Abstract

The increase in serum-thyroid-stimulating hormone (T.S.H.) levels measured twenty and sixty minutes after intravenous injection of 200 μg. of synthetic thyrotrophin-releasing hormone (T.R.H.) has been used as a test of pituitary-hypothalamic function. 77 patients with diseases of the pituitary or hypothalamus had T.R.H. tests and routine clinical and biochemical assessment of pituitary and thyroid function. Of 35 patients with acromegaly, 9 of whom had not received treatment directed to the pituitary, only 7 showed a normal response to T.R.H., and 4 of these were in the untreated group. No patient in whom growth hormone (G.H.) levels had returned to normal showed a normal T.S.H. reserve. In the acromegalic patients the T.S.H. reserve was impaired twice as frequently as the corticotrophin reserve (A.C.T.H.). Of 27 patients with various other pituitary lesions, 14 had an impaired or absent T.S.H. response, and 8 of these had other clinical or biochemical evidence of hypothyroidism. Unlike the acromegalic patients, T.S.H. and A.C.T.H. reserve were impaired with equal frequency in this group. Of 15 patients with various hypothalamic lesions, 8 had an impaired or absent response to T.R.H.; 3 patients who responded normally to T.R.H. had other evidence of hypothyroidism. A delayed response to T.R.H., where the twenty-minute T.S.H. level was less than the sixty-minute value, occurred in 13 of 15 in this group. This delayed pattern of response can be used to recognise hypothalamic disease. In patients with pituitary disease, but not in those with hypothalamic disease, a normal T.S.H. response to T.R.H. excludes the diagnosis of hypothyroidism. All patients with non-hormone-secreting pituitary lesions who had no response to T.R.H. were hypothyroid; this was not true in acromegaly or in a patient with active Cushing's disease. Since only 7 of the 26 patients with pituitary disease who showed impaired responses were hypothyroid by other criteria, it is suggested that impaired responses merely indicate a risk of the development of thyroid deficiency.

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