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PubMed1990

Erythrocyte sodium fluxes, ouabain binding sites, and Na+,K(+)-ATPase activity in hyperthyroidism.

Erythrocyte sodium pump activity, in contrast to other tissues, is decreased in hyperthyroidism. In order to examine whether the effect of thyroid hormones on erythrocytes is part of a generalized effect on other transport pathways, we measured sodium pump activity, Na+,K(+)-adenosine triphosphatase (ATPase) activity, ouabain binding sites, bumetanide-sensitive sodium potassium cotransport (SPC), sodium lithium countertransport (SLC), and ouabain- and bumetanide-insensitive passive efflux of sodium (sodium "leak") in erythrocytes from 20 healthy subjects and 18 untreated hyperthyroid subjects. Sodium pump activity (ouabain-sensitive sodium efflux rate constant), Na+,K(+)-ATPase activity, and the number of ouabain binding sites were lower and the erythrocyte sodium content was higher in hyperthyroid subjects. The rate constants of erythrocyte SPC (P less than .05), SLC (P less than .001), and sodium "leak" (P less than .05) were also significantly lower in hyperthyroidism. In 11 of the hyperthyroid subjects, sodium flux measurements were repeated after 20 weeks of treatment. Sodium pump activity, the number of ouabain binding sites, and the rate constant for SLC increased. These results suggest that the effect of thyroid hormones on the erythrocyte sodium pump is part of a generalized effect on membrane proteins, rather than a specific effect.

Adult↗
PubMed1992

Glucose tolerance and insulin secretion in spontaneously hyperthyroid cats.

Glucose tolerance and insulin secretion after administration of a glucose load were determined in 11 clinically normal cats and 15 cats with spontaneous hyperthyroidism. In six hyperthyroid cats, a glucose tolerance test was repeated after treatment with radioactive iodine (131I). All cats had similar baseline glucose concentrations. However, the cats with hyperthyroidism had a significantly decreased glucose clearance, which was worse after treatment. Hyperthyroidism also caused a marked increase in basal and glucose-stimulated insulin secretion, which was not improved with treatment. It is concluded that hyperthyroidism in cats may lead to long-lasting alterations of glucose tolerance and insulin secretion which may not be reversed by treatment.

Animals↗
PubMed1989

Behavioral modifications in relation to hypothyroidism and hyperthyroidism in adult rats.

1. Behavioural experiments were carried out on adult rats made hypothyroid and hyperthyroid. The hypothyroid rats in an "open field" situation reduced the number of squares crossed and boluses defecated, the hyperthyroid rats reduced the number of squares crossed. A swimming endurance was conducted to evaluate the physical resistance of the rats: only hypothyroidism affected the performance. 2. Two operant tests were studied: a) an "extinction" trial (60 min), in which the rats trained in a fixed ratio schedule (FR 1:10), were no longer rewarded with pellets of food and b) the "reversal" test in which the contingency for food delivery was switched four times from one lever, where responses were previously reinforced, to the other lever where responses had no programmed consequences. 3. Both hypo and hyperthyroid conditions caused a lower rate of responses during the "extinction" trial, while in the "reversal" test only hyperthyroid rats showed improved performances. 4. Our data clearly demonstrate behavioural changes in adult hypothyroid and hyperthyroid rats.

Animals↗
PubMed1988

Reduced cardiac vagal excitability in hyperthyroidism.

A great deal of uncertainty persists regarding the exact nature of the interaction between autonomic nervous activity and thyroid hormones in the control of heart rate. In the present work we investigated whether reduced vagal influence could contribute to the tachycardia in hyperthyroidism. Vagal excitability was studied in ten hyperthyroid patients. Prolongation of R-R interval in response to carotid baroreceptor stimulation by neck suction was found to be less in the hyperthyroid state compared to the control state after therapy. The extent of nocturnal bradycardia and the vagal excitatory response to the central effect of low dose atropin was significantly reduced in hyperthyroid patients compared to euthyroid controls. We concluded that in the hyperthyroid state cardiac vagal motoneurones were in low excitability state, and speculated that the inhibition might have resulted from thyroid hormone action on CNS structures integrating autonomic function and behaviour.

Adult↗
PubMedDate not supplied

The effect of propranolol, verapamil and dantrolene treatment on cardiac hypertrophy, enhanced myocardial contractility and tachycardia in the hyperthyroid rat.

Experimentally induced hyperthyroidism is associated with cardiac hypertrophy, tachycardia and elevated myocardial contractility. To investigate the possibility of ameliorating the cardiac changes pharmacologically, hyperthyroid rats were treated with propranolol, verapamil or dantrolene. Cardiac hypertrophy was assessed from the heart mass: body mass ratio and cardiac function was measured in vitro. Both verapamil and propranolol reversed the cardiac hypertrophy of the hyperthyroid animals from 0.92 +/- 0.02 mg.g-1 to 0.70 +/- 0.01 mg.g-1 (P less than 0.001) and 0.72 +/- 0.02 mg.g-1 (P less than 0.001) respectively. Verapamil was effective in reducing the spontaneous heart rate from 331 +/- 8 beats.min-1 to 273 +/- 7 beats.min-1 (P less than 0.001) while propranolol reduced the dP/dtmax of the hyperthyroid hearts from 4089 +/- 87 mmHg.s-1 to 3497 +/- 97 mmHg.s-1 (P less than 0.001). Dantrolene had no effect on any parameter. We conclude from our results that cardiac hypertrophy of the hyperthyroid heart can be reversed by treatment with propranolol and verapamil probably via their inotropic and chronotropic properties.

Animals↗
PubMed2005

Effect of prolonged exercise on oxidative damage and susceptibility to oxidants of rat tissues in severe hyperthyroidism.

We investigated effects of prolonged aerobic exercise and severe hyperthyroidism on indices of oxidative damage, susceptibility to oxidants, and respiratory capacity of homogenates from rat liver, heart and skeletal muscle. Both treatments induced increases in hydroperoxide and protein-bound carbonyl levels. Moreover, the highest increases were found when hyperthyroid animals were subjected to exercise. These changes, which were associated to reduced exercise endurance capacity, were in part due to higher susceptibility to oxidants of hyperthyroid tissues. Levels of oxidative damage indices were scarcely related to changes in antioxidant enzyme activities and lipid-soluble antioxidant concentrations. However, the finding that, following exercise the scavenger levels generally decreased in liver homogenates and increased in heart and muscles ones, suggested a net shuttle of antioxidants from liver to other tissues under need. Aerobic capacity, evaluated by cytochrome oxidase activity, was not modified by exercise, which, conversely, affected the rates of oxygen consumption of hyperthyroid preparations. These results seem to confirm the higher susceptibility of hyperthyroid tissues to oxidative challenge, because the mechanisms underlying the opposite changes in respiration rates during State 4 and State 3 likely involve oxidative modifications of components of mitochondrial respiratory chain, different from cytochrome aa3.

Animals↗
PubMed2005

Cardiovascular abnormalities in hyperthyroidism: a prospective Doppler echocardiographic study.

PURPOSE: We investigated the prevalence and clinical importance of cardiovascular abnormalities in patients with hyperthyroidism. METHODS: All consecutive patients diagnosed with hyperthyroidism during a period of 24 months were included in the study. Medical history, complete physical examination results, electrocardiographic findings, laboratory determinations, and Doppler echocardiographic findings were obtained for all patients within 24 hours of diagnosis, and after euthyroidism had been achieved. Age- and sex-matched controls also were studied. RESULTS: Thirty-nine patients (mean [+/-SD] age, 52 +/- 20 years; range, 25 to 86 years; 72% women), and 39 age- and sex-matched controls, were included. Atrial fibrillation was present in 7 patients (18%). Moderate or severe mitral or tricuspid regurgitation, or both, were present in 9 patients (23%) and in only 1 control (3%; P= 0.01). Mean pulmonary arterial systolic pressure was 38 +/- 12 mm Hg (range, 17 to 64 mm Hg) in patients and 27 +/- 4 mm Hg (range, 19 to 37 mm Hg) in controls (P= 0.001). Sixteen patients (41%) and 1 control (3%) had pulmonary arterial systolic pressure >or=35 mm Hg. Left ventricular systolic dysfunction was detected in 1 patient. After correction of hyperthyroidism, a significant decrease in pulmonary arterial systolic pressure was observed, and the levels became similar to those of controls. CONCLUSION: In patients with hyperthyroidism, there is a high prevalence of pulmonary hypertension and atrioventricular valve regurgitation. These abnormalities usually correct after treatment for hyperthyroidism.

Adult↗
PubMed2005

Hyperthyroidism changes nociceptive response and ecto-nucleotidase activities in synaptosomes from spinal cord of rats in different phases of development.

Changes in transport, receptors and production of extracellular adenosine have been observed after induction of hyperthyroidism. Adenosine is associated with inhibitory actions such as reduction in release of excitatory neurotransmitters and antinociception at spinal site. In contrast, ATP acts as an excitatory neurotransmitter and produces pronociceptive actions. ATP may be completely hydrolyzed to adenosine by an enzyme chain constituted by an ATP diphosphohydrolase and an ecto-5'-nucleotidase, as previously described in the spinal cord. Thus, we now investigated the effects of the hyperthyroidism on adenine nucleotide hydrolysis in the spinal cord and verified the nociceptive response in this pathology during different phases of development. Hyperthyroidism was induced in male Wistar rats, aged 5, 60 and 330 days by daily intraperitoneal injections of L-thyroxine (T4) for 14 days. Nociception was assessed with a tail-flick apparatus. Rats starting the treatment aged 5 days demonstrated a significant increase in ADP and AMP hydrolysis and increased tail-flick latency (TFL). In contrast, in the spinal cord from hyperthyroid rats aged 60 and 330 days old, the hydrolysis of ATP, ADP and AMP were significantly decreased. Accordingly, the tail-flick latency was decreased, indicating a hyperalgesic response. These results suggest the involvement of ecto-nucleotidases in the control of the hyperthyroidism-induced nociceptive response in rats at distinct developmental stages.

Adenosine Triphosphatases↗
PubMed2004

Possible link between glycated hemoglobin and lipid peroxidation in hyperthyroidism.

BACKGROUND: Glycated hemoglobin (HbA1C) levels are enhanced by elevated glucose concentrations. Glycation of hemoglobin is also modulated by lipid peroxides, ascorbic acid and reduced glutathione (GSH). We determined the strength of the relationships among these variables in a group of hyperthyroid patients. METHODS: Twenty-two untreated hyperthyroid patients and 17 healthy controls were recruited for the study. Whole blood GSH, HbA1C, plasma lipid peroxides, ascorbic acid and fasting glucose were analyzed in both the groups. Direct and partial correlation analysis was performed to explore the possible relationships between these variables. RESULTS: In hyperthyroid patients, HbA1C and lipid peroxides levels were found to be significantly increased than the controls. Ascorbic acid and GSH were decreased significantly in the test group when compared with the healthy control group. With partial correlation analysis, fasting glucose and lipid peroxides were found to have a significant positive correlation with HbA1C. Ascorbic acid and GSH showed no significant association with HbA1C levels. CONCLUSION: These data suggest that HbA1C levels are closely associated with fasting glucose and lipid peroxides in hyperthyroid patients. Therefore, serum lipid peroxides level should be kept in mind while interpreting HbA1C as a long-term glycemic index in hyperthyroid cases.

Adolescent↗
PubMed2005

Hyperthyroidism.

The clinical spectrum of hyperthyroidism varies from asymptomatic,subclinical hyperthyroidism to the life-threatening "thyroid storm". Hyperthyroidism is a common form of thyroid disease that mimics many of the common complaints in the emergency department. The diagnosis of hyperthyroidism is often challenging due to the multitude of physical and even psychiatric complaints. Recognition and treatment by emergency physicians of severe hyperthyroidism is critical and can be life saving.

Adult↗
PubMed1997

Myocardial damage does not occur in untreated hyperthyroidism unless associated with congestive heart failure.

Even in the absence of underlying cardiac disease, hyperthyroidism has seldom been reported to be associated with left ventricular dysfunction and congestive heart failure. The left ventricular function invariably improves with achievement of euthyroid status. Anecdotal autopsy reports have suggested that myocardial necrosis associated with hyperthyroidism may be responsible for congestive heart failure. This study prospectively evaluates the role of myocardial necrosis in untreated hyperthyroidism by imaging with Indium-111 antimyosin antibody. Thirteen consecutive patients (7 men and 6 women, mean age 36 +/- 11 years) with hyperthyroidism and Graves' disease (10 patients), subacute thyroiditis (2 patients), or multinodular goiter (1 patient) formed the basis of the study. The T4 levels ranged from 33 to 183 pmol/L (mean 103 +/- 47 pmol/L) and cardiac output from 5.47 to 11.0 L/min (mean 7.17 +/- 1.75 L/min). Two patients had clinical congestive heart failure and mildly depressed left ventricular ejection fraction. Both patients had scintigraphic evidence of myocardial damage with abnormal antimyosin scans. In the remaining 11 patients with normal left ventricular ejection fraction, no antimyosin uptake was observed. The reevaluation of two patients with abnormal initial scans 6 to 8 months after treatment revealed euthyroid status, resolution of antimyosin uptake, and normalization of left ventricular function. This study indicates that myocardial necrosis may be detected in a small proportion of patients with hyperthyroidism, which could contribute to left ventricular systolic dysfunction.

Adult↗
PubMed1996

Prediction of neonatal hyperthyroidism in infants born to mothers with Graves disease.

OBJECTIVE: To determine whether determinations of thyrotropin-receptor antibody (TRAb) levels in newborn infants of women with Graves disease would predict which infants will have hyperthyroidism. METHODS: The TRAb levels, assayed in the sera of 14 infants born to 14 women with Graves disease, were measured sequentially in the infants with hyperthyroidism during the course of antithyroid medication therapy. RESULTS: Seven infants had TRAb values less than 0.15 and remained euthyroid. In seven infants whose initial TRAb values were more than 0.25 (range, 0.48 to 0.88), clinical and biochemical signs of hyperthyroidism developed. The infants were treated with antithyroid medication until day 57 to day 123 of life. Therapy was discontinued when the infants were free of symptoms and when serum thyroxine and triiodothyronine and free thyroxine levels remained normal during therapy with decreasing doses of antithyroid medication. When the medication was discontinued, TRAb values were less than 0.20. CONCLUSIONS: Infants born to mothers with Graves disease with initial TRAb values less than 0.15 remained euthyroid. The TRAb values greater than 0.25 were associated with the development of neonatal hyperthyroidism. During treatment of neonatal hyperthyroidism, TRAb values less than 0.20 may be helpful in deciding when to withdraw antithyroid medication.

Antithyroid Agents↗
PubMed1998

Reduced metabolic efficiency of skeletal muscle energetics in hyperthyroid patients evidenced quantitatively by in vivo phosphorus-31 magnetic resonance spectroscopy.

Skeletal muscle energetics of seven hyperthyroid patients were investigated throughout a rest-exercise-recovery protocol using phosphorus-31 magnetic resonance spectroscopy (31P MRS) to quantitatively document in vivo the metabolic bases of impaired muscle performance in hyperthyroidism. The contributions of the main pathways of adenosine triphosphate (ATP) synthesis to energy production and proton efflux were measured and compared with results from normal muscle. At rest, a reduced concentration of phosphocreatine (PCr) was calculated for hyperthyroid patients when compared with controls, whereas pH and concentrations of inorganic phosphate (Pi) and phosphomonoesters (PME) were not different from controls. During exercise, the analysis of changes in pH and PCr concentration demonstrated that (1) at the onset of exercise, the magnitude of glycolysis activation is significantly larger for patients, resulting in a marked pH decrease; (2) the energy cost of exercise is higher for patients as compared with controls performing the same amount of work; and (3) both anaerobic and aerobic pathways are significantly more activated in the hyperthyroid group throughout the 3 minutes of exercise. During recovery, the rates of proton efflux and PCr resynthesis were similar in both groups, excluding any alteration in oxidative function and proton handling as a cause of initial glycolytic hyperactivation. The increased energy cost measured for patients during exercise evidences an increased need for energy, which is (1) probably linked to the existence of additional ATP-consuming mechanism(s), and (2) supported by hyperactivation of both aerobic and anaerobic pathways. These findings imply that, all things equal, a hyperthyroid muscle requires more energy to function than normal, and as a result is potentially more fatiguable.

Adolescent↗
PubMed2003

Hyperthyroidism.

Hyperthyroidism is a pathological syndrome in which tissue is exposed to excessive amounts of circulating thyroid hormone. The most common cause of this syndrome is Graves' disease, followed by toxic multinodular goitre, and solitary hyperfunctioning nodules. Autoimmune postpartum and subacute thyroiditis, tumours that secrete thyrotropin, and drug-induced thyroid dysfunction, are also important causes. The diagnosis of hyperthyroidism is generally straightforward, with raised serum thyroid hormones and suppressed serum thyrotropin in almost all cases. Appropriate treatment of hyperthyroidism relies on identification of the underlying cause. Antithyroid drugs, radioactive iodine, and surgery are the traditional treatments for the three common forms of hyperthyroidism. Beta-adrenergic blocking agents are used in most patients for symptomatic relief, and might be the only treatment needed for thyroiditis, which is transient. The more unusual causes of hyperthyroidism, including struma ovarii, thyrotropin-secreting tumours, choriocarcinoma, and amiodarone-induced thyrotoxicosis are, more often than not, a challenge to diagnose and treat.

Antithyroid Agents↗
PubMed1977

Diagnosis of hyperthyroidism when serum-thyroxine alone is raised.

31 patients admitted to hospital with different non-thyroidal intercurrent diseases were found to have raised total serum-thyroxine (T4) and free T4 together with normal serum-triiodothyronine (T3) concentrations. At admission none was clinically hyperthyroid. Patients were assigned to 3 groups according to clinical course and the laboratory findings. In the first group (14 patients) classic hyperthyroidism developed after recovery from the intercurrent disease. 11 out of these 14 patients had recently received iodine-containing preparations. In a second group (11 patients) the initially raised serum-T4 rapidly returned to normal with recovery from the non-thyroidal disease. In a third group (6 patients) serum-T4 concentrations remained raised well after recovery from intercurrent disease. In this group, there were 2 cases of transient iodine-induced (Jod-Basedow) hyperthyroidism in which raised serum-T4 returned spontaneously to normal after several months as iodine was eliminated. These results indicate that increase in serum-T4 with normal serum-T3 in patients with intercurrent systemic disease is not always the result of hyperthyroidism and in many cases probably reflects changes in peripheral metabolism of T4. It is suggested that careful clinical follow-up is needed in patients with raised serum-T4 and normal serum-T3 for the early detection and treatment of classic hyperthyroidism.

Adult↗
PubMed1998

Assessment of cardiac vagal activity in patients with hyperthyroidism.

Previous studies suggested that in patients with hyperthyroidism an autonomic imbalance and in particular a lower than normal vagal activity might be present. To verify this hypothesis we have evaluated the respiratory sinus arrhythmia (RSA, a measure of cardiac vagal activity) in ten hyperthyroid patients and in ten normal subjects. RSA was calculated from the power of the spectral component of the heart rate variability in high frequency band (HF-RR) during both spontaneous (supine and passive head-up tilt) and controlled breathing (supine). During controlled breathing the phase relation between heart rate and respiratory has been computed. The hyperthyroid patients showed a higher heart rate in all three conditions (P<0.001) and higher spontaneous respiratory rate in supine position (centered frequency of HF-RR: 0.342+/-0.015 vs 0.262+/-0.016 Hz; P<0.001). No difference was found in hyperthyroid patients compared to controls in terms of the HF-RR power in normalized units both during spontaneous breathing (supine, 43+/-8.3 vs 39.7+/-6.7%; tilt 18.8+/-5.9 vs 19.3 vs 4.1%; mean+/-SE) and controlled breathing (45.4+/-7.1 vs 48.9+/-6.9%). No difference was found also in terms of the phase relationship between the heart rate and the respiratory signals (77.5+/-32.3 vs 77.5+/-28.1, degrees). Hyperthyroid patients seem not to have an impaired cardiac vagal activity.

Adult↗
PubMed1999

Clinical and biochemical changes following 131I therapy for hyperthyroidism in patients not pretreated with antithyroid drugs.

BACKGROUND: Radioiodine therapy (131I) for the treatment of hyperthyroidism has been shown to be effective and safe. Despite the extensive experience with radioiodine therapy, the necessity for pretreatment with antithyroid drugs is controversial. Pretreatment is partly based on the concept that antithyroid drugs deplete the thyroidal hormonal stores, thereby reducing the risk of a radioiodine-induced aggravation of hyperthyroidism or thyroid storm. Few data are available on the frequency of clinically significant exacerbations of hyperthyroidism following 131I therapy without prior treatment with antithyroid drugs. The aim of the present study was to determine prospectively the early clinical and biochemical changes after 131I therapy in patients who were not pretreated with antithyroid drugs. METHODS: Patients with Graves' disease (n = 21), toxic multinodular goiter (n = 11) or toxic adenoma (n = 2) were studied before and after 131I therapy. Clinical and biochemical parameters of thyroid function were investigated before and 1, 2, 8, 11, 18 and 25 days after 131I treatment. Patients were given no antithyroid drugs prior to 131I therapy, all patients received beta-blocking agents for symptomatic relief. RESULTS: In 19 of 34 patients, a transient increase in thyroid hormone levels was observed, predominantly in the first week following 131I therapy. None of these patients experienced worsening of thyrotoxic symptoms. This transient increase in thyroid hormone levels was demonstrated in all patients with toxic multinodular goiter, whereas it was found in only six of 21 patients with Graves' disease. This difference could not readily be explained by differences in pretreatment thyroid hormone levels, administered dose or effectively absorbed dose of 131I. CONCLUSIONS: 131I treatment of hyperthyroidism without pretreatment with antithyroid drugs may cause a transient increase in thyroid hormone levels. Clinically significant exacerbations of hyperthyroidism were, however, not observed in our study population. Increased hormone levels following 131I therapy were more often seen in patients with toxic multinodular goiter than in patients with Graves' disease.

Adenoma↗
PubMed2001

Early postmenopausal bone loss in hyperthyroidism.

OBJECTIVES: To evaluate the effect of hyperthyroidism on bone in relation to the menopausal state. METHODS: Fifty-nine hyperthyroid (HYPER), 40 hypothyroid (HYPO), and 51 control euthyroid (EUTH) women were studied. Bone mineral density (BMD) was assessed by dual X-rays absorptiometry (DXA) at the lumbar spine, and at the femoral neck. A multi-site QUS device evaluated speed of sound (SOS) at the radius (RAD), tibia (TIB), metatarsus (MTR), and phalanx (PLX). Bone markers used were serum bone specific alkaline phosphatase (BSAP) and urinary deoxypyridinoline (DPD). RESULTS: At all sites, SOS was lower in HYPER than in EUTH (RAD P<0.05, TIB P<0.01, MTR P<0.05, PLX P=0.01). The low SOS was only noted at the early postmenopausal period. BMD at the femoral neck but not at the lumbar spine was lower in HYPER as compared to EUTH (P<0.05). Both femoral neck and tibia were the sites with the highest odds ratio for being hyperthyroid (2.3 and 2.04, respectively). There was no correlation between BMD or SOS and FT(4), TT(3) or duration of hyperthyroidism. BSAP and DPD positively correlated with FT(4) and TT(3) (P<0.05). CONCLUSIONS: This study suggests that hyperthyroidism affects bone mineralization especially during the early postmenopausal period, and the effect is mainly at the cortical bone.

Absorptiometry, Photon↗