Pretreatment with Betamethasone of Patients with Graves’ Disease Given Radioiodine Therapy: Thyroid Autoantibody Responses and Outcome of Therapy*

Abstract

The effects of betamethasone on thyroid autoantibody responses and outcome of radioiodine therapy were determined over a period of 1 yr in a prospective randomized study of 40 patients with Graves' disease. Twenty patients were given placebo tablets, and 20 patients were treated with beta-methasone from 3 weeks before until 4 weeks after 131I therapy. At the time of inclusion in the study, the mean serum concentrations of TSH receptor antibodies, thyroid peroxidase antibodies, and thyroglobulin antibodies (TgAb) were increased in both groups. Three weeks of treatment with betamethasone reduced the thyroid peroxidase antibody and TgAb titers as well as the serum concentrations of thyroid hormones. A decrease in the TSH receptor antibody level was not statistically significant. After radioiodine therapy, transient increases in thyroid autoantibody levels were observed. The titers of the different antibodies generally changed in parallel. In some patients a detectable level of a given antibody was found only after the radioiodine treatment, and in two cases, TgAb did not appear at all, although the two other antibodies increased temporarily. Betamethasone delayed, but did not abolish, the 131I-induced antibody peaks. Betamethasone also caused a reduction in the total serum immunoglobulin G, a reduction which persisted throughout the study period. When the study ended, 17 patients given placebo and 9 patients given betamethasone (P less than 0.001) were receiving replacement therapy due to the development of hypothyroidism. These patients at this point in time had lower antibody levels than those not requiring T4. The results of this study demonstrate that betamethasone reduces and modifies the thyroid autoantibody responses as well as the outcome of radioiodine therapy in patients with Graves' disease. From a clinical point of view, these effects may be in opposite directions.

Glucocorticoid Regimens for Prevention of Graves' Ophthalmopathy Progression Following Radioiodine Treatment: Systematic Review and Meta-Analysis

“…In two studies, no participant had preexisting GO (18,19), while in others, these patients represented 20-68% of the study population. Prednisone was evaluated in four studies (two RCTs and two retrospective), betamethasone in two RCTs, prednisolone in one retrospective study, and intravenous methylprednisolone in one retrospective study (Table 1).…”

“…Reasons for exclusion are detailed in Figure 1. Eight studies that were performed between 1986 and 2010 fulfilled inclusion criteria, including five RCTs and three retrospective controlled studies, evaluating 850 patients (Table 1) (3,(9)(10)(11)(12)(18)(19)(20). GCs used were oral prednisone in five studies, oral betamethasone in two studies, oral prednisolone in one study, and intravenous methylprednisolone in one study.…”

“…Six studies reported GO outcome following RAI treatment in patients with preexisting GO (3,(10)(11)(12)18,19). In one study, the entire patient population had preexisting GO (20), while in others, data were extracted from the treatment and control groups.…”

“…Patients with no preexisting GO GC treatment for the prevention of GO progression in patients without GO was evaluated in seven studies, of which four were RCTs and three were retrospective studies (3,(9)(10)(11)(12)18,19) (Table 1). In two studies, no participant had preexisting GO (18,19), while in others, these patients represented 20-68% of the study population.…”

Qualitative and Quantitative Impact of Protective Glucocorticoid Therapy on the Effective 131I Half-Life in Radioiodine Therapy for Graves Disease

“…In patients already presenting with EO-related symptoms, doses of 1.0-1.5 mg/kg are suggested. Although prednisolone has beneficial effects on the development or course of EO during RIT of GD, it is well established that glucocorticoids themselves change thyroid metabolism and triiodothyronine (T 3 ) and levothyroxine (T 4 ) levels and modulate the concentration of stimulating antithyroid antibodies (thyroid-stimulating hormone receptor antibody [TRAb]) (4)(5)(6)(7). Therefore, the aim of our study was to investigate the influence of prednisolone on the thyroidal 131 I half-life in RIT of GD patients and to assess this effect in comparison to other factors already known to change effective 131 I half-life during the course of RIT in GD patients-namely the thyroidal metabolic state, antithyroid medication, and TRAb level (8)(9)(10)(11)(12).…”