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At least 19 recordsLinked to original sources
PubMed1977

Evaluation of serum triiodothyronine and adjusted triiodothyronine (free triiodothyronine index) in pregnancy.

We measured serum thyroxine (free and total), triiodothyronine (free and total), thyroxine-binding globulin, and triiodothyronine uptake by talc in 97 normal men and 50 pregnant women. Mean serum thyroxine and triiodothyronine concentrations were higher in the pregnant subjects (104 vs. 78 mug/liter and 1.69 vs. 1.30 mug/liter) because of a higher mean thyroxine-binding globulin concentration (70 vs. 38 mg/liter). Mean triiodothyronine uptake by talc was lower in the pregnant subjects (0.82 vs. 1.03). Mean free thyroxine concentrations were similar in the two groups, but mean free triiodothyronine concentrations were 10% lower in the pregnant subjects. Triiodothyronine uptake by talc and the diayzable thyroxine and triiodothyronine fractions were highly correlated (r = 0.85 and r = 0.82, P less than 0.001). Calculated free thyroxine index and free triiodothyronine index values (hyroxine and triiodothyronine indirectly adjusted, using triiodothyronine talc uptake to compensate for differences in thyroxine-binding globulin concentration), were statistically similar (84 vs. 82 and 1.38 vs. 1.34) in pregnant and male subjects. The results indicate that the total triiodothyronine concentration can be normalized on the basis of the triiodothyronine uptake by talc to correct for variations in thyroxine-binding globulin concentration.

Adolescent↗
PubMed1978

Contributions of plasma triiodothyronine and local thyroxine monodeiodination to triiodothyronine to nuclear triiodothyronine receptor saturation in pituitary, liver, and kidney of hypothyroid rats. Further evidence relating saturation of pituitary nuclear triiodothyronine receptors and the acute inhibition of thyroid-stimulating hormone release.

Injections of triiodothyronine (T(3)) and thyroxine (T(4)) into chronically hypothyroid rats were used to evaluate the contribution of intracellular T(4) to T(3) conversion to nuclear T(3) in pituitary, liver, and kidney, and to correlate the occupancy of pituitary nuclear T(3) receptors with inhibition of thyroid-stimulating hormone (TSH) release. Injection of a combination of 70 ng T(3) and 400 ng T(4)/100 g body wt resulted in plasma T(3) concentrations of 45+/-7 ng/dl (mean+/-SD) and 3.0+/-0.4 mug/dl T(4) 3 h later. At that plasma T(3) level, the contribution of plasma T(3) to the nuclear receptor sites resulted in saturation of 34+/-7% for pituitary, 27+/-5% for liver, and 33+/-2% for kidney. In addition to the T(3) derived from plasma T(3), there was additional T(3) derived from intracellular monodeiodination of T(4) in all three tissues that resulted in total nuclear occupancy (as percent saturation) of 58+/-11% (pituitary), 36+/-8% (liver), and 41+/-11% (kidney), respectively. The percent contribution of T(3) derived from cellular T(4) added 41% of the total nuclear T(3) in the pituitary which was significantly higher than the contribution of this source in the liver (24%) or the kidney (19%). 3 h after intravenous injection of increasing doses of T(3), the plasma T(3) concentration correlated well with both the change in TSH and the nuclear occupancy, suggesting a linear relationship between the integrated nuclear occupancy by T(3) and TSH release rate. The contribution of intrapituitary T(4) to T(3) conversion to nuclear T(3) was accompanied by an appropriate decrease in TSH, supporting the biological relevance of nuclear T(3). Pretreatment of the animals with 6-n-propylthiouracil before T(4) injection decreased neither the nuclear T(3) derived from intrapituitary T(4) nor the subsequent decrease in TSH. These results indicate that intracellular monodeiodination of T(4) contributes substantially to the nuclear T(3) in the pituitary of the hypothyroid rat, and suggest a linear inverse relationship between nuclear receptor occupancy by T(3) in the pituitary and TSH release rate. The data further indicate that T(4) to T(3) monodeiodination is considerably more important as a source of nuclear T(3) in the pituitary than in the liver and kidney. This provides a mechanism whereby the TSH secretion could respond promptly to a decrease in thyroid secretion (predominantly T(4)) before a decrease in plasma T(3) would be expected to lead to significant metabolic hypothyroidism.

Animals↗
PubMed1977

No inhibition by Li+ of thyroxine monodeiodination to 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine (reverse triiodothyronine).

The possibility that lithium affects the conversion of thyroxine to 3,5,3"-triiodothyronine and 3,3',5'-triiodothyronine (reverse triiodothyronine) was studied by measurement of the serum concentractions of these parameters in five patients during the first week of lithium therapy. In three patients there was a decrease in serum thyroxine concentration and a slightly less pronounced decrease in that of serum 3,5,3'-triiodothyronine. In two patients, who also received L-tryptophan or flupentixol, no change was noted in the concentrations of these compounds. There was no increase in serum 3,3',5'-triiodothyronine concentration in any of the patients. No systematic change was found in the serum concentrations of thyrotropin or unsaturated thyroid-hormone binding proteins. The results obtained do not support the contention that lithium should inhibit the monodeiodenation of thyroxine to its active and inactive metabolites.

Adult↗
PubMed1977

Relation of triiodothyronine and reverse triiodothyronine administration in rats to hepatic L-triiodothyronine aminotransferase activity.

The effects of administration of 3,5,3'-triiodothyronine (T3) to normal and to hypothyroid male rats upon the hepatic activity of L-triiodothyronine aminotransferase were determined using 3,5-dinitro-L-tyrosine as substrate in the assay. Initial studies in normal rats demonstrated that basal enzyme activity was highest in liver and kidney of the organs tested, and that virtually no activity was detectable in skeletal muscle, serum, thyroid or pituitary gland. Hepatic enzyme activity increased from birth to a peak at 80-120 days and declined thereafter. Daily administration of T3 to normal rats in doses of 5 mug/100g BW for 8 days significantly elevated hepatic enzyme activity above normal. In daily doses of 2.5mug/100g BW, T3 restored the depressed enzyme activities in hypothyroid rats to normal. Daily administration of 3,3',5'-triiodothyronine (reverse T3) to normal rats in doses of 17.5 mug/100g BW and greater for 3 days increased L-T3 aminotransferase activity more than 30% above normal levels. Reverse T3 appeared to be approximately as active as T3 in increasing the hepatic activity of L-T3 aminotransferase.

Aging↗
PubMed1978

[Triiodothyronine, reverse-triiodothyronine, thyroxine, resin-triiodothyronine-uptake and protein bound jodide in the fluid of thyroid cysts (author's transl)].

T3, rT3, T4, PBI and the saturation of T3-T4-binding proteins in yellow and brown cyst fluids of nontoxic goiters differ from the values in sera. In the brown cyst fluids, resulting from a hemorrhage, T3, rT3, T4, PBI and T3 U are significantly higher than in sera and no correlation could be found with the values in sera. In the yellow cyst fluids T3 and T3 U are significantly higher then in sera, T4 is lower, PBI and rT3 do not differ from the values in sera. Only T3 and rT3 are not correlated. Various reasons for higher concentrations of hormones in the cyst fluid such as destruction of thyroid follicles and lymphvessels, a high protein concentration and direct secretion of hormones and iodoproteins from thyroid tissue in the cyst wall into the cyst fluid are taken into consideration. As these hormones in the cyst fluid may be absorbed, the results are also of clinical value.

Blood Proteins↗
PubMed1976

Changes of circulating thyroxine, triiodothyronine and reverse triiodothyronine after radiographic contrast agents.

Thyroid function was studied for 42 days in 58 patients, 28 of whome had euthyroid goiter, after urography (diatrizoic acid), cholangiography (ioglycamic acid), and cholecystography (Naiopanoate). After urography and cholangiography short-lived increases of the serum thyroxine occurred in a few patients, but the mean thyroxine and triiodothyronine concentration did not change. By contrast, 7 days after oral cholecystography serum thyroxine had risen consistently by 22% with a concomittant rise of the free thyroxine, while triiodothyronine declined by 15%. The thyroxine metabolite 3,3',5'-triiodo-1-thyronine (reverse T3) rose by 50% and serum thyrotropin concentration doubled. After 42 days thryoxine and triiodothyronine had returned to baseline, and none of the 58 patients developed clinical hyperthyroidism. In patients with severe myxoedema kept on a constant replacement dose with 1-thyroxine NA-iopanoate produced similar changes with the exception of the rise of the serum thyroxine. The primary event after Na-iopanoate seems to be a fall of the serum triiodothyronine, which in turn augments thyrotropin and indirectly thyroxine secretion. the marked and sometimes sustained rose of serum thyroxine after cholecystography may lead to the erroneous diagnosis of hyperthyroidism.

Adult↗
PubMed1977

Extrathyroidal conversion of thyroxine to 3,3',5'-triiodothyronine (reverse-T3) and to 3,5,3'-triiodothyronine (T3) in humans.

In order to estimate the relative magnitude of the two alternative pathways of monodeiodination of thyroxine (T4) in adult humans, the metabolic clearance rates (MCR) and production rates (PR) of 3,3',5'-triiodothyronine (reverse-T3,rT3) and of 3,5,3'-triiodothyronine (T3) were determined in six euthyroid control subjects (C) and in five hypothyroid patients (H) receiving L-T4 as replacement therapy (0.15-0.3 mg/day). MCR was computed by a non-compartmental method of analysis from the plasma disappearance of 125I rT3 and 131I T3 during 72 h following simultaneous injection of tracers. PR was calculated from MCR and the serum concentration of rT3 and T3, respectively, determined by radioimmunoassay. In the H subjects, rT3 MCR averaged 97.1 +/- 12.8 (SD) 1/day and rT3 PR, 34.3 +/- 12.8 microng/day; T3 MCR was 28.7 +/- 6.1 1/day and T3 PR, 20.3 +/- 6.6 microng/day (all corrected to 70 kg body weight). These results were not significantly different from those in the control group; rT3 MCR 104 +/- 24 1/day, rT3 PR 33.0 +/- 9.2 microng/day; T3 MCR 24.0 +/- 5.9, T3 PR 24.2 +/- 4.1. The proportionof total triiodothyronine (rT3 averaged 62% in H patients and was similar (57%) in the C group. The results obtained in the H subjects indicate that the production of rT3 is a major route of T4 metabolism, equal to or exceeding that of T3. From the close agreement between the mean values for rT3 PR in the C and H groups it is concluded that most, if not all of the rT3 produced in normal humans is derived by extrathyroidal conversion from T4.

Aged↗
PubMed1978

The relative distribution of thyroxine, triiodothyronine and 3,3',5'-(reverse)-triiodothyronine in various fractions of thyroglobulin.

Thyroglobulin fractions rich and poor in new thyroglobulin were separated by means of DEAE-cellulose chromatography of dog thyroid extracts and by zonal ultracentrifugation in a sucrose gradient of guinea pig thyroid extract incubated at low temperature. The distrubtion of thyroxine, triiodothyronine and 3,3',5'-(reverse)-triidothyronine in hydrolysates of the different fractions was estimated by radioimmunoassays. Following DEAE-cellulose chromatography there was a small but statistically significant increase in T4/T3 ratio in thyroglobulin fractions eluted at high ionic strength--that is fractions relatively rich in stable iodine but poor in fresh thyroglobulin. There was no differences in the T4/rT3 ratios between the different fractions. The ratios between iodothyronines were almost identical in the various thyroglobulin fractions following zonal ultracentrifugation in a sucrose gradient of cold treated guinea pig thyroid extract. These findings lend no support to the possibility that a relatively high content of triiodothyronines in freshly synthesized thyroglobulin modulates the thyroid secretion towards a preferential secretion of triiodothyronine and 3,3',5'-(reverse)-triidothyronine at the expense of the secretion of thyroxine.

Animals↗
PubMed1979

The effect of suppressive therapy of nontoxic diffuse goiter on serum levels of thyroxine, 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine.

We studied the effect of suppressive therapy with graded doses of thyroxine (T4) on serum levels of T4, 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyronine [rT3] in patients with diffuse, nontoxic goiter. For comparison and in order to elucidate the degree of suppression of the pituitary thyroid axis by T3 the effect of suppressive therapy with T3 was studied in the same type of patients. We found that T4 in serum rose significantly to a constant level during T4 treatment (0.10, 0.15 and 0.20 mg/day). Dose-related rises in T4 were only seen after 3 months of treatment. T3 and rT3 only changed minimally. The T4/T3 ratio rose to a constant level during the initial 3 months of treatment. T3/rT3 ratio remained unchanged. No dose-related differences in T4/T3 and T3/rT3 ratio were observed. Treatment with T3 in doses of 0.06 mg per day caused a significant but slow fall in T4 and rT3 to hypothroid levels while T3 only rose slightly. The T4/T3 ratio dropped significantly during T3 therapy.

Adult↗
PubMed1978

L-triiodothyronine and L-reverse-triiodothyronine generation in the human polymorphonuclear leukocyte.

Extrathyroidal monodeiodination of l-thyroxine (T(4)) is the principal source of l-triiodothyronine (T(3)) and l-reverse-triiodothyronine (rT(3)) production. To define some of the cellular factors involved, we examined T(3) and rT(3) generation from added nonradioactive T(4) in human polymorphonuclear leukocytes, using radioimmunoassays to quantify the T(3) and rT(3) generated. Under optimum incubation conditions which included a pH of 6.5 in sucrose-acetate buffer, the presence of dithiothreitol as a sulfhydryl-group protector, and incubation in an hypoxic atmosphere, significant net generation of T(3) and rT(3) was observed. Of the several subcellular fractions studied, the particulate fraction obtained by centrifugation at 27,000 g was found to possess the highest T(3)- and rT(3)-generating activities per unit quantity of protein. With respect to T(3) generation from substrate T(4), the K(m) was 5 muM and the V(max) was 7.2 pmol/min per mg protein. Propylthiouracil, methimazole, and prior induction of phagocytosis inhibited both T(3) and rT(3) generation, but T(3) generation was inhibited to a greater extent. rT(3), in a concentration equimolar to that of substrate T(4), did not alter T(3) generation, but inhibited T(3) generation when the molar ratio of rT(3) to T(4) approached 10:1. Under the incubation conditions employed, particulate fractions of leukocytes obtained from five cord blood samples displayed an essentially normal relationship between T(3)- and rT(3)-generating activities, despite the distinctly divergent serum T(3) and rT(3) concentrations in these samples. From our findings, we draw the following conclusions: (a) the human polymorphonuclear leukocyte possesses the ability to generate T(3) and rT(3) from substrate T(4); (b) the T(3)- and rT(3)-generating activities are associated principally with the 27,000 g particulate fraction and display enzymic characteristics with a sulfhydryl-group requirement; (c) T(3)-generating activity appears to be more susceptible to inhibitory influences than rT(3)-generating activity; and (d) in cord blood leukocytes, the putative enzymes catalyzing T(3) and rT(3) generation appear to be functionally intact under the experimental conditions employed.

Adult↗
PubMed1979

Effect of a single dose of glucocorticoid on the diurnal variations of TSH, thyroxine, 3,5,3'-triiodothyronine, 3,3'5'-triiodothyronine and cortisol in normal men.

Plasma thyrotropin (TSH) and cortisol concentrations were suppressed immediately after an intravenous bolus dose of 8 mg betamethasone in 6 male subjects. The circadian variations of these hormones disappeared for 40 hr (TSH) and 44 hr (cortisol). Plasma thyroxine (T4), 3, 5, 3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3) levels did not show diurnal variations before betamethasone administration. Plasma T3 levels decreased to 66% of the basal levels 20 hr after batamethasone administration, whereas plasma reverse T3 levels increased to 163% of the basal levels at 24 hr. These changes were reversed by 3 to 5 days after betamethasone. The earlier recovery of the diurnal rhythm of TSH than that of cortisol suggests that the TSH rhythm is not under the direct control of circulating cortisol.

Adult↗
PubMed1978

Urinary excretion of thyroxine, triiodothyronine, 3,3',5'-triiodothyronine (reverse T3) and renal function in human newborns.

The urinary excretion and serum levels of thyroxine (T4), triiodothyronine (T3) and 3,3',5'-triiodothyronine (reverse T3) was estimated in a longitudinal study of human newborns. The maternal and cord blood was also studied. Neonatal renal function was evaluated using endogenous creatinine clearance. In cord blood serum T3 was found to be lower than in maternal blood, but reverse T3 highly elevated. During the first 5 days of life serum T4 and T3 increased with maximum at 48 and 24 h in contrast to reverse T3 which remained high and then declined rapidly after 4 days. Creatinine clearance during the first 3 days of life increased from 5.3 to 21.9 ml/min/1.73 m2. In the same period the urinary T4 excretion increased from 79 to 281 ng/24 h, urinary T3 excretion from 16 to 44 ng/24 h and urinary reverse T3 from 4 to 15 ng/24 h. The renal excretion of thyroid hormones, corrected for body surface, was decreased compared to adult controls, corresponding to an immature renal function. The lack of ability to excrete thyroid hormones involved primary T3 and reverse T3 suggesting particular immaturity of tubular secretion of these hormones during the neonatal period.

Adult↗
PubMed1979

Effect of ACTH-stimulated glucocorticoid hypersecretion on the serum concentrations of thyroxine-binding globulin, thyroxine, triiodothyronine, reverse triiodothyronine and on the TSH-response to TRH.

The responses of serum concentrations of TSH, thyroxine (T4), triiodothyronine (T3) and of reverse triiodothyronine (rT3) to i. v. administration of 0.4 mg THR were examined prior to (and after) i. m. administration of ACTH (2 mg Synacthen Depot) in 7 euthyroid women using estrogen-containing oral contraceptives and in 8 controls, with the following results: (1) an increase in endogenous glucocorticoid secretion is associated with a depression of the TSH response to TRH; (2) TSH formed in decreased amounts is still capable of stimulating thyroid secretion; (3) the increased serum corticoid levels fail to affect the secretory response of the thyroid to TSH; (4) control of the pituitary-thyroid axis remains normal in the presence of increased serum thyroxine-binding globulin (TBG) levels. In a further series the serum levels of TBG, T4, T3, rT3 and cortisol under the effect of ACTH-induced endogenous glucocorticoid hypersecretion were studied in 6 normal untreated controls, in 6 normal women using oral contraceptives and in 10 untreated hyperthyroid patients. During four days subsequent to treatment the serum TBG levels decreased, maximum decrease being found in the users of oral contraceptives, minimum decrease in the controls. Serum T4 was found to decrease during 2 to 4 days, serum T3 parallel with an increase in serum rT3, for 1 to 2 days, subsequent for ACTH loading. In the euthyroid cases also the serum TSH levels showed a transitory decline. It is concluded that in case of endogenous hyperproduction of glucocorticoids (1) T4 leads to T3 monodeiodination decreases and T4 leads to rT3 conversion increases parallel with the changes in the serum cortisol levels; (2) TBG synthesis is inhibited by endogenous glucocorticoids; (3) the changes in serum TBG levels are accompanied by a decrease in the serum T4 concentrations.

Adrenocorticotropic Hormone↗
PubMed1979

Effect of insulin-induced hypoglycemia on the serum concentrations of thyroxine, triiodothyronine and reverse triiodothyronine.

The effect of insulin-induced hypoglycemia on serum thyroid hormone concentrations was studied in nine healthy individuals. Before, during and after the hypoglycemia blood samples were taken for measurement of the concentrations of glucose, thyroxine (T(4)), triiodothyronine (T(3)), reverse triiodothyronine (rT(3)), catecholamines and pituitary hormones.There was no change in the mean serum T(4) level (+/- the standard error of the mean) of 67 +/- 2 mug/l. However, the T(3) concentrations rose from a mean basal level of 1.86 +/- 0.06 mug/l to a mean peak of 2.51 +/- 0.21 mug/l (P < 0.01) at 45 minutes after the insulin injection, and the rT(3) concentrations fell from a mean basal level of 0.184 +/- 0.008 mug/l to a mean nadir of 0.171 +/- 0.022 mug/l (not a significant change). The mean peak epinephrine level was 545 +/- 103 ng/l and it occurred between 30 and 45 minutes after the insulin injection; the mean peak norepinephrine level was 584 +/- 114 ng/l and it occurred between 30 and 90 minutes after the injection. The growth hormone levels reached a mean peak of 26.1 +/- 4.8 mug/l and the plasma cortisol levels rose to 215 +/- 9 mug/l. The mean basal prolactin level was 8.5 +/- 0.9 mug/l; in five subjects there was a rise to a mean peak of 50.6 +/- 14.6 mug/l, whereas in the remaining four no significant increase occurred. No correlation was found between the changes in the serum T(3) concentration and any of the other factors studied.It was concluded that acute hypoglycemia is associated with a rapid increase in the serum T(3) concentration.

Adult↗
PubMed1977

Divergent changes of serum 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine in patients with acute myocardial infarction.

The serum levels of thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3, rT3), thyroxine-binding globulin and thyroid-stimulating hormone have been monitored in 13 patients with acute myocardial infarction. The major changes recorded were a transient decrease in T3 and a transient increase in rT3. They reached a nadir and a peak, respectively, within three days. A conceivable explanation for these alterations is that the monodeiodination of T4 is diverted from the activating pathway (T4 to T3) to the inactivating pathway (T4 to rT3).

Acute Disease↗
PubMed1977

Effects of dexamethasone, desoxycorticosterone, and ACTH on serum concentrations of thyroxine, 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine.

The effects of a pure glucocorticoid, dexamethasone, and a pure mineralocorticoid, desoxycorticosterone, on the serum concentrations of thyroxine (T4), 3,5,3'-triiodothyronine (T3), and 3,3',5'-triiodothyronine (reverse T3, rT3) were compared both in healthy subjects and in athyreotic T4-substituted patients. In addition, the effect of exogenous ACTH was examined in healthy subjects. Both in healthy subjects and in T4-substituted athyreotic patients, administration of a single oral dose of dexamethasone caused a rapid and sharp decrease in the serum concentration of T3, and a corresponding increase in the serum concentration of rT3. The T4 concentration was not changed. A single oral dose of desoxycorticosterone evoked no significant changes in the serum concentrations of T3, rT3, or T4 either in healthy subjects or in T4-substituted athyreotic patients. Like dexamethasone, ACTH (two i.v. injections of 60 IU each, at a 6-hour interval) evoked a serum T3 reduction and a serum rT3 increase. Hence, it appears that both endogenous and exogenous glucocorticoids, but not mineralocorticoids, may partially divert the deiodination of T4 from the activating (T4 lead to T3) to the inactivating (T4 leads to rT3) pathway.

Adrenal Cortex Hormones↗
PubMed1976

Effect of amiodarone on serum triiodothyronine, reverse triiodothyronine, thyroxin, and thyrotropin. A drug influencing peripheral metabolism of thyroid hormones.

2-n-Butyl-3-(4'-diethylaminoethoxy-3',5'-diiodobenzoyl)-benzofurane (amiodarone), a drug used in arrythmias and angina pectoris, contains 75 mg of organic iodine/200 mg active substance. Four studies were performed to test its effect on thyroid hormone metabolism: (a) nine male subjects were treated with 400 mg of amiodarone for 28 days; (b) five male subjects received, for the same period of time, 150 mg of iodine in the form of Lugol's solution; (c) five subjects received 300 mug L-thyroxine (T4) for 16 days; from the 10th to the 16th day, 400 mg of amiodarone was added; and (d) five euthyroid subjects received 300 mug L-T4 for 16 days. The changes in serum thyroid-stimulating hormone (TSH), serum total T4, 3,5,3'-triiodothyronine (T3), free T3, and 3,5',3'-triiodothyronine (reverse T3, rT3) were measured, and the pituitary reserve in TSH was evaluated by a thyrotropin-releasing hormone (TRH) test. The results show that amiodarone induced a decrease in serum T3 (28+/-5.1 ng/100 ml, mean+/-SEM, P less than 0.0S and 82.7+/-9.3 ng rT3/100 ml, P less than 0.01). The control study with an equal amount of inorganic iodine did not induce these opposite changes but slightly lowered serum rT3, T3, and T4. In the third study, serum rT3 increased as under amiodarone treatment, thereby proving that these changes were peripheral. It is suggested that amiodarone changes thyroid hormone metabolism, possibly by reducing deiodination of T4 to T3 and inducing a preferential production of rT3. Amiodarone also increased the response of TSH to TRH. The maximal increment of serum TSH above base line was 32+/-4.5 muU/ml under treatment and 20+/-3 muU/ml before treatment (P less than 0.01). During this test, the serum T3 increase was more pronounced than during the control period (83+/-13 and 47+/-7.4 ng/100 ml, P less than 0.05).

Adult↗