Abstract
A thyrotoxic woman became grossly hypothyroid after treatment with 131I. Bio-assay of her serum showed the presence of a high level of long-acting thyroid stimulator (LATS). By application of a concentration procedure which extracts TSH but not LATS, it was shown that her serum contained a high level of TSH, in addition to the LATS. After the patient had received 0.4 mg of thyroxine daily for 2 weeks, there was no change in the LATS content of her serum, but TSH was no longer detectable, nor was TSH detectable in a serum sample taken when the patient was thyrotoxic before receiving the 131I therapy. It is concluded that the patient's pituitary gland secreted TSH when the blood thyroxine level was below normal and that this secretion was stopped by the administration of thyroxine in suppressive dosage. There was no evidence of TSH secretion when the patient was in the untreated thyrotoxic state. These observations indicate that there is no defect in the control of TSH secretion in Graves' disease. This is in accord with the evidence that LATS is not of pituitary origin.
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