Jacqueline Golstein

PROLACTIN RELEASE AFTER INJECTION OF THYROTROPHIN-RELEASING HORMONE IN MAN

Abstract Five normal men were injected intra Summaryn venously 200 μg. of synthetic thyrotrophin-releasing hormone (T.R.H.). Blood was collected every 5 or 10 minutes and assayed for thyroid-stimulating hormone (T.S.H.), human growth hormone, luteinising hormone, hydrocortisone, and pituitary prolactin. T.S.H. levels reached peak values 20 to 40 minutes after the injection. Hydrocortisone, H.G.H., and L.H. did not exhibit any systematic variation. The T.R.H. injection was followed within 5 minutes by a release of prolactin, with a peak value at 10 minutes. These data indicate a lack of specificity of T.R.H. and suggest that in man it acts as a prolactin-releasing factor. Intravenous T.R.H. administration should become a very useful clinical test for the investigation of the hypothalamo-pituitary relationships, with special respect to prolactin secretion.

Cytotoxic effects of iodide on thyroid cells: Difference between rat thyroid FRTL-5 cell and primary dog thyrocyte responsiveness

In order to investigate whether the cytotoxic effect of iodide observed in the thyroid gland represented an apoptotic phenomenon, in vitro experiments were performed using the FRTL-5 thyroid cell line and dog thyrocytes in primary culture. These cells were exposed to iodide under various incubation conditions. Apoptosis was assessed through the analysis of DNA breakdown, i.e. the electrophoresis of internucleosomal DNA fragments generating a typical “ladder” and quantification of prelabelled DNA cleavage products. The FRTL-5 cells appeared to be sensitive only to high doses of iodide, far in excess of physiological levels. They exhibited the different characteristics of two different cell death phenomena: apoptosis and necrosis. The toxicity of iodide appeared to be partially relieved by anti-thyroid agents. This effect constitutes an additional example of the general paradigm of iodide action through oxidized intermediates. In contrast dog thyrocytes in primary culture did not appear to be sensitive to iodide under similar incubation conditions; species differences and/or types of culture could account for these discrepant effects.

Thyrotrophin, prolactin and growth hormone responses to TRH in barbiturate coma and in depression

The effects of 200 μg thyrotrophin‐releasing hormone (TRH) i.v. on thyrotrophin (TSH), prolactin (PRL), growth hormone (GH) and triiodothyronine (T3) were studied in eight patients with barbiturate coma due to attempted suicide, in the same patients after recovery, in eight depressive patients and in eight normal controls. The patients with barbiturate coma presented normal basal TSH and PRL, elevated basal GH and normal PRL but blunted TSH responses to TRH; their GH concentrations varied widely without consistent relation to TRH administration. The same patients after recovery from coma presented normal TSH and PRL, slightly elevated basal GH, and normal PRL but blunted TSH responses to TRH; in four of these patients, a clear‐cut rise in GH (i.e. more than 10 ng/ml) occurred after TRH administration. The depressive patients presented normal basal TSH and PRL, slightly elevated basal GH, and normal PRL but blunted TSH responses to TRH; in four of these patients, a moderate rise in GH (less than 10 ng/ml) occurred after TRH administration. The increment in T3 concentrations 120 min after TKH was found reduced in the comatose patients only. Basal cortisol was measured in all the subjects and found elevated in the comatose patients only. It is concluded that the abnormal TSH and GH responses to TRH observed in patients with barbiturate coma are more likely related to depressive illness than to an effect of barbiturates at the pituitary level. Barbiturates might affect thyroid secretion.

Rythmes neuroendocriniens dans les dépressions uni- et bipolaires

Eighteen patients with major depressive disorder of the endogenous subtype (8 unipolars and 10 bipolars) were submitted to blood sampling at 15 min interval for 24 h with polygraphic sleep recording during an acute episode of depression. Plasma growth hormone (GH), adrenocorticotrophin (ACTH) and cortisol were measured in each sample. The depressed patients hypersecreted GH during the daytime and had hypercortisolism which was evident throughout the 24 h span. The nadir of ACTH and cortisol rhythms was advanced by an average of 3 h as compared to the timing observed in normal subjects. These abnormalities were more pronounced and more consistent in patients with unipolar rather than bipolar depression. These results are consistent with the hypothesis that disorders of circadian time-keeping may characterize major endogenous depression.