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PubMed2003

Effect of hyperthyroidism on spontaneous physical activity and energy expenditure in rats.

Thyroid hormone excess is associated with increased energy expenditure. The contributions of increases in spontaneous physical activity and nonexercise activity thermogenesis (NEAT) to this effect have not been defined. To address the hypothesis that hyperthyroidism is associated with increased spontaneous physical activity and NEAT, we rendered rats hyperthyroid by using continuous infusion of high-dose triiodothyronine for 14 days and measured the effects on physical activity and NEAT. On day 14, in the hyperthyroid group the mean +/- SD triiodothyronine concentration was 755 +/- 137 (range 574-919) ng/dl and in the control group 59 +/- 0.5 (58-59) ng/dl. Over the 14-day treatment period, mean spontaneous physical activity increased in the hyperthyroid rats from 24 +/- 7 to 36 +/- 6 activity units (AU)/min; P < 0.001 but did not increase in the controls (23 +/- 7 vs. 22 +/- 4 AU/min). Also, over the 14-day period, daily NEAT increased in the hyperthyroid rats from 8.1 +/- 2.8 to 19.7 +/- 5.0 kcal/day (P < 0.001) but did not increase in the controls (8.7 +/- 3.5 cf 9.4 +/- 1.7 kcal/day; not significant). In conclusion, hyperthyroidism is associated with increased spontaneous physical activity and NEAT.

Animals↗
PubMed2003

Plasma levels of coenzyme Q10 in children with hyperthyroidism.

OBJECTIVES: In hyperthyroidism, increased oxygen consumption and free radical production in the stimulated respiratory chain leads to oxidative stress. Apart from its antioxidative function, coenzyme Q10 (CoQ10) is involved in electron transport in the respiratory chain. The aim of this study was to determine whether there is a correlation between an increased respiratory chain activity and the state of CoQ10 in children with hyperthyroidism. METHODS: The CoQ10 plasma concentration was measured by high-performance liquid chromatography in 12 children with hyperthyroidism before and after treatment. RESULTS: In the hyperthyroid state, the plasma level of CoQ10 was significantly decreased in comparison with the level in the euthyroid state. The correction of the hyperthyroid state resulted in a normalization of the CoQ10 level. CONCLUSION: Plasma CoQ10 deficiency appears to be related to the stimulated respiratory chain activity in children with hyperthyroidism.

Adolescent↗
PubMed1982

A Histochemical study of the coronary vasculature in euthyroid and hyperthyroid rats.

Coronary arteries and arterioles in the left and right ventricles from normal and hyperthyroid rats were examined histochemically to determine and to compare their metabolic activities. The test animals were made hyperthyroid by administration of desiccated thyroid for 8-10 weeks. Using histochemical techniques, selected enzymes and components of key metabolic pathways were examined. These pathways included an evaluation of aerobic (oxidative phosphorylation, Kreb's cycle and respiratory chain) and anaerobic metabolic capacity, hexose-monophosphate shunt activity, amounts of deoxyribonucleic and ribonucleic acids present and activity of beta-oxidation of fatty acids. Our results indicate that normal coronary arteriolar metabolism is predominantly aerobic. The findings also suggest a reduction in aerobic metabolism with an accompanying increase in anaerobic potential in the hyperthyroid coronary arterioles. Thus, during thyrotoxicosis, the coronary arterioles may partially shift from aerobic to anaerobic metabolism. Moreover, in both the normal and thyrotoxic rat heart, the coronary microvasculature appears quite stable with little cell proliferation. In contrast, both the control and hyperthyroid rat coronary arteries appear to utilize primarily anaerobic pathways, while the control and hyperthyroid myocardium seem highly dependent upon aerobic metabolism. The tremendous reduction in glucose-6-phosphate dehydrogenase activity in hyperthyroid, when compared to normal coronary arteries and some larger arterioles, implies a reduced capacity for nucleic acid and protein synthesis in the test animals.

Animals↗
PubMed1991

Acute effects of clonidine and growth-hormone-releasing hormone on growth hormone secretion in patients with hyperthyroidism.

Patients with hyperthyroidism have reduced growth hormone (GH) responses to pharmacological stimuli and reduced spontaneous nocturnal GH secretion. The stimulatory effect of clonidine on GH secretion has been suggested to depend on an enhancement of hypothalamic GH-releasing hormone (GHRH) release. The aim of our study was to evaluate the effects of clonidine and GHRH on GH secretion in patients with hyperthyroidism. Eight hyperthyroid females with recent diagnosis of Graves' disease (age range 20-55 years, body mass index range 19.2-26.2 kg/m2) and 6 healthy female volunteers (age range 22-35 years, body mass index range 19-25 kg/m2) underwent two experimental trials at no less than 7-day intervals: (a) an intravenous infusion of clonidine 150 micrograms in 10 ml of saline, or (b) a bolus intravenous injection of human GHRH (1-29)NH2, 100 micrograms in 1 ml of saline. Hyperthyroid patients showed blunted GH peaks after clonidine (7.1 +/- 1.7 micrograms/l) as compared to normal subjects receiving clonidine (28.5 +/- 4.9 micrograms/l, p less than 0.05). GH peaks after GHRH were also significantly lower in hyperthyroid subjects (8.0 +/- 1.7 micrograms/l) as compared to normal subjects receiving GHRH (27.5 +/- 4.4 micrograms/l, p less than 0.05). No significant differences in the GH values either after clonidine or GHRH were observed in the two groups of subjects examined. Our data demonstrate that the GH responses to clonidine as well as to GHRH in patients with hyperthyroidism are inhibited in a similar fashion with respect to normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Decreased lithium clearance in patients with hyperthyroidism.

Lithium clearance was studied to investigate proximal tubular function in patients with hyperthyroidism (n = 10) and control subjects (n = 7). Patients with hyperthyroidism showed significantly reduced fractional excretion of lithium (FELi) compared with control subjects (15.0 +/- 1.5%, n = 10, vs. 23.7 +/- 0.6%, n = 7, means +/- SE, p < 0.001). The reduced FELi of the hyperthyroid state was reversed toward control values with treatment by antithyroid drugs (12.6 +/- 2.6 toward 26.8 +/- 2.5% for 5 patients, means +/- SE). Tubular reabsorption of phosphate (TRP) was significantly increased in hyperthyroid patients compared with control subjects (96.1 +/- 0.7 vs. 87.5 +/- 0.7%, p < 0.001), and it returned to control values after the treatment. Our data demonstrate that lithium clearance is decreased and TRP is increased in patients with hyperthyroidism, which suggests that proximal tubular reabsorption of sodium and TRP is increased in hyperthyroidism.

Adult↗
PubMed1979

The influence of hyperthyroidism and hypothyroidism on the beta-adrenergic responsiveness of the turkey erythrocyte.

The mechanisms responsible for altered adrenergic tone in hyperthyroidism and hypothyroidism are not fully understood. To investigate these mechanisms, the beta-adrenergic receptor-cyclic AMP complex of the turkey erythrocyte was studied among groups of normal, hyperthyroid, and hypothyroid turkeys. In erythrocytes obtained from hypothyroid turkeys, there were fewer beta-adrenergic receptors than in normal cells as determined by the specific binding of [(125)I]iodohydroxybenzylpindolol, as well as associated decreases both in catecholamine-responsive adenylate cyclase activity and in cellular cyclic AMP content. In contrast, erythrocytes obtained from hyperthyroid turkeys contained the same number of beta-receptors and had the same catecholamine-responsive adenylate cyclase activity as cells from normal birds. Other characteristics of the beta-receptors in cells from hyperthyroid birds were indistinguishable from those present in normal erythrocytes. However, within the range of circulating catecholamine concentrations, 5-50 nM, the erythrocytes of the hyperthyroid turkeys generated substantially more cyclic AMP after exposure to isoproterenol than did normal cells. These results suggest that thyroid hormone affects beta-receptor-cyclic AMP interrelationships in the turkey erythrocyte by two distinct mechanisms: (a) In hypothyroidism, both beta-receptors and catecholamine-dependent cyclic AMP formation are coordinately decreased; (b) in hyperthyroidism, beta-receptors are unchanged but there is an amplification of the hormonal signal so that occupation of a given number of receptors at physiological concentrations of catecholamines leads to increased levels of cyclic AMP.

Adenylyl Cyclases↗
PubMed1981

Portal vein blood insulin and glucagon are increased in experimental hyperthyroidism.

Decreased glucose tolerance in hyperthyroidism has been long recognized; however, the mechanism(s) responsible for altered carbohydrate metabolism have not been elucidated. Studies of insulin secretion in hyperthyroidism have been reported by several investigators; however, the results are not conclusive since hormone secretion has been reported as increased, normal, or decreased. Few investigations of glucagon secretion in hyperthyroidism have been described; thus, the role of the alpha cell hormone in the glucose intolerance associated with thyrotoxicosis has not been established. To clarify these matters, experimental hyperthyroidism was induced in male rats by injecting T4 ip for 9 days. On the 10th day, blood was collected from the portal vein for measurement of insulin and glucagon. Animals injected with T4 (500 microgram/kg . day) became clearly thyrotoxic as evidenced by elevated plasma T4 and T3 and diminished weight gain. Rats receiving 750 micrograms T4/kg demonstrated marked enhancement of pancreatic insulin and glucagon release as evidence by elevated portal vein hormone values. Plasma insulin and glucagon in T4-treated rats were substantially elevated regardless of whether the animals were fed or were fasted for 20 h before blood samples were obtained. Insulin and glucagon in vena cava blood were far lower than in the portal vein in both control and hyperthyroid rats, and there was no significant difference between the two groups. We believe that portal vein hormone concentrations more accurately reflect insulin and glucagon secretion than do peripheral blood levels because the hormones and partially degraded in the liver. It is postulated that elevated T4 stimulates the alpha cell to release excess amounts of glucagon, which enhances hepatic glucose output. The possible increase in hepatic glucose output plus insulin resistance, which is characteristic of hyperthyroidism, may account for a secondary rise in insulin release.

Animals↗
PubMed1985

Activity of the hypothalamo-pituitary axis and testicular development in prepubertal ram lambs with induced hypothyroidism or hyperthyroidism.

Prepubertal (16 weeks old) ram lambs were used to investigate the effects of hyperthyroidism and hypothyroidism on development of reproductive endocrine function. Over a period of 8 weeks, ram lambs were made hypothyroid (serum T4 less than or equal to 3 ng/ml compared with controls congruent to 30 ng/ml) by daily oral administration of methyl thiouracil or hyperthyroid (serum T4 congruent to 135 ng/ml) by daily sc injection of T4. Hyperthyroidism was associated with decreases in LH pulse frequency (2.25 +/- 0.75/12 h compared with controls 5.75 +/- 0.48/12 h), basal LH, and mean LH concentrations, together with arrested testicular growth and aspermatogenesis. Hypothyroid rams showed normal pubertal development. After iv injection of LHRH, hyperthyroid ram lambs showed similar LH responses to control and hypothyroid rams. Basal testosterone production (5.6 +/- 1.0 ng/min) and plasma testosterone concentrations after human CG (2.0 +/- 0.7 ng/ml) in hyperthyroid rams were significantly lower than in controls (67.5 +/- 24.0 ng/min and 5.2 +/- 1.0 ng/ml, respectively). It is concluded that retarded testicular development in hyperthyroid ram lambs results from changes in hypothalamo-pituitary activity manifested in a decreased LH pulse frequency.

Animals↗
PubMed2006

Changes in skeletal muscle protein metabolism and myosin heavy chain isoform messenger ribonucleic acid abundance after treatment of hyperthyroidism.

BACKGROUND: Hyperthyroidism causes a hypermetabolic state and skeletal muscle dysfunction, but the underlying mechanism remains incompletely defined. OBJECTIVE: The objective of the study was to determine whether treatment of hyperthyroidism causes changes in amino acid fluxes, synthesis rates of muscle proteins, and expression of muscle myosin heavy chain (MHC) that may impact skeletal muscle function and metabolic rate. METHODS: Eight hyperthyroid patients were studied (TSH 0.008 +/- 0.001 mU/liter) before treatment and at least 9 months after correction of hyperthyroidism (TSH 2.3 +/- 0.4) (P < 0.03). Fluxes of leucine and phenylalanine as well as muscle protein synthesis rates were measured using L[1,2 13C] leucine and L(15N) phenylalanine as tracers. mRNA levels of selected genes were measured in muscle biopsy samples. RESULTS: Treatment decreased resting metabolic rate that paralleled changes in fluxes of leucine and phenylalanine accompanied by improved muscle strength and mass. Synthesis rates of mixed muscle proteins (P = 0.01), sarcoplasmic (P = 0.04), and mitochondrial (P = 0.08) proteins decreased, whereas MHC synthesis was unchanged. Selective increases in mRNA abundance of muscle MHC1 isoform (P = 0.04) and decrease of MHCIIA (P = 0.007) and MHCIIx (P = 024) were observed. Muscle mitochondrial oxidative enzymes and mRNA levels of mitochondrial proteins were unchanged, but uncoupling protein2 and uncoupling protein3 mRNA levels (P = 0.02) decreased. CONCLUSION: Increased amino acid flux, mixed muscle protein synthesis, and synthesis of sarcoplasmic proteins are consistent with the hypermetabolic state in hyperthyroidism. After treatment, MHC synthesis rates were unchanged, but mRNA levels of isoforms of MHC found in slow-twitch and fast-twitch fibers increased and decreased, respectively. These results offer a mechanistic explanation for posttreatment improvement in muscle functions in hyperthyroidism.

Adrenergic beta-Antagonists↗
PubMed1976

Catecholamines metabolism in thyroid diseases. I. Epinephrine secretion rate in hyperthyroidism and hypothyroidism.

We have measured the secretion rate of epinephrine in 6 euthyroid, 6 hyperthyroid, and 6 hypothyroid subjects infused at a constant rate for a one hour period with tritiated epinephrine (.01 muc/kg/min) (New England Nuclear Inc.). Plasma and urinary levels of epinephrine were measured by modifying the fluorometric method of Anton and Sayre. Plasma levels of epinephrine were 3.0 +/- 3.0 ng/100 ml (mean +/- SD) in normal subjects, compared to 4.4 +/- 3.5 ng/100 ml (mean +/- SD) in hyperthyroid subjects. In urine, epinephrine values ranged from 1.3 mug/day to 6.1 mug/day in normal subjects. Mean value observed in hyperthyroidism was 4.9 +/- 2.6 mug/day and 3.8 +/- 1.0 mu/day in hypothyroidism. Plasma secretion rates averaged 48 +/- 27 mug/kg/day in normal subjects, compared to 54 +/- 18 mu/kg/day in hyperthyroidism and 43 +/- 20 mug/kg/day in hypothyroidism. Likewise, the mean urinary secretion rate was 55 +/- 27 mug/kg/day in normal subjects compared to 60 +/- 22 mug/kg/day in hyperthyroidism and 50 +/- 28 mug/kg/day in hypothyroidism. There is no statistical difference between the values found in the three groups of subjects (plasma and urine). Therefore, these results would indicate that the signs and symptoms encountered in hyperthyroidism are not secondary to a high secretion rate of epinephrine.

Epinephrine↗
PubMed1984

The defect of intestinal calcium transport in hyperthyroidism and its response to therapy.

Skeletal demineralization occurs in thyrotoxicosis. Fecal calcium excretion may be enhanced, and calcium balance tends to be negative. We investigated intestinal calcium transport in 12 hyperthyroid patients. Absorption was measured by segmental perfusion in the proximal jejunum at calcium concentrations commensurate with those in the fasting and postprandial states. At low luminal concentrations, under conditions where calcium is transported predominantly by active processes, the calcium absorption rate was reduced though not abolished in hyperthyroid patients (16 +/- 4 (SE) mumol/h . 30 cm segment) as compared to normal subjects (71 +/- 8 mumol/h; P less than 0.001). When perfusate calcium was raised to 5 mmol/liter there was little increment of the net absorption rate in the hyperthyroid group (45 +/- 11 mumol/h), whereas that in the normal subjects rose to 183 +/- 17 mumol/h. Likewise, the unidirectional calcium flux out of the lumen was low in hyperthyroidism (43 +/- 7 mumol/h), suggesting that low net absorption rates were not due to transmucosal calcium loss. D-Xylose permeation was similar in all study groups. Treatment of the thyroid disease led to a marked increase in calcium absorption rates from 33 +/- 10 to 124 +/- 20 mumol/h (at 2 mmol/liter P less than 0.001; n = 5) into the range of values in normal subjects (124 +/- 9 mumol/h). Circulating levels of 1,25-dihydroxyvitamin D were low in hyperthyroid patients (38 +/- 11 pg/ml) and increased during treatment to 63 +/- 11 pg/ml (P less than 0.025; n = 9), whereas 25-hydroxyvitamin D was normal and remained unchanged. We conclude that intestinal calcium transport, particularly its active component, is reversibly decreased in hyperthyroidism. The association with low plasma levels of the active vitamin D metabolite suggests that the decrease in calcium absorption may be related to calcium-regulating mechanisms as a consequence of the net calcium efflux from bone in this disease.

Adult↗
PubMed1986

Reduced binding and antilipolytic effect of prostaglandin E2 in adipocytes from patients with hyperthyroidism.

The present study was undertaken to evaluate the effect of thyroid hormones on prostaglandin E2 (PGE2) binding and action in human adipocytes. The study consisted of 12 patients with hyperthyroidism and 20 normal subjects. In adipocytes from hyperthyroid patients, there was a 32% decrease in [3H]PGE2-binding sites (P less than 0.01). This reduced binding was accompanied by a 46% reduction in the relative antilipolytic effect of PGE2 in adipocytes from patients with hyperthyroidism. These changes might, then, account for some of the enhanced lipolysis that occurs in hyperthyroid patients. Thyroid hormones significantly increased the lipolytic effect of isoproterenol (P less than 0.01). However, the lipolytic effect of theophylline plus adenosine deaminase and basal lipolysis also were increased in adipocytes from hyperthyroid subjects. The latter findings indicate that thyroid hormones induce a state of increased activation of lipolysis under both basal and stimulated conditions. It is concluded that thyroid hormones reduce the binding and action of PGE2 in human adipocytes, possibly via a cAMP dependent mechanism. These alterations will contribute to accelerated lipid metabolism in the hyperthyroid state.

Adipose Tissue↗
PubMed1989

Glucose turnover in hyperthyroid patients with normal glucose tolerance.

To determine the diabetogenic effect(s) of thyroid hormones, we simultaneously measured glucose turnover in six hyperthyroid patients and six normal subjects. All had normal fasting blood glucose concentration and oral glucose tolerance test values. We determined hepatic total glucose output (HTGO) and total glucose phosphorylation with [2-3H]glucose and hepatic glucose production (HGP) and irreversible glucose uptake using [6-3H]glucose. The difference between the two turnover rates indicates the extent of hepatic glucose cycling (glucose in equilibrium glucose-6-phosphate). Measurements were made both in the postabsorptive steady state and during a 2-h glucose infusion (11.1 mumol/kg.min). The postabsorptive HTGO and total glucose phosphorylation were increased in the hyperthyroid patients [13.5 +/- 0.8 (+/- SE) vs. 11.3 +/- 0.4 mumol/kg.min; P less than 0.05]. HGP and irreversible glucose uptake also were slightly but not significantly higher. During the glucose infusion, HTGO and HGP were less suppressed in the hyperthyroid patients than in the normal subjects, while the increments in peripheral glucose uptake were normal. In hyperthyroidism, glucose cycling was increased both postabsorptively (2.35 +/- 0.27 vs. 1.17 +/- 0.25 mumol/kg.min; P less than 0.025) and during glucose infusion (2.57 +/- 0.34 vs. 1.31 +/- 0.35 mumol/kg.min; P less than 0.05). We conclude that increases in HTGO and HGP are important features of hyperthyroidism, especially during glucose infusion. The increase in GC indicates increased activities of both glucokinase and glucose-6-phosphatase. The diabetogenic effect of hyperthyroidism, as revealed most markedly by [2-3H]glucose, could be accounted for by augmented glucose production, possibly due to increased glucose-6-phosphatase activity.

Adult↗
PubMed1990

The effect of hyperthyroidism on in vivo aging of erythrocyte ouabain-binding sites and intracellular sodium and potassium.

The sodium pump activity of erythrocytes is inhibited in hyperthyroidism, whereas in all other cells it is increased. To examine the possibility that thyroid hormones cause an accelerated loss of membrane proteins during in vivo aging, we determined the number of ouabain-binding sites (OBS) in young and old erythrocytes from 13 hyperthyroid and 13 euthyroid subjects. Erythrocytes were separated according to their cell age by centrifugation. In euthyroid subjects, the median number of OBS decreased from 415 (range, 341-551; mean +/- SEM, 440 +/- 19.1) in young cells to 336 (range, 287-453; mean, 340 +/- 13.6) in old cells. In hyperthyroid subjects the median number of OBS decreased from 290 (range, 190-370; mean, 280 +/- 13.3) in young cells to 207 (range, 155-244; mean, 208 +/- 7.5) in old cells. In hyperthyroid subjects the number of OBS of erythrocytes of all ages was lower than that in euthyroid subjects. The ratio of OBS between young and old cells in hyperthyroid subjects (median, 1.27; mean +/- SD, 1.34 +/- 0.16) was similar to that in euthyroid subjects (median, 1.29; mean, 1.30 +/- 0.12). We conclude that these results do not support the hypothesis that in hyperthyroidism there is accelerated loss of sodium pump sites during the lifespan of erythrocytes in circulation.

Adult↗
PubMed1991

Nature of altered growth hormone secretion in hyperthyroidism.

Hyperthyroidism is accompanied by various neuroendocrine regulatory disturbances that affect not only the thyrotropic, but also the gonadotropic, corticotropic, and somatotropic axes. To examine the nature of alterations in neuroendocrine control mechanisms that direct the somatotropic axis in hyperthyroidism, we have applied a novel deconvolution technique designed to estimate the number, amplitude, and mass of significant underlying GH secretory events after the influence of GH metabolic clearance has been removed mathematically. To this end, blood was sampled at 10-min intervals for 24 h in seven hyperthyroid and seven age-matched euthyroid men. The subsequent GH time series were assayed by immunoradiometric assay (sensitivity, 0.08 ng/mL) and submitted to quantitative deconvolution analysis. We found that hyperthyroid compared to euthyroid men 1) had significantly more GH secretory bursts per 24 h (viz. 15 +/- 1.0 vs. 10 +/- 1.1; P = 0.017); 2) secreted 3 times as much GH per burst (3.7 +/- 0.80 vs. 1.3 +/- 0.42 ng/mL distribution vol; P = 0.013); 3) achieved a maximal rate of GH secretion in each burst 2.3-fold higher than that in control men (0.14 +/- 0.028 vs. 0.060 +/- 0.015 ng/mL.min; P = 0.017); and 4) had 3.7-fold higher 24-h endogenous GH production rates (P less than 0.01). Neither hyperthyroid nor euthyroid men had significant interburst (tonic) GH secretion. We conclude that the somatotropic axis in hyperthyroid men is marked by a higher frequency of spontaneous GH secretory bursts, a higher rate of maximal GH secretion attained per burst, and a larger mass of GH released per burst. These neuroregulatory disturbances result in a nearly 4-fold increase in the 24-h production rate of GH in thyrotoxicosis.

Adult↗
PubMed1994

Comparison of second and third generation methods for measurement of serum thyrotropin in patients with overt hyperthyroidism, patients receiving thyroxine therapy, and those with nonthyroidal illness.

We compared serum TSH results determined in second and third generation assays in patients with thyroid disease and nonthyroidal illnesses (NTIs) to evaluate the usefulness of the more sensitive assay. We studied 19 subjects with untreated hyperthyroidism, 12 hyperthyroid subjects sampled at 4-week intervals after beginning carbimazole, 153 subjects receiving T4 replacement, and 300 hospital in-patients with a variety of NTIs. Serum TSH was measured, using a second generation immunometric method, together with free T4 and free T3. Samples with subnormal TSH (< 0.5 mU/L) were reassayed, using a more sensitive chemiluminescent immunometric method. Both assays revealed undetectable serum TSH levels in 18 of 19 overtly hyperthyroid patients. Undetectable TSH values (in both assays) were found in 30 of 33 patients with low serum TSH levels who were receiving treatment for hyperthyroidism, in association with normal thyroid hormone levels in 11. Undetectable TSH was evident in both patients receiving T4 and those with NTI, but use of the more sensitive assay led to a reduction in the number of subjects with undetectable TSH compared with the second generation results (T4-treated, 55 vs. 77 cases; NTI, 13 vs. 19 cases). There was a significant correlation between serum TSH and free T4 in the whole group on T4 (P < 0.001) and in those receiving T4 with low TSH (r = -0.33; P < 0.05); no significant correlation was evident in subjects with low serum TSH levels associated with NTI. An improvement in assay sensitivity led to a reduction in the number of patients being treated with T4 or with NTI in whom serum TSH was undetectable and, hence, an increase in those in whom overt hyperthyroidism could be excluded. Undetectable TSH results, even in a third generation assay, are not diagnostic of overt hyperthyroidism, but are also found in subjects with treated thyroid disease and NTI.

Analysis of Variance↗
PubMed1996

Power spectral analysis of heart rate in hyperthyroidism.

The aim of the present study was to evaluate the impact of hyperthyroidism on the cardiovascular system by separately analyzing the sympathetic and parasympathetic influences on heart rate. Heart rate variability was evaluated by autoregressive power spectral analysis. This method allows a reliable quantification of the low frequency (LF) and high frequency (HF) components of the heart rate power spectral density; these are considered to be under mainly sympathetic and pure parasympathetic control, respectively. In 10 newly diagnosed untreated hyperthyroid patients with Graves' disease, we analyzed power spectral density of heart rate cyclic variations at rest, while lying, and while standing. In addition, heart rate variations during deep breathing, lying and standing, and Valsalva's maneuver were analyzed. The results were compared to those obtained from 10 age-, sex-, and body mass index-matched control subjects. In 8 hyperthyroid patients, the same evaluation was repeated after the induction of stable euthyroidism by methimazole. Heart rate power spectral analysis showed a sharp reduction of HF components in hyperthyroid subjects compared to controls [lying, 13.3 +/- 4.1 vs. 32.0 +/- 5.6 normalized units (NU; P < 0.01); standing, 6.0 +/- 2.7 vs. 15.0 +/- 4.0 NU (P < 0.01); mean +/- SEM]. On the other hand components were comparable in the 2 groups (lying, 64.0 +/- 6.9 vs. 62.0 +/- 6.5 NU; standing, 77.0 +/- 6.5 vs. 78.0 +/- 5.4 NU). Hence, the LF/HF ratio, which is considered an index of sympathovagal balance, was increased in hyperthyroid subjects while both lying (11.3 +/- 4.5 vs. 3.5 +/- 1.1; P < 0.05) and standing (54.0 +/- 12.6 vs. 9.8 +/- 2.6; P < 0.02). This parameter was positively correlated with both T3 (r = 0.61; P < 0.05) and free T4 (r = 0.63; P < 0.05) serum levels. Among traditional cardiovascular autonomic tests, the reflex response of heart rate during lying to standing was significantly lower in hyperthyroid patients than in controls (1.12 +/- 0.03 vs. 1.31 +/- 0.04; P < 0.002). No statistically significant difference in reflex responses between the two groups was found in deep breathing or Valsalva's maneuver. In the 8 patients reexamined after methimazole treatment, we observed complete normalization of altered cardiovascular parameters, with slight predominance of the vagal component compared with controls. These results suggest that thyroid hormone excess may determine reduced parasympathetic activity and, thus, a relative hypersympathetic tone.

Adolescent↗
PubMed1997

Both hypothyroidism and hyperthyroidism enhance low density lipoprotein oxidation.

Hypothyroidism is frequently associated with hypercholesterolemia and an increased risk for atherosclerosis, whereas hyperthyroidism is known to precipitate angina or myocardial infarction in patients with underlying coronary heart disease. We have shown previously that L-T4 functions as an antioxidant in vitro and inhibits low density lipoprotein (LDL) oxidation in a dose-dependent fashion. The present study was designed to evaluate the changes in LDL oxidation in subjects with hypothyroidism and hyperthyroidism. Fasting blood samples for LDL oxidation analyses, lipoprotein determinations, and thyroid function tests were collected at baseline and after the patients were rendered euthyroid. The lag phase (mean +/- SEM hours) of the Cu+2-catalyzed LDL oxidation in the hypothyroid state and the subsequent euthyroid states were 4 +/- 0.0.65 and 14 +/- 0.68 h, respectively (P < 0.05). The lag phase during the hyperthyroid phase was 6 +/- 0.55 h, and that during the euthyroid phase was 12 +/- 0.66 h (P < 0.05). The total and LDL cholesterol levels were higher in hypothyroidism than in euthyroidism and were lower in hyperthyroidism than in the euthyroid state. We conclude that LDL has more susceptibility to oxidation in both the hypothyroid and hyperthyroid states. Thus, the enhanced LDL oxidation may play a role in the cardiac disease process in both hypothyroidism and hyperthyroidism.

Adult↗