抄録
Studies on what factors might produce elevations in plasma TSH concentration have been carried out in normal subjects with no history of endocrine disorder and patients in. euthyroid state and primary hypothyroidism. TSH concentration was determined by radioimmunoassay using purified HTSH and potent anti-HTSH serum, which had been kindly supplied to us by the National Pituitary Agency, U. S. A. No significant elevation of plasma TSH concentration was observed, 1) when regular insulin (0.1U/kg of body weight) was intravenously injected in. normal subjects, 2) when arginine (0.5g/kg of body weight for 30 minutes) was intravenously infused in. normal subjects, and 3) when 20mg of estrogen was intravenously injected in. normal subjects. No increase in plasma TSH concentration was found after exposure of. healthy volunteers to 4° for. hours and during hypothermic cerebral surgery under general anesthesia with fluothane and nitrous oxide. But significant changes of plasma TSH concentration were observed, 1) when 30mg of MMI per day was given to. euthyroid patients for 10-14 days, 2) when 2mg of L-thyroxine was injected to those cases at the end of MMI treatment and 3) when 75μg of triiodothyronine or 2mg of L-thyroxine was subcutaneously injected into patients of primary hypothyroidism.
Plasma TSH and thyrotropic activity in the pituitary glands of patients with Graves' disease was also studied as follows. Plasma TSH concentration in the 10 patients not treated for Graves' disease was not detectable but plasma TSH levels after treatment by an antithyroid drug for 2-3 month was elevated to within normal ranges. In. patients who have suffered from Graves' disease with LATS and are in. euthyroid state after treatment, serial changes in TSH, LATS and plasma thyroxine levels, following administration of MMI or L-thyroxine. were simultaneously determined by means of their specific methods, respectively. The administration of MMI led to. decrease in plasma thyroxine concentration and. 6-10 times increase of the initial values in the plasma TSH concentration. But no significant changes were observed in the LATS activity. The immunological and biological thyrotropic activity in the pituitary glands of. patients with Graves' disease (GC-1, GC-2 and GC-3) was studied by using radioimmunoassay and McKenzie bioassay, and found to be immunologically abnormal. The time response curve obtained by bioassay for the pituitary thyrotropic activity in any of the patients was normal. Multiple doses of saline-extracted pituitary powder of patients with Graves' disease resulted in a parallel curve to that obtained for saline-extracted normal pituitary powder and to that for Human Thyrotropin Research Standard. in bioassay. The biological thyrotropic activity in GC-1 and GC-2 who died in. hyperthyroid state was found to be about 1/60 and 1/20 respectively, and the activity in GC-3 who died in an upper limit of. euthyroid state for receiving treatment was found to be about 1/3 of the normal average. No effect was observed when 0.02-200μg of GC-1 and GC-2 were assayed by radioimmunoassay, and also they failed to be neutralized by anti-HTSH serum and anti γ globulin serum in the bioassay. On the other hand, TSH activity in GC-3 was detectable by radioimmunoassay and resulted in. parallel curve to that obtained for the Human Thyrotropin Research Standard A, but the ratio of bioassay potency/immunoassay potency was 7.8, whereas it was 4.6±1.4 in the normal pituitary gland in our laboratory. 0hen Human Thyrotropin Research Standard. was used as the standard in both assays.
