We studied responsiveness to synthetic thyrotropin-releasing hormone (TRH), 200 μg iv, in 13 patients with Graves' opthalmopathy, 10 of whom were euthyroid on the basis of serum concentration of free T3 and free T4. Two hyperthyroid and 4 euthyroid patients (Group I) responded abnormally by failing to show an increase in serum thyrotropin (TSH) or triiodothyronine (T3). The remaining patients (Group II), of whom 1 was hyperthyroid (Group IIA) and 6 euthyroid, also responded abnormally but with exaggerated serum TSH response to TRH. The serum TSH increased in these patients from a mean baseline value of 22 to a mean peak value of 91 μU/ml. The mean net 2-hr TSH secretion response of 5627 μU min in these patients was significantly higher than that observed in 14 normal subjects. Thyroid 131I uptake was not suppressible with T3 in all 5 of the Group I patients so studied and in 3 Group II patients. In the latter, serum immunoassayable TSH, supranormal initially, declined normally to undetectable levels during administration of T3, while serum T4 was unaffected. In the Group II patients with normal suppressibility by T3, serum T4 fell in those in whom it was studied. In the nonsuppressible patients of Group II, serum T3 did not rise after TRH, whereas it rose normally in those with normal T3-suppression tests. Two patients in Group II whose thyroid function was unaffected by T3 and who had high normal or high baseline serum TSH were given dexamethasone (2 mg every 6 hr for 4 doses). In one case, GD, it resulted in a fall in serum TSH from 8.5 μU/ml to undetectable levels and a fall in serum T3 from 220 to 120 ng/100 ml and serum T4 from 7.8 to 5.0 μg/100 ml; the minimum TSH, T3 and T4 was noted at 6, 28 and 72 hr, respectively, following the start of dexamethasone treatment. In another case, BG, serum TSH fell from 75 to a minimum of 15 μU/ml and serum T3 from 185 to a minimum of 130 ng/100 ml. The variations in response to TRH may represent different stages of the same disease or may signify that there are different types of Graves' disease. It is suggested that suppression of thyroid function by dexamethasone may be a result of a direct effect of the glucocorticoid on a putative thyroid abnormality in Graves' disease or a result of suppression of an as yet undefined thyroid stimulator.
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CHOPRA et al. (1973) studied this question.