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PubMed1985

Sleep-related growth hormone release in thyrotoxic patients before and during propylthiouracil therapy.

Hyporesponsiveness of GH to insulin-induced hypoglycemia has previously been reported in hyperthyroid patients. In order to clarify the GH secretion in thyrotoxic patients, sleep-related increases in the serum GH concentration were investigated. Eight thyrotoxic females ranging in age from 7 to 15 were treated with PTU. Blood samples for measurement of GH were drawn every 15 minutes during the first few hours of sleep before and during the treatment lasting about three months. The mean maximum serum GH level before the treatment was 10.0 +/- 5.5 ng/ml (mean +/- SD); this rose to 23.2 +/- 14.6 ng/ml (P less than 0.02) during the treatment. The maximum value of more than 10 ng/ml was detected in only 3 out of the 8 patients before treatment. On the other hand, serum GH levels during PTU administration rose to above 10 ng/ml in all patients except one. It was revealed that sleep-related elevations of GH occurred early in sleep and in close association with a slow-wave EEG pattern. The results show that sleep-related GH release is low in the hyperthyroid state, but becomes significantly elevated during PTU administration. However, even in the hyperthyroid state, the sleep-related secretion of GH is closely correlated with the slow-wave sleep stage as in the euthyroid condition.

Adolescent↗
PubMed1986

Effects of thyroidectomy and administration of propylthiouracil (PTU) or thyrotropin (TSH) to pregnant rats on the functional development of the fetal thyroid gland an immunohistochemical study.

In order to elucidate the maternal factors influencing the functional development of the fetal rat thyroid gland, pregnant rats were subjected to either thyroidectomy or administration of PTU or TSH and the thyroid glands of the fetuses were examined chronologically by immunohistochemistry to detect thyroglobulin (Tg), T4 and T3. In the group undergoing thyroidectomy, the occurrence of immunoreactive Tg, T4 and T3 was the same as in the control group in spite of slight retardation of the development of the thyroid gland. On the other hand, PTU administration caused remarkable degeneration of the hyperplastic epithelium of the follicles, where immunoreactivity of T4 and T3 was barely detectable, suggesting a transplacental effect of PTU on the fetal thyroid gland. However, Tg remained unaffected and was stained as well as in the controls. Injection of TSH led to a delay in the occurrence of T4 and T3 by one day, probably due to increased levels of thyroid hormone from the stimulated thyroid gland of the mother rats.

Animals↗
PubMed1982

The effect of thyroxine, the antithyroid drug propylthiouracil and thyroidectomy on mineral metabolism in rat tissues.

The administration of thyroxine produces a significant increase in the copper, magnesium, iron and zinc contents of liver, with a concomitant decrease of heart iron. Magnesium in heart tissues was also increased. The administration of antithyroid drugs produces a significant decrease in the concentration of the same metals in the liver with concomitant increases in kidney copper and calcium, and in heart magnesium and calcium. Brain magnesium was found to be significantly decreased after antithyroid treatment and increased to a lesser extent after thyroxine administration. Thyroidectomy did not produce an appreciable effect on minerals in various tissues, except heart zinc which was significantly decreased. These findings suggest the involvement of thyroid hormones in tissue mineral metabolism, especially in the liver.

Animals↗