Thyrotropin (TSH) release during altered adrenergic alpha and beta receptor influence.
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Biomedical subjects
Publications and source records attributed to U B Lauridsen.
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Fifty-five normal subjects were studied following intravenous injection of increasing doses of bovine thyrotropin (b-TSH) from 0.5 to 250 mU/kg. Serum triiodothyronine (T3) and thyroxine (T4) were measured 1, 2, 3 and 4 h after the TSH injection. Dose-related increments in serum T3 and T4 were demonstrated with doses of b-TSH = 2.5 mU/kg and a maximum response was obtained after approximately 100 mU/kg. The fractional increase in serum T3 was greater than in serum T4, but the ratio between the increase in serum T4 and serum T4 and serum T3 (21.3/l ng/ng) was independent of the dose of b-TSH and time after TSH stimulation. The T3 response was reproducible and unaffected by sex and age.
Thyroid levels were estimated in 15 patients with endogenous depressions. Before electroconvulsive treatment (ECT), serum thyroxine (T4) and free T4 index values were elevated (P less than .02). After recovery from depression, the levels were normal. Serum triiodothyronine (T3) and free T3 index were normal both before and after ECT. Serum thyrotropin (TSH) levels were also normal and not substantially altered by the ECT procedure. The mean maximal TSH response to protirelin (thyrotropin-releasing hormone) was diminished in the depressed patients and normal after recovery. In three patients, the increase in TSH response to protirelin after recovery did not occur and they relapsed within six months, while in seven patients with increased TSH response to protirelin after recovery only one relapse occurred. The disturbances in the free T4 index, T4, and the protirelin test may in some depressed patients resemble hyperthyroidism, but this condition can be excluded by means of serum, T3 and free T3 index.
Thyrotropin-releasing hormone (TRH) stimulation tests were performed in 19 patients with endogenous depression before treatment and when they had apparently recovered following antidepressive treatment. An increase in the maximal serum thyrotropin (TSH) response to TRH of more than 2.0 muU/ml was found in all of ten patients who did not relapse, while such an increase was found in only one of nine patients who did relapse within 6 months. I. e., a correct prognosis was possible in 94.7% (95% confidence limits 74.0 - 99.9%). Through significant changes were found in serum thyroxin (T4), free T4 index, serum triiodothyronine (T3) and free T3 index, these findings were of no prognostic value.
During antithyroid treatment a total of 88 TRH tests was performed in 56 clinical euthyroid patients. 56% had negative response to TRH (i.e. delta TSH smaller than 2 muU/ml) after being treated in average 12.6 months and no relation between the duration of treatment and the outcome of the TRH test was found. In the group with positive TRH tests (i.e. delta TSH greater than 2 muU/ml) the mean T4 value was slightly decreased (5.8 plus or minus SD 2.5 mug/100 ml) while the mean T3 value was normal (121 plus or minus SD 32 ng/100 ml). The group with negative TRH tests had quite normal serum T4 values (9.3 plus or minus SD 3.1 mug/100 ml) but in general high normal or elevated serum T3 values (175 plus or minus SD 31 ng/100 ml). Our results seem to indicate that serum T3 is of greater importance than serum T4 with regard to the outcome of the TRH test. The majority of the cases with negative TRH tests, however, had serum T3 and T4 values within normal range. In almost all patients with a negative TRH test a negative T3 suppression of 131I uptake in the thyroid gland was found while a positive TRH test was not correlated with suppressibility of 131I uptake.
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