We described a significant clinical response to RTX treatment in patients with active TAO. In order to understand the possible mechanisms of action of RTX, we measured serum concentrations of IL-6 and its soluble receptor (sIL-6R). We treated 10 patients with RTX: 8 women, 2 men aged 3151 yr with Graves disease. We also treated 14 patients with i.v. steroids (IVGC). All had active TAO. In all patients we studied thyroid function, serum autoantibodies and peripheral blood lymphocytes and by ophthalmologic evaluation the clinical activity score (CAS). Patients were treated with RTX (1000 mg i.v. twice at 2-week interval) or with IVGC (500 mg i.v. for 16 weeks). Serum cytokines were measured by highly sensitive assays (Quantikine, R&D Systems, USA) at baseline and at the time of CD20+ depletion, 30 and 50 weeks from therapy. Basal serum IL-6 concentrations were 30.6±83.6 and 9.4±17.4. in patients treated with RTX and IVGC respectively, and did not change after therapy (ANOVA; P=NS). Serum IL-6 did not change in relation to CD20+ depletion (ANOVA; P=0.17). There was no correlation between serum IL-6 and either thyroid autoantibodies or the CAS. Mean basal serum sIL-6R concentrations were 478.2±132.3 and 578.6±172.7 pg/ml in patients treated with RTX and IVGC respectively, and did not change after therapy (Anova). Serum sIL-6R did not change in relation to CD20+ depletion (ANOVA; P=0.30). There was no correlation between serum sIL-6R and either thyroid autoantibodies or the CAS (P=NS) We did not observe any significant change of either serum IL-6 or sIL-6R with respect to the modality of treatment (ANOVA). These findings suggest that: a) the RTX effect on TAO does not seem to involve the IL-6/sIL-6R system; b) the therapeutic action of IVGC is also not modifying the secretion of these cytokines; and c) the beneficial effects of RTX may be solely related to the consequences of B cell depletion.
03 - 07 May 2008
European Society of Endocrinology