Study of urinary 17-ketosteroids in hyperthyroidism and hypothyroidism

Abstract

In hyperthyroidism, urinary 17-ketosteroids are in the lower limit of the normal value or low, and 17-hydroxycorticosteroids are normal or slightly increased. These data are widely accepted but the cause of the dissociation of these data is based on conjecture.The author tried to clarify this dissociation with hormonal examinations as follows : 1. Urinary 17-KS were measured by Holtorff-Koch and var. Masuda's method. 2. Microscale liquid column chromatography by Edwards and var. Ohno's method. 3. Urinary 17-OHCS were hydrolyzed by bacterial beta-glucuronidase and measured by Porter-Silber's reaction. 4. Plasma 17-OHCS by var. Silber-Porter's method. 5 Urinary gonadotropin by the mouse uterine weight method. 6. ACTH-test by I. V. dripping of 25 units of ACTH for 6 hrs., and GTP-test by I.M. injection three to five times a day of Gonagenforte (Gonadotropin protamin) every three days.In hyperthyroidism, urinary 17-KS were almost in the lower limit of the normal value or low but 17-OHCS in urine and blood were normal. GTP in urine were more than normal, but the chromatography of urinary 17-KS disclosed decreased androgenic 17-KS in more than half of the cases. In androgenic, 17-KS androsterone increased and etiocholanolone decreased. ACTH-test revealed increased urinary 17-KS, 17-OHCS, and androgenic 17-KS with normal response, though plasma 17-OHCS responded poorly in some cases. Urinary 17-KS and 17-OHCS measured by GTP-test were in the range of daily variation, and androgenic 17-KS did not increase.Urinary 17-KS returned almost to normal value, and chromatography showed almost normal pattern after treatment.In hypothyroidism, urinary 17-KS and 17-OHCS decreased remarkably and 17-OHCS in blood were normal. Urinary GTP and androgenic fraction of urinary 17-KS were both low. In androgenic 17-KS androsterone decreased and etiocholanolone increased. These data were opposite of hyperthyroidism. After treatment, urinary 17-KS and 17-OHCS returned almost to normal level and androsterone increased.From these data I presume that in hyperthyroidism, over-secreted thyroxin supresses the reactivity of the gonadal tissue and adrenal glands to GTP and so the response of the adrenal gland to GTP decreases as compared to the response to ACTH and these factors cause the decrease of urinary 17-KS especially of the androgenic fraction. I also presume that in hypothyroidism, because of the decreased removal rate of steroid, plasma 17-OHCS are normal but urinary 17-KS, 17-OHCS become low, and that the decrease of GTP causes less production of androgenic 17-KS.Thyroxin effects to metabolic changes of androgenic 17-KS in the peripheral tissues mainly in liver, and so in hyperthyroidism androsterone increases and in hypothyroidism decreases.