甲状腺機能異常症の視床下部下垂体副腎系に関する研究
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The effects of abnormal thyroid function on the hypothalamo-pituitary-adrenal system were studied in 37 hyperthyroid and 16 hypothyroid patients and compared to 38 normal subjects.<BR>1) Plasma corticotropin (ACTH), growth hormone (GH) and cortisol responses to insulin hypoglycemia (0.1 U/kg, iv) were examined. Plasma ACTH was determined by radioimmunoassay (RIA) using two antisera, one directed against the C-terminal portion of ACTH molecule, the other (NPA, 699 FRED) directed against the N-terminal portion. The mean basal ACTH levels determined by C-terminal antibody in normal, hyperthyroid and hypothyroid subjects were 59 ± 11 (SE), 111 ± 35 and 33 ± 20 pg/ml respectively, where a statistically significant difference was not present. However, the maximum levels attained during insulin hypoglycemia were 410 ± 34, 1,379 ± 216 (P<0.01) and 269 ± 58 pg/ml (P<0.05) in the same order. The significant correlation between the maximum ACTH concentration and RT<SUB>3</SUB>U was revealed (r = 0.766, P<0.005). The maximum ACTH levels determined by the N-terminal antibody were also increased in hyperthyroid patients (537± 116 pg/ml, P<0.05), when compared with normal subjects (249 ± 53 pg/ml). By contrast, the plasma GH responses to hypoglycemia were markedly suppressed in both hyper- and hypothyroid patients. The plasma cortisol responses were not significantly different between normal subjects and patients with thyroid dysfunction.<BR>2) t 1/2, V, and MCR of cortisol were obtained from the disappearance curve of intravenously injected 2.5-5 mg of cortisol after overnight dexamethasone suppression, using one pool model. MCR's in normal, hyper- and hypothyroid subjects were 244 ± 22,696 ± 88 (P<0.001) and 129 ± 19 1/24 hrs (P<0.005) respectively.<BR>3) The maximum cortisol production rate (PRmax) was obtained by plasma cortisol levels during 30 and 90 minutes after iv injection of 250 μg of 1-24 ACTH, and t 1/2 and V of cortisol by the formula of Hellman (1970). PRmax's in normal, hyper- and hypothyroidism were 56.7 ± 4.8,102.9 ± 11.6 (P<0.05) and 31.2 ± 2.8 pig/min (P<0.01). The mean plasma cortisol level at 120 minutes after the priming dose-constant infusion of the excess amount of 1-24 ACTH following overnight dexamethasone suppression in hyperthyroidism was significantly less than that of normal subjects (22.6 1.5 vs. 27.3 ± 1.1, P<0.05), while that of hypothyroidism was not significantly different (24.6 ± 0.9 μg/ 100 ml)).<BR>4) The amount of cortisol produced (Pph) and the availability of cortisol secreted in response to a physiological dose (1 μg) of 1· 24 ACTH after overnight dexamethasone suppression were investigated. From the response curve of plasma cortisol, determined by competitive protein binding method, cortisol production (Pph) was calculated by the formula, P = MCR <I>∫</I><SUP>∞</SUP><SUB>o</SUB> C<SUB>F</SUB> dt = MCR × S (S : area under cortisol response curve). Pph's in normal, hyper- and hypothyroid subjects were 3.00 ± 0.15, 3.48 ± 0.56 (N.S.) and 1.88 ± 0.17 mg (P<0.01) respectively. But, the availability of cortisol secreted (area under cortisol concentration curve) after iv injection of 1 μg of 1-24 ACTH in hyperthyroidism was markedly decreased (808 ± 165, P<0.001), while that in hypothyroidism (2,459 ± 313) was not significantly different from normal subjects (1,872 ± 143 min·μg/ 100 ml).
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