Effect of Diethylstilbestrol on the Binding of Thyroxine in Serum*†

Dowling, J. Thomas; Freinkel, Norbert; Ingbar, Sidney H.

doi:10.1210/jcem-16-11-1491

Cited by 140 publications

(32 citation statements)

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“…This is well illustrated in the euthyroid pregnant subjects with the characteristic elevation of PBI attributable to increased TBG concentration (1,(17)(18)(19)(20)(21)(22)(23)(24), but a low per cent free thyroxine, giving a computed free thyroxine iodine concentration in the low normal range. It is considered likely that the physiological activity of thyroxine depends upon the concentration of unbound hormone.…”

Section: Methodsmentioning

confidence: 74%

Free thyroxine in human serum: simplified measurement with the aid of magnesium precipitation.

Sterling¹,

Brenner²

1966

J. Clin. Invest.

407

110

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Section: Methodsmentioning

confidence: 74%

Free thyroxine in human serum: simplified measurement with the aid of magnesium precipitation.

Sterling¹,

Brenner²

1966

J. Clin. Invest.

407

110

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“…Eumetabolic subjects. Previously described effects of large doses of estrogen on PBI (13,18) and on the binding activity of TBG (13) Certain data suggest that estrogens may directly influence cellular oxidative metabolism and its response to thyroid hormone. While estrogens generally stimulate genital structures, several estrogens have been found to depress oxygen consumption of homogenates of rat brain (20) and liver (21), and of fresh rat liver mitochondria incubated with Krebs' cycle intermediates and diphosphopyridine nucleotide (22).…”

Section: Resultsmentioning

confidence: 95%

“…has been necessary to assess the effects of alterations in thyroxinebinding induced by pharmacological means. Large doses of estrogen have been shown to induce pronounced increases in the thyroxine-binding activity of TBG (13), with little or no change in the binding activity of TBPA (14). The present studies concern the effects of estrogens and of the increase in thyroxine-binding by TBG which they induce on the peripheral metabolism of thyroxine in patients with diverse states of thyroidal function.…”

mentioning

confidence: 99%

The Effect of Estrogens Upon the Peripheral Metabolism of Thyroxine *†

Dowling¹,

Freinkel²,

Ingbar³

1960

J. Clin. Invest.

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In plasma, thyroxine is avidly bound to specific proteins present in low concentration, particularly the so-called thyroxine-binding globulin (TBG) and thyroxine-binding pre-albumin (TBPA) (1-4). Several observations indicate that such protein-hormone interactions are of physiological importance. In vitro, the ability of cellular systems to accumulate thyroxine from suspending media is conditioned by the thyroxine-binding potency of the proteins within the media (5, 6). In addition, the volume of distribution and rate of turnover of thyroxine in vivo resemble those of certain plasma proteins (7, 8)'. Finally, abnormal thyroxine-binding by TBG and TBPA has been observed in a variety of states in which the peripheral metabolism of thyroid hormone is disturbed (9-12). It therefore seemed possible that interactions with plasma proteins might in part regulate the peripheral utilization and degradation of thyroxine.An ideal test of this hypothesis would be provided by studies of hormonal metabolism performed before and during the administration of large quantities of purified binding protein. However, adequate quantities of these materials are not yet available. Therefore, it. has been necessary to assess the effects of alterations in thyroxinebinding induced by pharmacological means. Large

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“…The existence of a protein-binding system for tetrahydrocortisone, as yet undescribed, which may be influenced by the administration of estrogens, should be considered. There is evidence for a diversity of protein-binding systems affected by estrogens in the reported increases in thyroid-binding globulin induced by the administration of diethylstilbestrol (21).…”

Section: Methodsmentioning

confidence: 99%

Studies on the Mechanism of the Plasma 17-Hydroxycorticosteroid Elevation Induced in Man by Estrogens*

Wallace¹,

Carter²

1960

J. Clin. Invest.

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The administration of estrogens to man produces sustained elevation above normal levels of plasma (1, 2). The elevated levels of plasma 17-OHCS are associated with an augmented response of plasma levels of these steroids to exogenous adrenocorticotropic hormone (ACTH) and with a marked delay in the rate of clearance of exogenous cortisol from plasma (2). The last trimester of pregnancy is associated with similar changes in levels of plasma 17-OHCS and in their response to exogenous ACTH (3-9). In the last trimester of pregnancy there is a variable increase in urinary 17-OHCS excretion, a decrease in the rate of clearance of exogenous cortisol from plasma (9-11), a decrease in the rate of clearance of exogenous tetrahydrocortisone from plasma (11) and an increase in corticosteroid-binding protein (12). The apparently normal adrenal status of pregnant women and of patients treated with estrogens for long periods of time suggests that the administration of estrogens to man elevates plasma 17-OHCS levels by altering the normal metabolism of endogenous cortisol by a mechanism similar to that seen in pregnancy. Studies have been made of urinary 17-OHCS excretion, of clearance of tetrahydrocortisone from plasma, and of plasma corticosteroid-binding protein after the administration of estrogens to man. MATERIALS AND METHODSThe patients studied were primarily adult females ranging in age from 37 to 75 years, all of whom either had been surgically castrated or were at least 3 years past a spontaneous menopause. A number of these subjects were patients with metastatic carcinoma of the * This work was supported in part by a research grant from The National Cancer Institute, Bethesda, Md. breast. One male was studied during recovery from a myocardial infarction.After appropriate control studies, the patients were treated for periods of 2 weeks to 6 months with either oral ethinyl estradiol (Estinyl), diethylstilbestrol or conjugated equine estrogens (Premarin). Only doses of these preparations which uniformly elevated plasma 17-OHCS levels above normal were used in the studies (Table I). Ethinyl estradiol 0.1 and 0.5 mg, diethylstilbestrol 15 mg, and Premarin 10 mg, daily by mouth, all caused significant increases in the levels of plasma 17-OHCS.The effect of oral ethinyl estradiol, 0.5 mg daily, on urinary excretion of free and total 17-OHCS and of 17-ketosteroids was studied. Twenty-four hour urinary excretion of steroids was determined in each patient before estrogen therapy and again after plasma 17-OHCS

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Effect of Diethylstilbestrol on the Binding of Thyroxine in Serum*†

Cited by 140 publications

References 0 publications

Free thyroxine in human serum: simplified measurement with the aid of magnesium precipitation.

Free thyroxine in human serum: simplified measurement with the aid of magnesium precipitation.

The Effect of Estrogens Upon the Peripheral Metabolism of Thyroxine *†

Studies on the Mechanism of the Plasma 17-Hydroxycorticosteroid Elevation Induced in Man by Estrogens*

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