Treatment of Graves disease and associated ophthalmopathy with the anti-CD20 monoclonal antibody rituximab: an open study

M Salvi, G Vannucchi, I Campi, N Currò, D Dazzi, S Simonetta, P Bonara, S Rossi, C Sina, C Guastella, R Ratiglia and P Beck-Peccoz. Hyperthyroidism in Graves’ disease is mediated by a B cell mechanism, which causes an overproduction of immunoglobulin G and subsequent stimulation of the thyroid stimulating hormone (TSH) receptor. Thyroid-associated ophthalmopathy (TAO) has an active inflammatory phase lasting between 6 and 18 months, followed by clinical stabilisation. The anti-CD20 monoclonal antibody rituximab (RTX) specifically eliminates pre-B and mature B lymphocytes.Although the pathogenesis of TAO is not understood, Salvi and colleagues aimed to determine whether RTX therapy could affect the degree and the duration of the disease’s active phase. Salvi and colleagues assessed the effect of RTX on nine patients with Graves’ disease, and they report that the antibody was well tolerated and positively affected the clinical course of TAO after B cell depletion was attained. Compared with the 20 control subjects who received intravenous glucocorticoids (IVGC), those receiving RTX had a more prompt and significant decrease of the TAO clinical activity score. No relapse of active TAO was reported in the RTX patients, compared with a 10% relapse in the IVCG group. This study was an open, phase 2b trial so the findings will need testing in larger randomised controlled trials to confirm the results. There is a strong indication that RTX may be a useful therapy for patients with active TAO. EJE 156-1