Using a radioreceptor assay and serum immunoglobulin (Ig) prepared by ammonium sulfate precipitation, significant TSH displacement activity (TDA) was demonstrated in 5 of 15 patients with subacute thyroiditis tested during the acute phase. Using a cAMP generation assay, adenyl cyclase stimulation by Ig from patients with subacute thyroiditis was not demonstrated. The nature of the TDA demonstrated in subacute thyroiditis was investigated to determine whether the factor measured was TSH receptor antibody, as is found in Graves' hyperthyroidism, or thyroglobulin, which is know to give false positive responses in the radioreceptor assay. When Ig was prepared by DEAE+-Sephadex chromatography, mean TSH displacement indices were similar to those given by ammonium sulfate-prepared Ig for both Graves' disease and subacute thyroiditis. On the other hand, when Ig was prepared by DEAE+-cellulose chromatography, which isolates highly purified IgG, mean indices were significantly less than for ammonium sulfate-prepared Ig for both Graves' hyperthyroidism and subacute thyroiditis. Thyroglobulin was not detected in Ig prepared by any of the 3 methods. Although high concentrations of crude thyroid-soluble fraction and purified thyroglobulin gave strongly positive responses in the radioreceptor assay, concentrations of thyroglobulin over the range found in the sera of patients with subacute thyroiditis could not be shown to give positive responses. Moreover, TSH displacement indices did not correlate with serum thyroglobulin levels. As determined by species cross-reactivity and dose-responses studies, the TDAs demonstrated in subacute thyroiditis and Graves' hyperthyroidism were similar. It was concluded that the TDA demonstrated in subacute thyroiditis represents antibody which binds to, but does not stimulate, the TSH receptor.
Blood mononuclear cells bearing Fc receptors for immunoglobulin G were measured in patients with thyroid disorders as the percentage of EA rosette-forming cells (% EA-RFC). Levels were normal in patients with untreated Graves' hyperthyroidism, Graves' ophthalmopathy, and Hashimoto's thyroiditis. On the other hand, the % EA-RFC was increased in eight of nine patients with subacute thyroiditis (SAT) tested during the acute phase, returning to normal during recovery. Levels were normal in all five patients with "silent" thyroiditis tested. The majority of the Fc receptor-bearing cells in SAT patients was shown to be phagocytic. There was no evidence for increased killer cell or suppressor cell activity, functions which reside in Fc receptor-bearing mononuclear cell populations, in SAT patients. There was no close correlation between the % EA-RFC and parameters of thyroid damage (erythrocyte sedimentation rate and serum T4 levels) or thyroid antibody titers. While an increase in the % EA-RFC in SAT patients may represent a nonspecific response to a viral inflammation of the thyroid gland, the abnormalities may be markers of a more specific immunological response to thyroid antigen release. Abnormalities of blood mononuclear cell numbers in Graves' hyperthyroidism and SAT are reviewed.
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