title: 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.
authors.affiliation: Department of Internal Medicine, Orebro Medical Center Hospital, Sweden.
authors.forename: A
authors.initials: A
authors.lastname: Gamstedt
authors.forename: A
authors.initials: A
authors.lastname: Karlsson
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001323:Autoantibodies / Q000097:blood*; D001623:Betamethasone / Q000627:therapeutic use*; D005260:Female; D006111:Graves Disease / Q000188:drug therapy / Q000276:immunology / Q000532:radiotherapy*; D006801:Humans; D007457:Iodine Radioisotopes / Q000627:therapeutic use*; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011989:Receptors, Thyrotropin / Q000276:immunology; D013954:Thyroglobulin / Q000037:antagonists & inhibitors; D013961:Thyroid Gland / Q000276:immunology*; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D001323:Autoantibodies; D007457:Iodine Radioisotopes; D011989:Receptors, Thyrotropin; C006606:anti-thyroglobulin; C056626:thyroid microsomal antibodies; D014284:Triiodothyronine; D013954:Thyroglobulin; D001623:Betamethasone; D013974:Thyroxine