is a marker for ciclosporin-responsiveness in patients with chronic spontaneous urticaria

Functional factors including histamine-releasing autoantibodies have been identified by the BHRA in the sera of 20–30% of patients with CSU [1-3]. CSU patients with a positive BHRA also have a higher incidence of thyroid antibodies than those without [4]. A double-blind placebo controlled study of ciclosporin for chronic idiopathic urticaria showed that more patients with a positive BHRA responded to ciclosporin than those with a negative BHRA [5] but this observation is not widely known. If confirmed, the BHRA could be used as a biomarker to predict a good response to treatment with ciclosporin and provide additional justification for using this third-line immunosuppressive agent in CSU patients with antihistamine-unresponsive disease.The electronic case records of CSU patients attending a specialist Urticaria Clinic at St John’s Institute of Dermatology, London, who had a BHRA performed on their sera by RefLab, Copenhagen (HR-Urtikaria Test？) [6] between November 2004 and March 2011 were reviewed retrospectively by one of the authors to identify those with H1 antihistamine-unresponsive CSU treated with ciclosporin and their response to it. None of the patients had an autologous serum skin test. The usual starting dose of ciclosporin was 4 mg/kg/d and the usual duration of treatment was between 3 and 4 months. Patients with other patterns of chronic urticaria including inducible urticarias (physical, cholinergic and other types), angio-oedema without weals and urticarial vasculitis were excluded. The global response to ciclosporin was designated as complete, partial or none based on the assessment made by their attending clinician. The time to respond to ciclosporin was also noted when this information could be gleaned from the notes. The time to onset of a complete or partial response was categorised as immediate (within days), early (within a month), late (from 1-3 months) and delayed (beyond 3 months). An increase in autoantibodies to thyroid peroxidase, thyrogl