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PubMed1989

Kinetics of triiodothyronine uptake by erythrocytes in hyperthyroidism, hypothyroidism, and thyroid hormone resistance.

We studied the initial uptake of L-T3 in erythrocytes isolated from normal subjects and patients with abnormal thyroid function. The uptake was saturable, with a mean maximum velocity (Vmax) of 3.60 pmol/min.10(8) cells and a Km of 248 nmol/L in normal subjects. Women had a somewhat lower Km but a similar Vmax compared to those in men. The Vmax was increased in patients with hyperthyroidism and decreased in those with hypothyroidism. Successful treatment lowered the initially high Vmax in hyperthyroid patients and raised the low Vmax in hypothyroid patients. One subject with the rare syndrome of thyroid hormone resistance had a Vmax in the upper normal range. The mean Km values of the hyperthyroid and hypothyroid groups and of the subject with thyroid hormone resistance were similar to that of the normal subjects. The results indicate that the initial saturable uptake of T3 by the human erythrocyte is increased in hyperthyroidism and decreased in hypothyroidism.

Adult↗
PubMed1990

Fructose-6-phosphate cycling and the pentose cycle in hyperthyroidism.

Hepatic fructose-6-phosphate (fructose-6-P) cycling and pentose cycle activity were quantified in hyperthyroid patients. A measure of the fructose-6-P cycle was the incorporation of 14C, on administering [3-3H,6-14C]galactose, into carbon 1 of blood glucose and the 3H/14C ratio in blood glucose. The measure of the pentose cycle was the randomization of 14C to carbon 1 of blood glucose on administering [2-14C]galactose. [2-3H]Galactose was also administered, so the 3H/14C ratio in blood glucose measured the extent of equilibration of glucose-6-P with fructose-6-P. Patients given [3-3H,6-14C]galactose were restudied when euthyroid. Of the 14C from [3-3H,6-14C]galactose, 7.7-9.5% was in carbon 1 of glucose in both states. 3H/14C ratios were also the same in both states. Fructose-6-P cycling was estimated to be 13 +/- 1% the rate of glucose turnover in the euthyroid and 15 +/- 1% that in the hyperthyroid state. The pentose cycle contributed about 2% to glucose utilization, similar to previous estimates in healthy humans. As in healthy individuals, about 25% of 3H was retained in the conversion of [2-3H]glucose-6-P to glucose. Thus, the fractions of glucose turnover participating in hepatic fructose-6-P and pentose cycling are similar in hyperthyroid and healthy subjects. As a result, augmented fructose-6-P cycling does not substantially contribute to increased hepatic oxygen consumption in hyperthyroidism.

Adult↗
PubMed1991

Serum osteocalcin in patients taking L-thyroxine who have subclinical hyperthyroidism.

Serum osteocalcin, an index of osteoblastic activity, is increased in hyperthyroidism. Serum osteocalcin levels are negatively correlated with bone density in patients with overt hyperthyroidism. Osteocalcin levels are also elevated in patients with multinodular goiter and subclinical hyperthyroidism. We therefore measured serum osteocalcin levels in patients taking T4 to determine if they correlated with the degree of TSH suppression. Despite an upward trend in serum osteocalcin measurements with decreasing TSH concentrations, there was no significant difference in serum osteocalcin among groups of patients with normal (0.5-5.0 mu/L), mildly reduced (0.1-0.5 mU/L), or undetectable serum TSH (less than 0.01 mU/L). However, a weak negative correlation was seen between serum TSH and osteocalcin concentrations (r = 0.29, slope = -0.28, P less than 0.05). Osteocalcin did not correlate with either serum free T4 or free T3 concentrations. Serum PTH concentrations were not different among the three patient groups. Our data suggest that osteocalcin is not a useful clinical marker for increased bone turnover in patients with subclinical hyperthyroidism due to T4 therapy. However, the trend towards higher osteocalcin levels in patients with suppressed serum TSH values, and the weak negative correlation between serum TSH and osteocalcin are consistent with findings of reduced bone density in these patients.

Adult↗
PubMed1991

Enhanced left ventricular diastolic function in hyperthyroidism: noninvasive assessment and response to treatment.

Hyperthyroidism is associated with a marked effect on the cardiovascular system. Despite enhanced resting ventricular systolic performance, thyrotoxicosis has been implicated as a primary cause of cardiomegaly, congestive heart failure, and decreased exercise tolerance. To further assess potential alterations in ventricular function we have noninvasively studied diastolic performance in nine newly diagnosed and untreated hyperthyroid patients. Parameters including diastolic flow velocities, isovolumic relaxation time (IVRT), and the rate of diastolic flow deceleration were compared to those of an age- and sex-matched control population, and then repeat determinations were made after beta-adrenergic blockade and again when the patients were chemically and clinically euthyroid. Before treatment the IVRT was 33.0 ms, which was significantly (P less than 0.005) shorter than the control value (57.9 ms) and in combination with other measures of diastolic function indicated enhanced left ventricular relaxation. beta-Adrenergic blockade slowed the resting heart rate from 97 to 80 beats/min (P less than 0.005) and partially normalized the rate of diastolic deceleration, but had no effect on the IVRT (33.8 ms). When patients were euthyroid, the IVRT was 51.7 ms, and other measures of diastolic performance were the same as those in controls. The current data assessing resting diastolic function in hyperthyroidism are similar to those previously reported for systolic function. Our findings of enhanced cardiac diastolic performance do not support the hypothesis that thyrotoxicosis is associated with compromised left ventricular function and suggest the possibility that the cardiac symptoms that accompany hyperthyroidism may be due to noncardiac mechanisms.

Adult↗
PubMed1992

Effect of administration of thyroxine on the risk of postpartum recurrence of hyperthyroid Graves' disease.

In our previous study, we reported that the administration of T4 to patients with Graves' disease who were under treatment with methimazole (MMI) decreased the level of antibodies to thyroid-stimulating hormone (TSH) receptors and the rate of recurrence of hyperthyroidism. In this study, the effect of T4 administration on the rate of postpartum recurrence of hyperthyroidism was examined. Seventy-eight patients with Graves' disease had been treated with MMI for 1-3 yr before pregnancy, and MMI was discontinued 5-6 months after the onset of pregnancy because the levels of antibodies to TSH receptors decreased during early pregnancy. The patients were then divided into two groups. Group A (n = 40) was given T4 (100 micrograms/day) and group B (n = 38) was not given any drugs from 5 months after the onset of pregnancy until 1 yr after delivery. The levels of the antibodies to TSH receptors and serum concentrations of thyroxine-binding globulin (TBG) and T4 were not different between the two groups before and during pregnancy, although a transient increase in serum T4 and TBG concentrations were observed during the pregnancy in both groups. After delivery, levels of antibodies to TSH receptors increased in both groups. The rate of increase, however, was more rapid in group B than in group A. The levels were significantly higher in group B than A at 3, 6, 9, and 12 months after delivery. Serum T4 and TBG concentrations decreased after delivery in both groups. Serum concentrations of T4 increased after delivery in group B but not in group A. The concentration of T4 was significantly higher in group B than in group A at 9 and 12 months after delivery. Postpartum recurrence of hyperthyroidism was 5.0% in group A and 31.6% in group B, respectively, during the first year after delivery. These results suggest that administration of T4 during pregnancy and after delivery is effective in decreasing the level of antibodies to TSH receptors and to prevent the postpartum recurrence of hyperthyroidism.

Adolescent↗
PubMed1993

Lipoprotein(a) and apolipoprotein B plasma concentrations in hypothyroid, euthyroid, and hyperthyroid subjects.

Overt hypothyroidism is associated with premature coronary artery disease, and this is assumed to be due to a deteriorated metabolism of atherogenic lipoproteins. The effect of thyroid status on plasma concentrations of lipoprotein(a) [Lp(a)], a recently recognized highly atherogenic lipoprotein in man, is unknown. In a cross-sectional study, plasma Lp(a) concentrations were higher in overtly hypothyroid subjects [255 +/- 28 (+/- SD) mg/L; n = 19] and lower in hyperthyroid subjects (75 +/- 28 mg/L; n = 27) compared to those in 54 euthyroid subjects (150 +/- 36 mg/L) and a reference population of local blood bank donors (155 +/- 31 mg/L; n = 114). These findings were confirmed in a follow-up study of 19 hypothyroid and 8 hyperthyroid individuals. In the hypothyroid subjects, initial levo-T4 substitution therapy (25 micrograms daily) caused a 55% decrease in plasma Lp(a) concentrations and a 27% decrease in total plasma apolipoprotein B (apo B). Good agreement was found between the decrease in Lp(a) and apo B at a normal free T4 index. Follow-up of 8 hyperthyroid subjects revealed that their plasma Lp(a) and apo B concentrations significantly increased with return of euthyroidism. In conclusion, good agreement was found between the direction and magnitude of the responses of apo B and Lp(a) to changes in thyroid status. The following findings suggest that different thyroid hormone-dependent mechanisms modulate plasma Lp(a) concentrations in man, in part analogous to modulation of apo B: 1) impaired catabolism in the hypothyroid state, and 2) a combination of suppressed secretion of apoB and Lp(a) with increased catabolism in hyperthyroid subjects. Increased plasma Lp(a) concentrations may contribute to the increased risk of premature coronary artery disease in the hypothyroid state.

Adult↗
PubMed1996

Criteria of cure and follow-up of central hyperthyroidism due to thyrotropin-secreting pituitary adenomas.

The recorded number of patients with central hyperthyroidism due to TSH-secreting pituitary adenoma doubled in the last few years after the introduction of ultrasensitive TSH assays in the assessment of thyroid function; however, information about the results and the criteria for cure after pituitary surgery is scanty. Seventeen patients with a TSH-secreting adenoma, diagnosed on the basis of detectable TSH levels in the face of high free thyroid hormone concentrations and pituitary lesion at neuroimaging, underwent pituitary surgery. Hypersecretion of other pituitary hormones was diagnosed in 5 of 17 patients. Four patients were initially misdiagnosed and treated with thyroid surgery or radioiodine therapy. The majority (86%) of hyperthyroid patients normalized thyroid hormone concentrations and regained euthyroidism, although pituitary imaging, alpha-subunit, and alpha-subunit/TSH molar ratio normalized in only 47%, 54%, and 58% of patients, respectively. Moreover, TSH secretion was normally suppressed by T3 in 40% of the patients. Interestingly, the finding of undetectable TSH levels 7 days after surgery was highly predictive of successful outcome. During long term follow-up, there was one relapse of hyperthyroidism. Early diagnosis of TSH-secreting adenomas permits a high rate of remission of hyperthyroidism after surgery. However, normalization of thyroid function alone does not necessarily reflect complete removal of the tumor, and more comprehensive criteria of cure based on pituitary imaging, hormone measurement, and suppression of TSH during T3 administration should be used. Lastly, all patients need an accurate long term follow-up to monitor the possible recurrence of the adenoma.

Adenoma↗
PubMed1998

Severe congenital hyperthyroidism caused by a germ-line neo mutation in the extracellular portion of the thyrotropin receptor.

Gain of function mutations in the TSH receptor (TSHR) have been identified as the molecular basis for congenital and acquired forms of autonomous thyroid function. Herein, we report the molecular characterization of a case of severe congenital hyperthyroidism with a history of hyperthyroidism in the paternal aunt and the paternal grandmother, who were both found to be heterozygous for a mutation (R528H) located in exon 10 of the TSHR gene. Functional expression of the mutant TSHR-R528H in COS-7 cells, however, did not result in constitutive activity of the TSHR. Subsequent analysis of exons 1-9 led to the detection of an additional heterozygous mutation (S281N) in the patient, but not in other family members. Interestingly, the latter mutation is located in the extracellular domain of the TSHR, and functional studies revealed a marked increase in basal cAMP levels when the mutant receptor was expressed in COS-7 cells. To address the question of whether both mutations were present on the same allele, a double mutant TSHR (S281N/R528H) was generated and characterized. These functional studies in conjunction with RT-PCR analysis of thyroid tissue obtained from subtotal thyroidectomy performed at the age of 6 yr revealed that the patient bears two distinct mutations on different alleles: the familial paternal R528H mutation to be regarded as a polymorphism and a de novo mutation (S281N) on the maternal allele accounting for the clinical picture. Thus, the main conclusions to be drawn from this case are 1) a search for mutations in cases of congenital nonautoimmune hyperthyroidism should not remain restricted to exon 10 of the TSHR gene, because germ-line gain of function mutations of the TSH receptor can be located outside of the transmembrane core of the receptor; and 2) this case illustrates the necessity for careful functional characterization of any novel mutation before a causal relationship to hyperthyroidism can be established.

Alleles↗
PubMed2001

Usefulness of L-carnitine, a naturally occurring peripheral antagonist of thyroid hormone action, in iatrogenic hyperthyroidism: a randomized, double-blind, placebo-controlled clinical trial.

Old studies in animals and unblinded studies in a few hyperthyroid patients suggested that L -carnitine is a periferal antagonist of thyroid hormone action at least in some tissues. This conclusion was substantiated by our recent observation that carnitine inhibits thyroid hormone entry into the nucleus of hepatocytes, neurons, and fibroblasts. In the randomized, double-blind, placebo-controlled 6-month trial reported here, we assessed whether 2 or 4 g/d oral L-carnitine were able to both reverse and prevent/minimize nine hyperthyroidism- related symptoms. We also evaluated changes on nine thyroid hormone-sensitive biochemical parameters and on vertebral and hip mineral density (bone mineral density). Fifty women under a fixed TSH-suppressive dose of L -T(4) for all 6 months were randomly allocated to five groups of 10 subjects each. Group 0 associated placebo for 6 months; groups A2 and A4 started associating placebo (first bimester), substituted placebo with 2 or 4 g/d carnitine (second bimester), and then returned to the association with placebo. Groups B2 and B4 started associating 2 and 4 g/d carnitine for the first two bimesters, and then substituted carnitine with placebo (third bimester). Symptoms and biochemical parameters worsened in group 0. In group A, symptoms and biochemical parameters worsened during the first bimester, returned to baseline or increased minimally during the second bimester (except osteocalcin and urinary OH-proline), and worsened again in the third bimester. In group B, symptoms and biochemical parameters (except osteocalcin and urinary OH-proline) did not worsen or even improved over the first 4 months; they tended to worsen in the third bimester. In both the A and B groups, the two doses of carnitine were similarly effective. At the end of the trial, bone mineral density tended to increase in groups B and A (B > A). In conclusion, L-carnitine is effective in both reversing and preventing symptoms of hyperthyroidism and has a beneficial effect on bone mineralization. Because hyperthyroidism depletes the body deposits of carnitine and since carnitine has no toxicity, teratogenicity, contraindications and interactions with drugs, carnitine can be of clinical use.

Administration, Oral↗
PubMed2006

Differential effects of experimental and cold-induced hyperthyroidism on factors inducing rat liver oxidative damage.

Thyroid hormone-induced increase in metabolic rates is often associated with increased oxidative stress. The aim of the present study was to investigate the contribution of iodothyronines to liver oxidative stress in the functional hyperthyroidism elicited by cold, using as models cold-exposed and 3,5,3'-triiodothyronine (T3)- or thyroxine (T4)-treated rats. The hyperthyroid state was always associated with increases in both oxidative capacity and oxidative damage of the tissue. The most extensive damage to lipids and proteins was found in T3-treated and cold-exposed rats, respectively. Increase in oxygen reactive species released by mitochondria and microsomes was found to contribute to tissue oxidative damage, whereas the determination of single antioxidants did not provide information about the possible contribution of a reduced effectiveness of the antioxidant defence system. Indeed, liver oxidative damage in hyperthyroid rats was scarcely related to levels of the liposoluble antioxidants and activities of antioxidant enzymes. Conversely, other biochemical changes, such as the degree of fatty acid unsaturation and hemoprotein content, appeared to predispose hepatic tissue to oxidative damage associated with oxidative challenge elicited by hyperthyroid state. As a whole, our results confirm the idea that T3 plays a key role in metabolic changes and oxidative damage found in cold liver. However, only data concerning changes in glutathione peroxidase activity and mitochondrial protein content favour the idea that dissimilarities in effects of cold exposure and T3 treatment could depend on differences in serum levels of T4.

Animals↗
PubMed1980

Assessment of cardiac reserve in patients with hyperthyroidism.

Radionuclide multigated cardiac imaging was performed to assess functional cardiac reserve in patients with hyperthyroidism. In 11 normal individuals, submaximl supine exercise increased heart rate (HR) by 60 percent, systolic blood pressure (BP) by 54 percent, and the left ventricular ejection fraction (LVEF) by 13 percent. All of these increments were statistically significant (p < 0.001). Eight patients with hyperthyroidism were studied. Their mean +/- standard error of the mean (SEM) serum thyroxine level was 17.7 +/- 0.5 micrograms percent. There was a negative correlation between serum thyroxine levels and LVEF, both at rest and during exercise, in the patients with hyperthyroidism. Our data suggest that hyperthyroidism is associated with impaired functional cardiac reserve.

Adult↗
PubMed2005

Increased calcium influx mediates increased cardiac stiffness in hyperthyroid rats.

Cardiac remodeling (hypertrophy and fibrosis) and an increased left ventricular diastolic stiffness characterize models of hypertension such as the SHR and DOCA-salt hypertensive rats. By contrast, hyperthyroidism induces hypertrophy and hypertension, yet collagen expression and deposition is unchanged or decreased, whereas diastolic stiffness is increased. We determined the possible role of increased calcium influx in the development of increased diastolic stiffness in hyperthyroidism by administering verapamil (15 mg/[kg x d] orally) to rats given triiodothyronine (T3) (0.5 mg/[kg x d] subcutaneously for 14 d). Administration of T3 significantly increased body temperature (control: 36.7 +/- 0.2 degrees C; T3: 39.6 +/- 0.2 degrees C), left ventricular wet weight (control: 2.09 +/- 0.02 mg/kg; T3 3.07 +/- 0.07 mg/kg), systolic blood pressure (control: 128 +/- 5 mmHg; T3: 156 +/- 4 mmHg), and left ventricular diastolic stiffness (control: 20.6 +/- 2.0; T3: 28.8 +/- 1.4). Collagen content of the left ventricle was unchanged. Contractile response to noradrenaline in thoracic aortic rings was reduced. Relaxation in response to acetylcholine (ACh) was also reduced in T3-treated rats, whereas sodium nitroprusside response was unchanged. Verapamil treatment of hyperthyroid rats completely prevented the increased diastolic stiffness and systolic blood pressure while attenuating the increased body temperature and left ventricular weight; collagen content remained unchanged. ACh response in thoracic aortic rings was restored by verapamil. Thus, in hyperthyroid rats, an increased calcium influx is a potential mediator of the increased diastolic stiffness independent of changes in collagen.

Animals↗
PubMed1983

[Fasting serum gastrin, motilin and secretin in treated and untreated hyperthyroidism].

To study the gastrointestinal hormones involved in hyperthyroidism and the interrelationship with the thyroid hormones, the preprandial serum concentrations of gastrin, motilin and secretin were measured by radioimmunoassay in 33 normal subjects and in 104 patients before and after treatment. The following results were obtained. 1) Serum gastrin concentrations in hyperthyroid patients were significantly higher than that of the control, and when the patients reached euthyroidism or hypothyroidism after treatment, the gastrin concentrations in the serum decreased to the normal level. There was a positive correlation between thyroid hormones and serum gastrin. 2) The changes in serum motilin concentrations in hyperthyroidism before and after treatment did not show any significant differences from that of the control. There was a slightly negative relationship between motilin and gastrin and also between T4 and motilin. 3) The mean serum secretin level rose significantly in hypothyroid patients after treatment for hyperthyroidism, but there was no individual correlation between serum secretin and thyroid hormone.

Adult↗
PubMed2001

Serum concentration of androstenediol and androstenediol sulfate in patients with hyperthyroidism and hypothyroidism.

Androstenediol (5-androsten-3beta, 17beta-diol, ADIOL) and androstenediol 3-sulfate (ADIOLS) are active metabolites of dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS), respectively, and have estrogenic activity and immunoregulatory function. We examined serum concentrations of ADIOL, ADIOLS, DHEA, DHEAS and pregnenolone sulfate (5-pregnen-3beta-ol-20-one sulfate, PREGS) in patients with Graves' thyrotoxicosis (male/female 9/14), hypothyroidism (11/20) and in normal controls (14/29). In hypothyroidism serum levels of all these steroids were significantly decreased in both genders. In hyperthyroidism, in contrast, serum levels of ADIOLS (male 1.49 +/- 0.69, female 0.64 +/- 0.31 micromol/l), DHEAS (male 7.43 +/- 3.91, female 5.13 +/- 2.03 micromol/l), and PREGS (male 1.13 +/- 0.58, female 1.07 +/- 0.85 micromol/l) were markedly increased, but serum concentrations of ADIOL and DEHA were not significantly different from controls (ADIOLS male 0.36 +/- 0.33, female 0.14 +/- 0.09 micromol/l; DHEAS male 2.88 +/- 1.70, female 1.86 +/- l1.03pmol/l; PREGS male 0.18 +/- 0.12, female 0.11 +/- 0.08 micromol/l; ADIOL male 3.76 +/- 1.35, female 1.91 +/- 1.17 nmol/l; DHEA male 9.23 +/- 3.49, female 13.5 +/- 10.8nmol/l). Serum concentrations of all these steroids correlated with the serum concentration of the thyroid hormones in these patients. Serum albumin and sex hormone-binding globulin concentrations were not related to these changes in the concentrations of steroids. These findings indicate that serum concentrations of ADIOLS, ADIOL, DHEAS, DHEA and PREGS were decreased in hypothyroidism, whereas serum ADIOLS, DHEAS and PREGS concentrations were increased but ADIOL and DHEA were normal in hyperthyroidism. Thyroid hormone may stimulate the synthesis of these steroids and sulfotransferase is speculated to be increased in hyperthyroidism. Increased ADIOLS might contribute to menstrual disturbances and gynecomastia in hyperthyroidism.

Adult↗
PubMed2004

Plasma homocysteine levels in hyperthyroid patients.

Hyperhomocysteinemia is a risk factor for premature atherosclerotic vascular diseases. It is known that plasma homocysteine levels are higher in hypothyroid patients compared to healthy subjects. The aim of our study was to assess plasma total homocysteine concentrations in hyperthyroid patients before and after treatment when euthyroid status was reached and compare them with control group. Thirteen hyperthyroid patients (age, 42.9 +/- 15.6 year) and eleven healthy subjects (age, 39.9 +/- 12.5 year) were involved in the study. Plasma levels of homocysteine and serum cholesterol, triglyceride, HDL cholesterol, urea, creatinine, vitamin B12, folate were measured before and after treatment. LDL cholesterol and creatinine clearances were calculated. Pretreatment homocycteine levels of the hyperthyroid patients were significantly lower than healthy controls (11.5 +/- 3.6 micromol/L vs. 15.1 +/- 4.5 micromol/L, respectively, p<0.05). Posttreatment homocysteine levels were significantly higher than pretreatment levels (13.9 +/- 6.3 micromol/L vs. 11.5 +/- 3.6 micromol/L, respectively, p<0.05) and posttreatment creatinine clearance were lower than pretreatment level (103.5 +/- 12.7 ml/min vs. 114.2 +/- 9.3 ml/min, respectively, p<0.01). Lower homocysteine levels in hyperthyroidism can be partially explained with the changes in creatinine clearance.

Adult↗
PubMed2006

Sporadic congenital hyperthyroidism due to a germline mutation in the thyrotropin receptor gene (Leu 512 Gln) in a Japanese patient.

Constitutively activating thyrotropin receptor (TSHR) germline mutations have been identified as a molecular cause of congenital hyperthyroidism. We here describe a Japanese woman who had presented with severe hyperthyroidism and advanced bone age as a neonate. She underwent neurosurgical intervention for craniosynostosis, and presented with perodactylia and mild mental retardation with hydrocephalus. Hyperthyroidism has been refractory to antithyroid drug therapy in the absence of antithyrotropin receptor antibodies during follow-up of 20 years, resulting in an enlarged goiter. Analysis of the patient's genomic DNA showed a heterozygous thymine-to-adenine point mutation in exon 10 of TSHR at position 1535 which was not present in the parents' DNA. This mutation, changing leucine to glutamine in codon 512 in the third transmembrane region, was previously identified as a somatic mutation in toxic thyroid nodules and was shown to increase basal cAMP production in vitro. To our knowledge, this is the first report of a germline mutation of TSHR causing sporadic congenital nonautoimmune hyperthyroidism in a Japanese patient.

Adult↗
PubMed1975

Serum T3 level in the patients with hyperthyroidism after therapy.

Serum T3 level in various thyroid diseases was determined in unextracted serum with the Dainabot kit for T3 RIA. The serum T3 level in 33 normal subjects was 0.8-1.6 ng/ml. It was 5.7 +/- 3.5 ng/ml (mean +/- S.D.) in 36 hyperthyroid patients, and undetectable to 0.8 ng/ml in 21 hypothyroid patients. Generally the serum T4 and serum T3 decreased in parallel after radioiodine therapy for hyperthyroidism. However, in some cases the serum T3 level remained high in spite of normalized serum T4 after radioiodine therapy. This state indicated "T3-toxicosis", and hyperthyroidism was apt to recur. When thyroid function was observed for 2 years following radioiodine treatment, the ratio of serum T3 (T3 level before treatment/T3 level after treatment) decreased more significantly as compared with the ratio of serum T4 in euthyroid cases. Serum T3 provides a more sensitive index of thyroid function than serum T4 in euthyroid states after radioiodine or anti-thyroid drug therapy. The present data indicate that the serum T3 level and the T4/T3 ratio are valuable aids in the estimation of prognosis of hyperthyroid patients after various treatments.

Adult↗
PubMed1990

Differential effects of 3 beta blockers on lipid peroxidation in hyperthyroid muscle.

To determine whether beta blockade protects against the acceleration of lipid peroxidation in hyperthyroid rat soleus (slow-oxidative) muscle, in vivo chronic (3 weeks) effects of 3 beta blockers with different ancillary properties on mitochondrial oxidative enzymes, antioxidant enzymes, and thiobarbituric acid-reactive substances were investigated. The rats were rendered hyperthyroid by the administration of thyroxine and treated simultaneously with either carteolol (a nonselective blocker with partial agonist activity; 30 mg/kg/day), atenolol (a beta 1-selective blocker; 50 mg/kg/day), or arotinolol (a nonselective blocker with weak alpha-blocking action; 50 mg/kg/day) over a 3 week period. Hyperthyroidism induced tachycardia, an increase in the mitochondrial oxidative enzymes, manganese (mitochondrial) superoxide dismutase and thiobarbituric acid-reactive substances, and a decrease in the other antioxidant enzymes. The tachycardia was alleviated completely by either atenolol or arotinolol, but partially by carteolol. Arotinolol, but neither carteolol nor atenolol, inhibited the increase in oxidative enzymes and thiobarbituric acid-reactive substances. The levels of antioxidant enzymes were minimally affected by the beta-blocker treatment. Beta 2-, and possibly alpha- as well, but not beta 1-, blockade suppressed mitochondrial hypermetabolism and protected against peroxidative injury in the hyperthyroid soleus muscle. Partial agonist activity was not beneficial.

Adrenergic beta-Antagonists↗