John Q. Thompson’s research while affiliated with Scott & White and other places

Forty-five patients with Graves' disease were studied prospectively to determine if 24-hour I-131 uptake measurements alone or in combination with serum thyroid hormone levels at six weeks would determine the necessity for retreatment of the thyrotoxicosis. All patients with an I-131 uptake greater than 30% at six weeks required retreatment. No patient with an I-131 uptake of less than 15% required retreatment. Patients with uptakes between 15% and 30% were variable. An elevated free thyroxin index at 6 weeks is not helpful to determine which patients will remain thyrotoxic. Patients with a free thyroxin index within the normal range at six weeks can be predicted to be euthyroid by 12 weeks if their 24-hour I-131 uptake is between 15% and 30% and to be hypothyroid if their 24-hour I-131 uptake is below 15%. There was no difference between patient groups treated initially with antithyroid medication and those who were not.

Twenty normal adult volunteers were systematically tested with five known provocative agents of human growth hormone (HGH) release in order to ascertain which procedure was the most effective stimulus for pituitary testing purposes. Ninety-five per cent responded normally (5 ng/ml increment) to levodopa (l-dopa) and 90 per cent to insulin-hypoglycemia. Arginine, vasopressin and glucagon were less potent stimuli; however, arginine (80 per cent response rate) was superior to vasopressin and glucagon (60 and 55 per cent, respectively).

In this systematic survey of patients with various features of hypercortisolism, 39 patients were found to have at least one elevated corticosteroid measurement. Only 24 were proved to have Cushing's syndrome; the condition in the remaining 15 patients was termed "Cushingoid obesity." Plasma cortisol was the least helpful assay parameter. In the patients with Cushing's syndrome, 25 per cent of the 8 AM and 8 PM values were normal, and in the patients with Cushingoid obesity, 47 per cent of the values were spuriously high. The presence or absence of diagonal variation was of little diagnostic significance. After overnight dexamethasone, only one patient with Cushing's syndrome showed normal suppression, however, 53 per cent of the patients with Cushingold obesity falled to show adequate suppression. Routine 17-hydroxycorticosteroid (17-OHCS) and 17-oxogenic steroid (17-KGS) assays also proved to be relatively poor diagnostic parameters. Of the patients with Cushing's syndrome, 17 per cent had normal levels of excretion, and of the patients with "Cushingoid obesity," the 17-OHCS levels were falsely elevated in 53 per cent and the 17-KGS levels in 62 per cent. During high dosage dexamethasone therapy, none of the patients with Cushing's syndrome showed adequate suppression, however, in all the patients with Cushingoid obesity suppression was normal. Free cortisol excretion provided the most definitive index of adrenocortical hyperfunction. Urinary free cortisol was increased only in the 24 patients with Cushing's syndrome and was not adequately suppressible with dexamethasone. There were no false elevations in any of the 15 patients with Cushingoid obesity, in all of whom suppression was normal with dexamethasone.