A group of 20 patients affected with thyroid carcinoma, all from Southern Italy, was typed for HLA-A, -B, -C and -DR antigens. Sixteen of them (80%) typed for DRl, while in the control group (120 unrelated healthy individuals from the same region) only 22 (18.3%) shared the same antigen (x2 = 32.96). The data indicate a highly significant association between the HLA-DR1 gene and the thyroid carcinoma.
Plasma TSH responses after an i.v. injection of 100 mg of L-dopa were evaluated by radioimmunoassay in 4 normal euthyroid subjects and in 8 patients with primary hypothyroidism. In agreement with previous results, no variations in plasma TSH levels were observed in the euthyroid subjects. In contrast, in primary hypothyroidism L-dopa induced a biphasic response in plasma TSH. In fact, we observed a transitory increase with a maximum at 30 min (mean ± SEM = 54 ± 18%) followed by a decrease reaching a minimum level of plasma TSH basal values at 90 min (mean ± SEM = 15 ± 6%). These findings demonstrate that the plasma TSH response to L-dopa in primary hypothyroidism is time-dependent. Some speculation on the possible mechanism of this action is presented.
In 12 patients with primary hypothyroidism the somatotrophic and corticotrophic functions were evaluated before and after thyroxine treatment.
The results confirm a significant decrease, reversible by treatment, of plasma HGH responses to insulin-induced hypoglycaemia and to arginine infusion. Moreover, the results indicate that the impairment of the hypothalamic-pituitary function may also involve the response of plasma ACTH after provocative tests (insulin-induced hypoglycaemia and metyrapone). It must be stressed that the impairment of the corticotrophic function can be revealed only when the responses to provocative tests are evaluated by a direct assay of plasma ACTH and not by plasma corticosteroid modifications. These different responses may account for the conflicting results obtained by other investigators and may be justified by the multiple interference of the thyroid deficiency with the hypothalamic-pituitary-adrenal axis at different levels.
Plasma TRH was determined by radioimmunoassay in normal and abnormal thyroid state. In euthyroid adult subjects, the plasma TRH level were 31.9 \m=+-\11 pg/ml (mean \ m=+-\ sd). No significant differences were observed with regard to sex, pregnancy or age, except for the acute increase in newborn infants. The plasma TRH levels evaluated in abnormal thyroid states were found significantly (P < 0.001) increased in hyperthyroidism (49.1 \m=+-\14 pg/ml) and decreased in hypothyroidism (22.1 \ m=+-\6 pg/ml). Nor were any significant differences observed in simple goitre, pituitary adenoma and empty sella. Lastly, plasma TRH and TSH levels were also evaluated after acute administration of L-dopa, 2-Br-\g=a\-ergocriptineand chlorpromazine in normal and hypothyroid subjects. Contemporaneous modifications of plasma TRH and TSH levels (decreased after L-dopa and 2-Br-\g=a\-ergocriptine,increased after chlorpromazine) were observed in hypothyroidism. The results indicate that plasma TSH modifications at birth as well as under catecholaminergic influences are at least partially mediated by variations of TRH secretion. Moreover, the inverse plasma TRH and TSH modifications in abnormal thyroid states agree with different feedback effects at the hypothalamic (positive) and pituitary (negative) level. It is possible that the significance of the positive feedback at the hypothalamic levels can be interpreted when taking into account the extrapituitary effects of TRH.
The study reported here extends investigation on the pituitary thyroid axis in newborn infants, including the assay of plasma immunoreactive TSH levels at different intervals after delivery. Blood samples were collected at birth and after 30, 60, 120 minutes, 6, 24 and 48 hours. Plasma TRH levels were also estimated in normal adult subjects and pregnant women. No significant difference was observed with regard to sex, pregnancy or age, except for a marked increase in newborn infants after delivery. Plasma TRH values, already moderately high at birth (mean 46 pg/ml, range 34-57) reached rapidly a peak of 78 pg/ml (range 60-93) 30 minutes after delivery, decreased rapidly between 30 minutes and 2 hours post-partum, then fell gradually to normal range at 24 hours. A comparison of plasma TRH and TSH levels measured simultaneously suggests that the acute TSH surge at delivery is mediated by TRH secretion.
Plasma hGH response to provocative tests (insulin-induced hypoglycaemia and arginine infusion) appears normal in Turner's syndrome. Two cases are reported of the chromatin positive variety of ovarian dysgenesis (XO/XX mosaicism) with unusual absence of plasma hGH response to provocative tests (arginine infusion, insulin-induced hypoglycaemia). Study of other pituitary functions supports the view that a hypothalamic-pituitary impairment is present in these cases. In fact, in these cases we observed low values of gonadotrophin excretion and limited responses of plasma ACTH and plasma corticosteroids to provocative tests (insulin-induced hypoglycaemia, metopyrone). Moreover, markedly abnormal plasma TSH response to TRF was observed in Case 2. The results are discussed with reference to the significance of this rare association.
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