The effect of methadone on hypophyseal and peripheral glandular hormones during withdrawal.
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Biomedical subjects
Publications and source records attributed to K H Rudorff.
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Radioimmunoassay of thyroxine and triiodothyronine in a 14-year-old girl with primary hypothyroidism and nodular goitre as a result of Hashimoto's thyroiditis gave falsely low values due to the presence of hormone-binding antibodies. Such antibodies occur in Hashimoto's thyroiditis and thyroid carcinoma. Their presence requires special methods for determining these hormones.
The effect of a new analogue of the gonadotrophin-releasing hormone LH-RH, D-Ser(TBU)6-EA10-LH-RH, on the secretion of LH, FSH, as well as testosterone, oestradiol, HGH, prolactin, TSH, and cortisol was studied in normal men. The same subjects were injected intravenously in 4-day intervals with 1.0, 2.5, 5.0, and 10.0 mug of this substance. A significant LH but no FSH release was seen after doses of 1.0 and 2.5 mug LH-RH analogue, while after 5.0 and 10.0 mug dose-dependent increases of LH and imposed elevations of FSH were observed. Peak levels of LH were reached after 30 min, those of FSH after intravenous injection after 120 min. LH and FSH remained elevated for 8-10 h. LH peak levels after 5 mug of LH-RH analogue were comparable to those seen after injection of 100 mug of the decapeptide LH-RH. Following the release of LH and FSH after doses of 5.0 and 10.0 mug LH-RH analogue, there was a late stimulating effect in testosterone and oestradiol secretion. HGH, TSH, prolactin, and cortisol were not influenced by the LH-RH analogue.
The competitive ligand binding assay (CLBA) first described by Chopra et al. ((1972) J. Clin. Endocrinol. Metab. 35, 565-573) is a convenient routine method for the accurate measurement of thyroxine binding globulin in large numbers of serum samples. The assay is based on the partition of a constant quantity of radiolabelled T3 between a fixed quantity of rabbit T3 antibodies and the thyroxine binding globulin of the serum, after prior removal of T3 and T4 from the serum with an anion exchange resin (Amberlite IRA 400). In euthyroid subjects serum thyroxine binding globulin was 25.5 +/- 5.0 mg/1, in hyperthyroid patients thyroxine binding globulin was significantly decreased to 13.0 +/- 4.0 mg/1 and was significantly increased in hypothyroid patients to 36.8 +/- 6.2 mg/1 as well as in pregnant women to 41.3 +/- 6.2 mg/1. No difference was found between normal subjects and young women taking contraceptive pills with low oestrogen content. There were significant negative correlations between the thyroxine binding globulin in serum on the one hand side and the free T4-and free T3-fraction on the other. The low thyroxine binding globulin estimates in hyperthyroid patients increased gradually to normal during treatment with thyroid blocking drugs, the elevated thyroxine binding globulin in hypothyroid patients decreased to normal during treatment with thyroid hormones. The competitive ligand binding assay used here seems to be convenient as a routine method for the precise and reproducible measurement of thyroxine binding globulin in serum.
In a 41-year-old woman and a 3-year-old girl, both of them with T3-thyrotoxicosis, serum levels of total and free T4 and T3 were measured serially during anti-thyroid drug treatment. Attempts to substitute thyroxine during the antithyroid treatment had to be interrupted because the patients became hyperthyroid again with excessive increases in total and free serum T3, even when concentrations of total and free T4 were brought to subnormal levels. The increased conversion of administered thyroxine ceased later on and higher amounts of oral T4 were tolerated after one year of treatment. In both patients there was an extremely low serum T4/T3 ratio, differing in this respect significantly from six other patients with T3-thyrotoxicosis and 41 patients with "conventional" T3/T4-hyperthyroidism. It is concluded that, in patients with T3-thyrotoxicosis due to excessive peripheral T4 to T3 conversion, substitution during antithyroid drug treatment should be either with very low doses of thyroxine or with triiodothyronine in divided daily doses. In such cases the level of serum T3 represents the most reliable biochemical measurement for the control of treatment, serum T4 levels being irrelevant.
The synthetic linear tetradekapeptide somatostatin (growth-hormone release inhibitory hormone: GHRIH) inhibits the liberation of growth hormone in normal persons in the insulin hypoglycaemia test without influencing the rise of cortisol and prolactin, while the concentrations of LH, FSH and TSH remain unchanged. In patients with florid acromegaly there occurs during administration of GHRIH a marked fall in the raised STH level without influencing the basal level of the other anterior-pituitary hormones. As a further effect there is suppression of the insulin level. The somatostatin at present available has a very short biological half-life and in its present form is, therefore, without therapeutic importance.
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