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PubMed2004

Radioiodine treatment of hyperthyroidism: prognostic factors affecting outcome.

OBJECTIVE: To assess the effectiveness of radioactive iodine (RAI) treatment in patients with hyperthyroidism and to evaluate prognostic factors affecting outcome. RESEARCH DESIGN AND METHODS: Our cohort comprised 115 consecutive patients with hyperthyroidism treated with RAI at the Endocrinology Clinic at the Farabi Hospital, Trabzon, between 1994 and 2002. Data were retrieved from the endocrinology clinic database. Patients were categorized into three diagnostic groups: Graves' disease (GD), toxic multinodular (TMN) hyperthyroidism, and toxic adenoma. Our policy, over the period of the study, was to offer a single fixed first dose (10 mCi) 131I to all patients with toxic nodular goiter (TNG) for the first time and to all patients with relapsed GD. RESULTS: There was no significant difference in the cure rate between GD and TNG, but Graves' patients had a significantly higher incidence of hypothyroidism (p < 0.001). In contrast, incidence of euthyroidism was significantly increased in TNG than those of the patients with GD (p < 0.05). The incidences of hyperthyroidism, euthyroidism, cure rate, and persistent hyperthyroidism did not vary significantly between females and males. Age at onset of hyperthyroidism at diagnosis was not associated with outcome of RAI therapy. The incidence of hypothyroidism in patients who had nonpalpable goiter was higher than those in patients who had medium or large goiter (p < 0.05). The means of serum FT3 and TT4 at presentation were correlated with the development of hypothyroidism after RAI therapy. Logistic regression analysis showed serum FT3 concentration at presentation to be significant contributing factor to failure to respond to a single dose of RAI. Patients who had higher FT3 concentrations at diagnosis were more likely to fail to respond to RAI therapy. CONCLUSION: The results of the present study of a cohort of patients with hyperthyroidism demonstrate that a single fixed dose of 10 mCi of RAI is highly effective in curing GD as well as toxic nodular hyperthyroidism. Therefore, treatment protocols for these groups should be identical. The most important factors that determine efficacy of RAI treatment are serum FT3 concentrations at diagnosis before the initiation of treatment and goiter size. Therefore, these factors should be taken into consideration when planning treatment. If such factors are present, the initial dose of RAI should be increased.

Adenoma↗

PubMed1984

[Serum angiotensin I converting enzyme activity in patients with hyperthyroidism and hypothyroidism: relation to renin and aldosterone].

In order to ascertain whether angiotensin I converting enzyme (ACE) activity might be regulated by thyroid hormone, serum ACE activity was measured in a variety of thyroid states, including hyperthyroid and hypothyroid subjects. In addition, the correlation of serum ACE activity to plasma renin activity (PRA) and plasma aldosterone concentration (PAC) was evaluated in these patients. In hyperthyroid patients, the mean (+/- SD) serum ACE activity was 32.7 +/- 6.7 U/ml (n = 30), which was significantly higher than that in hypothyroid patients (20.4 +/- 4.3 U/ml, n = 7, p less than 0.001) and in normal subjects (22.5 +/- 3.4 U/ml, n = 51, p less than 0.001). No significant difference in serum ACE activity was found between the hypothyroid patients and normal subjects. There was a significant positive correlation between serum ACE activity and PRA (r = 0.524, n = 30, p less than 0.01) and also between serum ACE activity and PAC (r = 0.473, n = 30, p less than 0.01) in the patients with hyperthyroidism. By contrast, no significant relationship was observed between serum ACE activity and thyroid hormones (r = 0.115, for T3; r = 0.143, for T4) in hyperthyroid patients. Treatment with furosemide (1 mg/kg i.v.) and upright posture (2h) significantly increased PRA, PAC and serum ACE activity in both hyperthyroid patients and normal subjects, but not in hypothyroid patients. There was a significant positive correlation between changes in serum ACE activity and in PRA (r = 0.418, n = 23, p less than 0.05) in response to the treatment in hyperthyroid patients, while no significant relationship was observed between them in either hypothyroid patients (r = 0.216, n = 6, p less than 0.10) or normal subjects (r = 0.620, n = 10, 0.05 less than p less than 0.01). In one patient with hyperthyroidism, administration of propranolol decreased PRA from 3.4 to 2.3 ng/ml/h, corresponding to an apparent decrease in serum ACE activity from 38.7 to 29.6 U/ml. From these results, it is suggested that serum ACE activity in the hyperthyroid state is modulated by the renin-angiotensin system rather than by thyroid hormone.

Adult↗

PubMed1986

[Responses of plasma bradykinin and the renin angiotensin axis to angiotensin II in hyperthyroid patients].

The present investigation was undertaken to elucidate the possible interplay between the circulating kinin(s) and the renin angiotensin axis in hyperthyroidism. The responsiveness of plasma aldosterone (p-Ald), kinin (p-BK), plasma renin activity (PRA) and serum angiotensin converting enzyme activity (ACEA) to infusion of angiotensin II at a dose of 4, 8 and 16 ng/kg.min. was asessed in 15 hyperthyroid patients and 10 euthyroid controls. There was impaired angiotensin II induced response of blood pressure in hyperthyroid patients, and basal concentrations of p-Ald were 7.7 +/- 3.8 ng/dl in euthyroid controls and 12.6 +/- 3.1 ng/dl in hyperthyroid patients (p less than 0.05). As compared to the euthyroid controls, the hyperthyroid patients showed a reduced response of plasma aldosterone to angiotensin II infusion. Angiotensin II infusion increased p-BK from basal levels of 19.1 +/- 8.2 pg/ml to 31.0 +/- 7.8 pg/ml (p less than 0.05) only in hyperthyroid patients and did not increase ACEA in either group. Next, the effects of a single administration of captopril (50 mg p.o.) on blood pressure and p-BK in hyperthyroid patients and euthyroid controls were studied. In the two groups blood pressure was not changed by captopril, but p-BK increased significantly. The present results do not support the view that there may be a direct linkage between the kallikrein kinin system and the renin angiotensin axis mediated by kininase II or angiotensin converting enzyme in human peripheral blood. Also it is unlikely that kinin may play a role in the mechanism of reduced responsiveness of aldosterone and blood pressure to angiotensin II in hyperthyroidism.

Adult↗

PubMed1986

Pharmacokinetics of methimazole in normal subjects and hyperthyroid patients.

Serum and urinary concentrations of methimazole (MMI) were measured by high-performance liquid chromatography (HPLC) with an electrochemical detector (ECD) in 10 normal subjects and 43 hyperthyroid patients after intravenous and oral administration of the drug. The pharmacokinetic parameters of MMI were estimated in 5 normal subjects and 15 hyperthyroid patients according to a two-compartment model after intravenous injection of a 10 mg dose. The mean half-life of the distribution phase (T1/2 alpha) was 2.7 +/- 1.0 h (mean +/- SD) and 3.1 +/- 1.4 h and that of the slower-phase (T1/2 beta) was 20.7 +/- 9.6 h and 18.5 +/- 12.9 h in normal subjects and hyperthyroid patients, respectively. There were no significant differences between pharmacokinetic parameters of normal subjects and those of hyperthyroid patients. No correlations between free T4 index (FT4I) and pharmacokinetic parameters were observed. Maximum serum MMI concentrations (Cmax) (213 +/- 84 and 299 +/- 92 ng/ml) were attained 1.8 +/- 1.4 h and 2.3 +/- 0.8 h after a single dose of 10 mg in 5 normal subjects and in 15 hyperthyroid patients, respectively. In hyperthyroid patients the time taken to reach the peak concentration (Tmax) after a single dose of 10 mg was similar to that after a single 15 mg and 30 mg dose. The pharmacokinetic parameters, except Cmax and the area under the curve (AUC), were not affected by the administered dose and those, except Cmax, were not affected by the thyroid function. All urine was collected at intervals of 3 h for the first 12 h and then at 24 h and 48 h after intravenous and oral administration of MMI. In all subjects, MMI rapidly appeared in the urine and the rate of excretion was highest in the first 3 h. The cumulative urinary excretion of MMI was 5.5-8.5% of administered doses in normal subjects and hyperthyroid patients. These findings in the present study are compatible with the assumption that the extent of absorption of MMI is high, if not complete, and hyperthyroidism does not affect the kinetics of MMI, and that interindividual variation is observed in the time taken to reach the peak concentration after oral administration.

Administration, Oral↗

PubMed1991

Diagnostic relevance of suppressed basal concentrations of TSH compared with the negative TRH test in detection and exclusion of hyperthyroidism.

To evaluate the sensitivity of basal TSH concentrations as determined by an "ultrasensitive" IRMA-assay (RIA-gnost h-TSH-monoclonal, Behring) versus a "negative" TRH test (defined as an increment of TSH less than or equal to 0.2 mU/l 20 min after administration of 400 micrograms TRH iv) in the diagnosis of hyperthyroidism we examined 193 consecutive patients from our thyroid outpatient clinic: 34 patients displayed hyperthyroidism (total T4: 184.4 +/- 26.0 mumol/l, effective thyroxine index: 1.25 +/- 0.08), whereas 12 had isolated T3-hyperthyroidism (total T3: 3.47 +/- 0.48 nmol/l). Employing the producer's definition of subnormal ("suppressed") bTSH concentrations (less than or equal to 0.1 mU/l), only 19 (41.3%) hyperthyroid patients would have been detected; on the other hand, one euthyroid patient would have been recognized false positively as hyperthyroid. Using the TRH test as criterion led to the correct diagnosis in 42 (sensitivity: 91.3%) hyperthyroid patients, whereas two had low bTSH concentrations (less than or equal to 0.5 mU/l), but a normal TSH response to TRH (greater than 2.0 mU/l). Raising the threshold concentration to 0.2 and, subsequently, to 0.4 mU TSH/l increased the number of correct results to 38 (sensitivity: 82.6%) and 43 (93.5%), respectively. This was associated with a concomitant decrease in specificity in the diagnosis of hyperthyroidism from 93.7 (0.1 mU/l) to 27.9% (0.4 mU/l). In conclusion, despite ultrasensitive methods for estimation of low TSH concentrations, the TRH test remains an irreplaceable tool for the correct diagnosis of hyperthyroidism.

Adult↗

PubMed1992

Increased lymphocyte thermogenesis in hyperthyroid patients. Role of Na/K pump function. Evaluation of aerobic/anaerobic metabolism.

The role of the Na/K pump for the increased cell energy expenditure in hyperthyroidism was studied by measuring total lymphocyte heat production rate in samples with and without ouabain inhibition of Na/K ATP-ase. In addition, the relative contribution of aerobic processes to lymphocyte thermogenesis was calculated from oxygen consumption measurements. In 12 patients with clinical and laboratory hyperthyroidism total lymphocyte heat production rate was 3.19 +/- 0.21 pW/cell, significantly higher than in 7 patients with subclinical hyperthyroidism (2.14 +/- 0.11 pW/cell) and in 15 euthyroid subjects (2.26 +/- 0.11 pW/cell) (p less than 0.001). The relative decrease in lymphocyte heat production rate after ouabain, giving a quantitative measure of the activity of the Na/K ATP-ase and reflecting the importance of Na/K pump function for the overall rate of lymphocyte metabolism, was not significantly different between the groups: 19.5 +/- 3.6% in hyperthyroid patients, 14.2 +/- 2.3% in subclinical hyperthyroid patients and 17.8 +/- 3.1% in euthyroid subjects. According to the rate of lymphocyte oxygen consumption, aerobic processes represented 58.4 +/- 6.7% of total lymphocyte energy expenditure in hyperthyroid patients, not significantly different from subclinical hyperthyroidism (62.6 +/- 8.4%) or from euthyroidism (66.6 +/- 2.7%). These data do not support the hypothesis of a specific role of the Na/K pump function for the increased cell thermogenesis in hyperthyroidism and indicate a parallel stimulation of aerobic and anaerobic processes by thyroid hormone excess.

Adult↗

PubMed2006

Effects of hyperthyroidism induced by L-thyroxin administration on lipid peroxidation in various rat tissues.

Thyroid dysfunctions are associated with many pathological signs in the body. One of these is lipid peroxidation that develops due to over- or under-secretion of thyroid hormones. The present study was conducted to determine lipid peroxidation that develops in different tissues including the brain, liver and heart of rats in experimental hyperthyroidism induced by L-thyroxin. The study was carried out on 30 male Sprague-Dawley rats. They were divided into three groups as control, sham hyperthyroidism and hyperthyroidism. Malondialdehyde (MDA) and glutathione (GSH) levels in rat tissues were determined at the end of a 3-weeks period of L-thyroxin administration. It was observed that MDA levels in the hyperthyroidism group were significantly higher in the cerebral cortex, liver and ventriculer tissue of heart (p < 0.001) than in the control and in sham hyperthyroidism groups. GSH levels were higher in the hyperthyroidism group than in control and sham hyperthyroidism groups in all tissues (p < 0.001). Results demonstrate that hyperthyroidism induced by L-thyroxin activates both oxidant and antioxidant systems in cerebral, hepatic and cardiac tissues. However, the increase in antioxidant activity cannot adequately prevent oxidative damage.

Animals↗

PubMed2000

Serum cytokine levels in autoimmune and non-autoimmune hyperthyroid states.

Although the role of interleukin-2 (IL-2) and interferon gamma (gammaIFN) is still poorly understood in hyperthyroid diseases, it is reasonable to assume that these cytokines may be present at higher levels in Graves' disease (GD) than in other primarily non-autoimmune thyroid diseases. In order to look for an easy method to distinguish GD from primarily non-autoimmune causes of hyperthyroidism, we compared 13 healthy individuals with 21 treated and untreated hyperthyroid GD patients and with 19 patients with hyperthyroidism due to other etiologies: 7 cases of multinodular goiter, 5 cases of excessive hormone replacement and 7 cases of amiodarone-associated hyperthyroidism. All patients presented low TSH levels and a dubious clinical thyroid state. We found a good correlation between TSH and serum IL-2 levels (r = 0.56; P<0.01). Serum IL-2 (P<0.01) and gammaIFN (P<0.01) levels were lower in the hyperthyroid group of patients than in control subjects, suggesting a depressed TH1 pattern in the T-cell subset of hyperthyroid patients. GD had normal IL-2 levels, while patients with other forms of thyrotoxicosis presented decreased IL-2 levels (P<0.05). There was no difference between treated and untreated GD patients. We suggest that the direct measurement of serum IL-2 level may help to confirm hyperthyroidism caused by GD.

Adolescent↗

PubMed1985

Spermatogenesis, seminal characteristics and reproductive hormone levels in mature rams with induced hypothyroidism and hyperthyroidism.

Mature Merino rams were made hypothyroid by daily oral drenching with methylthiouracil or hyperthyroid by daily subcutaneous injections of thyroxine for 8 weeks. Neither hypothyroidism nor hyperthyroidism had any apparent effect on either spermatogenesis or daily sperm production, but motility of ejaculated spermatozoa and circulating testosterone concentrations were reduced in both conditions. The ratio of testosterone concentrations in plasma from the internal spermatic vein to those in peripheral blood plasma was higher in hyperthyroid (21.2 +/- 3.5) than in control (11.1 +/- 4.4) and hypothyroid (7.6 +/- 1.4) rams. The basal secretion rate for testosterone was slightly lower in hypothyroid rams and testosterone responses to human chorionic gonadotrophin and after LH-releasing hormone (LHRH) were very much reduced. Basal serum LH levels were low in both hypothyroid and hyperthyroid rams compared with controls whereas there were no differences in FSH levels. The LH response to exogenous LHRH was reduced in hypothyroid rams but not in hyperthyroid rams. Serum prolactin levels on the other hand were higher than control in both hypothyroid and hyperthyroid rams. Reduced testosterone secretion in hypothyroid rams indicates that the normal function of Leydig cells depends on an adequate level of thyroid hormones. The decrease in circulating testosterone concentrations in hyperthyroid rams with normal secretion rates suggests an increased testosterone clearance rate in these animals. The decreased spermatozoal motility in hypo- and hyperthyroid rams suggests that the lowered testosterone level in these animals has altered the androgen-dependent maturation of spermatozoa in the epididymis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Relationship between the resting metabolic rate and hepatic metabolism in rats: effect of hyperthyroidism and fasting for 24 hours.

We have examined the relationship between the changes in resting metabolic rate (RMR) and those in hepatic metabolism induced by hyperthyroidism and fasting for 24 h. We found that hyperthyroidism induced a significant increase in RMR, while fasting for 24 h reduced RMR in euthyroid but not in hyperthyroid rats. We have also measured oxygen consumption in isolated hepatocytes from euthyroid and hyperthyroid rats, fed or fasted for 24 h. Hyperthyroidism induced an increase in oxygen consumption in rat liver cells; fasting for 24 h increased respiratory rates in isolated liver cells from euthyroid but not from hyperthyroid rats. The findings showed that hyperthyroidism and fasting for 24 h have opposite effects on RMR but similar effects on hepatic metabolism. The results also indicated that the increase in RMR found in hyperthyroid rats is partly due to an increase in hepatic metabolism, while no correlation exists between variations in resting and hepatic metabolism induced by 24-h fasting.

Animals↗

PubMed2004

Analysis of differentially expressed genes in hyperthyroid-induced hypertrophied heart by cDNA microarray.

Experiments were carried out to identify the altered genes in hyperthyroid rat heart and their influence on the functions of cardiac myocytes. Chronic treatment of rats with 3,5,3' triiodo-L-thyronine (T3) resulted in a prominent increase in the size of the left ventricle with increased wall thickness and reduced chamber volume leading to concentric cardiac hypertrophy. The heart weight to body weight ratio (HW/BW) in hyperthyroid rats was increased by about 58% over that of normal rats. Using cDNA microarray comprising 588 genes, we compared the differences in mRNA expression of hyperthyroid and normal rat heart. Based on a threshold of greater than 10% change, about 37 genes were found to be regulated by T3. Further analyses by Western blotting, Northern blotting and real-time quantitative RT-PCR of some of the genes confirmed the microarray results. The T3-altered genes encode various types of proteins related to metabolism, matrix and cytoskeletal structures, growth factors, transcription factors, Ca(2+)-channels etc. The physiological significance of one of these altered proteins in hyperthyroid heart, insulin-responsive glucose transporter (GLUT) type 4 (GLUT4), was studied in detail. The expression of GLUT4 was drastically reduced in the ventricular tissues of hyperthyroid heart. Insulin-induced glucose uptake in hyperthyroid cardiomyocytes was reduced significantly, indicating the impaired glucose transport in cardiac cells. Interestingly, a few genes such as GLUT4, cytochrome P450 isoforms, superoxide dismutase (SOD), collagens, matrix metalloproteinases (MMP), tissue inhibitors of matrix metalloproteinases etc. which had not been reported earlier were found to be altered in hyperthyroid heart. Our results show some new aspects of hyperthyroid heart which will be important in assessing the pathophysiology of hypertrophied cardiomyocytes.

Animals↗

PubMed1998

Hyperthyroidism. Current treatment guidelines.

Hyperthyroidism is common and affects approximately 2% of women and 0.2% of men. The most common cause of hyperthyroidism is Graves' disease, an autoimmune disorder associated with circulating immunoglobulins that bind to and stimulate the thyrotropin (TSH) receptor, resulting in sustained thyroid overactivity. Toxic nodular goitres cause hyperthyroidism due to autonomous hyperfunctioning of localised areas of the thyroid. There are 3 recognised modalities of treatment for hyperthyroidism: antithyroid drugs, surgery and radioiodine. All are effective but no single method offers an absolute cure. Patients with Graves' disease may be prescribed antithyroid drugs over a period of 12 to 18 months with a view to inducing a long term remission. These drugs are also often given for a short period to render the patient euthyroid before definitive therapy with radioiodine or thyroidectomy. However, antithyroid drugs will not 'cure' hyperthyroidism associated with a toxic nodular goitre. The use of radioiodine as a first-line therapy for hyperthyroidism is growing. It is well tolerated, with the only long term sequelae being the risk of developing radioiodine-induced hypothyroidism. Radioiodine can be used in all age groups other than children, although it should also be avoided in pregnancy and during lactation. Pregnancy should be avoided for 4 months following its administration. Radioiodine may cause a deterioration in Graves' ophthalmopathy and corticosteroid cover may reduce the risk of this complication. The treatment of choice for toxic nodular goitre hyperthyroidism is radioiodine. Surgery, either subtotal or near-total thyroidectomy, has limited but specific roles to play in the treatment of hyperthyroidism: this approach is rarely used in patients with Graves' disease unless radioiodine has been refused or there is a large goitre causing symptoms of compression in the neck. The goal of surgery is to cure the underlying pathology while leaving residual thyroid tissue to maintain postoperative euthyroidism.

Adrenergic beta-Antagonists↗

PubMedDate not supplied

Gastric inhibitory polypeptide (GIP) responses after oral glucose ingestion in hyperthyroidism.

Gastric inhibitory polypeptide (GIP) is a gastrointestinal hormone stimulated after oral nutrient ingestion, but not after intravenous nutrient administration. GIP stimulates insulin release in the presence of hyperglycemia and as such is considered a major enteroinsular hormone. Since elevated glucose and insulin levels are found in hyperthyroidism, we compared the GIP responses to oral glucose ingestion in 12 hyperthyroid patients and 10 age-matched controls. Seventy-five grams of oral glucose was ingested after overnight fasting and samples were obtained at 0, 30, 60, 90, 120, and 180 min for serum glucose and immunoreactive insulin (IRI) and GIP (IRGIP). The mean serum glucose levels in hyperthyroid subjects were significantly higher (P less than or equal to 0.05) at every time studied except at 180 min. At 60 min, peak mean glucose was 171 +/- 14 mg/dl versus 128 +/- 7 mg/dl in controls (P less than 0.02). Except for fasting, mean IRI levels were significantly higher (P less than 0.001) in hyperthyroid subjects than in controls at all times studied. At 60 min, IRI rose to a peak of 125 +/- 11 microU/ml in hyperthyroid subjects versus 50 +/- 9 microU/ml in controls (P less than 0.001). Mean fasting, stimulated, and incremental IRGIP levels were slightly higher but not statistically different in the hyperthyroid subjects versus controls. Glucose and IRI responses are exaggerated in hyperthyroidism after oral glucose ingestion. Even though GIP has insulinotropic action, its role in the hyperinsulinism found in hyperthyroid subjects appears to be minimal.

Adult↗

PubMed2006

[Effects of short-term rapid atrial pacing on electrophysiological characteristics of atrium in hyperthyroidism].

OBJECTIVE: To investigate the effects of short-term rapid atrial pacing on the electrophysiological characteristics of atrium in hyperthyroidism. METHODS: Forty-six adult rabbits were randomly divided into 4 groups: normal control group (n=10), pacing group (n=10), hyperthyroidism group (n=14), hyperthyroidism/pacing group (n=12). Baseline AERP and AERPs after pacing 2, 4, 6 h were determined in all groups at driver cycle length (DCL) of 200 ms, 150 ms and 130 ms. RESULT: In pacing group, AERPs at different DCL (200 ms, 150 ms and 130 ms) were shortened after rapid pacing 2, 4, 6 h when compared with before pacing and control group (P<0.01). AERPs (at DCL of 200 ms, 150 ms and 130 ms) in hyperthyroidism group were shorter than those in control group at all time points (P<0.01). AERPs (at DCL of 200 ms, 150 ms and 130 ms) in hyperthyroidism/pacing group after rapid pacing 2, 4, 6 h were shorter than those in pacing 0 h (P<0.01) and hyperthyroidism group (P<0.05). AERP200-150 and AERP200-130 in pacing group after rapid pacing 2, 4, 6 h were significantly different from at pacing 0 h and control group (P<0.01). AERP200-150 and AERP200-130 in hyperthyroidism and hyperthyroidism/pacing group were significantly different from control group at all time points (P<0.01). No differences were observed in AERP200-150 and AERP200-130 between hyperthyroidism group and hyperthyroidism/pacing group. CONCLUSION: Hyperthyroidism and short-term atrial pacing in the presence of hyperthyroidism can lead to remodeling of atrial electrophysiology.

Animals↗

PubMed2000

[Contribution of the renin-angiotensin system to blood pressure variability in hyperthyroid rats].

OBJECTIVES: To produce a chronical thyrotoxicosis model in rat, and to evaluate, using spectral analysis, the involvement of the renin-angiotensin system (RAS) in short-term variability of blood pressure (BP) in experimental hyperthyroidism. DESIGN AND METHODS: Thyrotoxicosis was produced by a daily intraperitoneal (i.p.) injection of L-thyroxine (T4: 0.1 mg/kg for 15 days) in Wistar rats. Control (euthyroid) rats received i.p. daily injection of the thyroxine solvent. Two series of experiments were performed in conscious and unrestrained rats. In the first series, 10 euthyroid and 14 hyperthyroid rats were surgically prepared with a femoral artery catheter to measure BP and heart rate (HR) and to collect blood samples on the last day of treatment. In the second series of experiments (n = 12 in each group), on the fifteenth day of treatment, BP and HR were recorded by telemetry in control conditions and after a specific blockade of the RAS by the angiotensin type I receptors antagonist: valsartan (10 mg/kg, i.p.). BP recordings were analysed by the Fast Fourier Transform on consecutive 204.8-s stationary periods. RESULTS: The dose and duration of T4 treatment was sufficient to induce a significant degree of hyperthyroidism with characteristic features including: tachycardia, systolic hypertension, myocardial hypertrophy, hyperthermia, and weight loss. In addition, we measured an increase in free fractions of thyroid hormones, and a 3 fold-increase of plasma renin activity. Hyperthyroidism modified systolic BP (SBP) variability profiles. An amplification of low frequency (LF) oscillations (2.37 +/- 0.12 mmHg vs 1.78 +/- 0.11 mmHg, p < 0.01) was observed after T4 treatment. In hyperthyroid rats, valsartan diminished the slow fluctuations of SBP (p < 0.001) and increased the mid-frequency oscillations (2.44 +/- 0.20 mmHg vs 1.32 +/- 0.18 mmHg, p < 0.001). CONCLUSION: The cardiovascular alterations of hyperthyroidism are reproduced with thyroid hormone injections in rats. Activation of the RAS in hyperthyroid rats was accompanied by increased SBP variability in the LF range. Using the angiotensin type I receptors antagonist, valsartan, we demonstrated that the RAS impinged on the LF oscillations of the SBP in our experimental hyperthyroidism model.

Angiotensin I↗

PubMed1992

[Influence of dexamethasone and epinephrine on glycogen content and cytosol glucocorticoid receptors in hyperthyroid rat liver].

The influence of hyperthyroidism on the action of drugs affecting rat liver glycogen content and its mechanism were investigated. The thyroid-induced hyperthyroidism of rat served as the model. In normal rats, dexamethasone (5 mg.kg-1, ip) increased the content of liver glycogen and decreased the Bmax of glucocorticoid receptors (GCR) in liver cytosol. These effects were minimized or even disappeared in hyperthyroid rat models. On the other hand, in normal rats, epinephrine (0.20 mg.kg-1, ip) decreased the content of liver glycogen. This effect was potentiated in hyperthyroid rat models. Epinephrine did not affect the Bmax of GCR in liver cytosol of normal and hyperthyroid rats. These results suggested that hyperthyroidism may be one of the causes effecting the individual differences of drug action, and that the influence of hyperthyroidism on the glycogen-increasing action of dexamethasone correlated well with the changes in glucocorticoid receptor. The mechanism of the influence of hyperthyroidism on the glycogen-decreasing action of epinephrine is to be further explored.

Animals↗

PubMed2005

Pinealectomy inhibits antioxidant system in rats with hyperthyroidism.

OBJECTIVE: Thyroid hormones regulate energy metabolism and act on the mitochondria, which is an important source of free radicals in the cell. Reactive oxygen types play a significant role in physiological mechanisms, but in excessive amounts they can cause oxidative damage in molecules. The aim of the present study was to determine levels of lipid peroxidation caused by induced hyperthyroidism in cerebral, hepatic and cardiac tissues of pinealectomized rats. METHODS: Experimental animals used in the study were allocated to three groups as general control group, hyperthyroidism-sham pinealectomy group and hyperthyroidism-pinealectomy group. GSH and MDA levels in cerebral, hepatic and cardiac tissues were evaluated at the end of the 3-week study period. RESULTS: It was found that MDA levels in cerebral, hepatic and cardiac tissues were the highest in hyperthyroidism and pinealectomy group and that these values were higher in hyperthyroidism-sham pinealectomy group than in the control group (p<0.001). It was seen that tissue GSH levels significantly increased in hyperthyroidism-sham pinealectomy group (p<0.001) and that the increase in hyperthyroidism and pinealectomy group was higher than the increase in the control group only (p<0.001). CONCLUSION: Results of our study show that MDA and GSH levels in cerebral, hepatic and cardiac tissues increased due to hyperthyroidism and that the increase in MDA levels became more evident and GSH levels were significantly suppressed after pinealectomy.

Animals↗

PubMed2006

Work capacity and oxygen uptake abnormalities in hyperthyroidism.

AIM: The aim of our study was to evaluate the haemodynamic and the respiratory response to exercise in patients with hyperthyroidism before and 30 days after normalized thyroid hormones levels. These findings were compared with those of 10 control patients. METHODS: Thirty patients (23 women, aged 34.3 +/- 12 years) with untreated hyperthyroidism were studied. Twenty-four patients were treated with methimazole, 13 of which were also treated with propranolol. Six patients underwent surgery. A symptom-limited cardiopulmonary exercise test and an echocardiography were performed in all patients. RESULTS: At rest patients with hyperthyroidism showed at echocardiography an increased cardiac index (P = 0.006 vs euthyroid, P = 0.007 vs normal) and a higher ejection fraction (P = 0.008 vs euthyroid, P = 0.007 vs normal). The duration of the exercise was lower in hyperthyroid patients (P = 0.006 vs euthyroid; P = 0.0068 vs normal). Anaerobic threshold was reached at 49.6% of peak VO2 during hyperthyroidism, at 60.8% during euthyroidism (P = 0.01) and at 62% in normal (P = 0.01). Work rate was lower in patients with hyperthyroidism at anaerobic threshold (P = 0.01 vs euthyroid, P = 0.03 vs normal) and at maximal work (P = 0.001 vs euthyroid, P = 0.01 vs normal). Patients in hyperthyroidism showed a lower increment of heart rate between rest and anaerobic threshold (P = 0.021 vs euthyroid, P < 0.0001 vs normal) and a lower VO2 at anaerobic threshold (P = 0.03 vs euthyroid; P = 0.04 vs normal). Oxygen pulse at anaerobic threshold was significantly reduced in hyperthyroidism (P = 0.04 vs euthyroid, P = 0.005 vs normal). CONCLUSIONS: The mean result is that after only 30 days of appropriate antithyroid treatment there was an appreciable improvement of exertion capacity.

Adult↗