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PubMed2007

Melatonin protects against oxidative damage and restores expression of GLUT4 gene in the hyperthyroid rat heart.

To understand the mechanism of cardiovascular dysfunction in the hyperthyroid condition, the role of oxidative stress was examined in rats treated with 3,5,3'-triiodo-l-thyronine (T3). Treatment of rats daily with T3 (8 microg/100 g BW) for 15 days resulted in an increase in heart weight to body weight ratio, which was ameliorated by antioxidants, melatonin (2 mg/100 g BW) or vitamin E (4 mg/100 g BW). Both melatonin and vitamin E also inhibited rises of lipid peroxidation and hydroxyl radical generation and prevented the inhibition of Cu,Zn-superoxide dismutase in the hypertrophic heart. The expression of the glucose transporter, GLUT4, was reduced in response to T3, which was completely restored by melatonin and partially by vitamin E. However, neither antioxidant prevented down regulation of peroxisome proliferator-activated receptor-alpha in the hyperthyroid heart. Furthermore, the reduced level of myocyte enhancer factor-2, a regulator of GLUT4 transcription was restored completely by melatonin and partially by vitamin E treatment. Glucose uptake in hypertrophic left ventricular cells was also restored by these antioxidants. The expression of B-type natriuretic peptide, a marker of heart failure, was significantly increased by T3 and ameliorated by melatonin or vitamin E treatments. In general, the beneficial effects of melatonin given as a co-treatment with T3 were better than those induced by vitamin E. These data show that melatonin ameliorates hypertrophic growth of the myocardium induced by hyperthyroidism and provide an insight into the mechanism of reactive oxygen species-mediated down regulation of metabolically important genes such as GLUT4 in the heart.

Animals↗
PubMed1986

Hypercalcemia: an unusual complication of hyperthyroidism in a child.

Although well known in adults the association of hypercalcemia with hyperthyroidism has not been reported in children. We described how its occurrence in a hyperthyroid child obscured the manifestations of hyperthyroidism and discuss the factors that led to its appearance and regression.

Child↗
PubMedDate not supplied

Effects of methimazole on thyroid gland uptake of 99mTC-pertechnetate in 19 hyperthyroid cats.

Nineteen cats with abnormally high serum T4 concentrations underwent thyroid scintigraphy using technetium-99m pertechnetate (99mTcO4) before and after 36 +/- 6 days of methimazole administration (approximately 2.5mg PO q 12 h). Thyroid-to-salivary gland ratios (T:S ratios) and percentage thyroidal uptake of injected radioactivity at 20 and 60min after injection of 99mTcO4 were compared before and after methimazole treatment. Serum thyroid stimulating hormone (TSH) concentration was measured before and after methimazole treatment. Quantitatively, there was a positive association between the thyroid uptake of 99mTcO4 and the serum T4 before treatment (r = 0.74-0.83). TSH suppression was present when cats were first evaluated for hyperthyroidism. Methimazole treatment did not relieve TSH suppression in 17 cats. Two cats with unilateral thyroid uptake developed bilateral, asymmetric thyroid uptake of 99mTcO4 after treatment and had the greatest increase in TSH concentration after treatment. Quantitatively, thyroid scintigraphy did not significantly change after methimazole treatment (P>0.1). Evaluation of serum TSH concentration may be helpful in identifying methimazole-induced changes in the scintigraphic features of hyperthyroidism in mildly hyperthyroid cats.

Animals↗
PubMed2003

The thermogenic function of the sarcoplasmic reticulum Ca2+-ATPase of normal and hyperthyroid rabbit.

After formation of a Ca(2+) gradient, the amount of heat released during the hydrolysis of each mol of ATP cleaved (DeltaH(cal)) varies depending on the Ca(2+)-ATPase isoform expressed by the muscle cell. In vesicles derived from the sarcoplasmic reticulum of white muscle (SERCA 1) most of the ATP cleaved is not coupled to Ca(2+) transport, and the DeltaH(cal) varies between -20 and -22 kcal/mol. In contrast, in vesicles derived from red muscle (SERCA 2a) the hydrolysis of ATP is coupled with Ca(2+) transport, and the DeltaH(cal) varies between -12 and -14 kcal/mol. Hyperthyroidism increases the rate of heat production by the Ca(2+)-ATPase fourfold in white muscle and 40-fold in red muscle. In hyperthyroid rabbits, the amount of sarcoplasmic reticulum protein recovered from white and red muscle is four- to fivefold greater than that obtained from control rabbits. Hyperthyroid red muscle expresses SERCA 1, and the vesicles derived from these muscle hydrolyze ATP through a catalytic route that is not coupled to Ca(2+) transport, thus increasing the amount of heat released during ATP hydrolysis, the DeltaH(cal) varying between -20 and -22 kcal/mol.

Adenosine Triphosphate↗
PubMedDate not supplied

Methimazole treatment of 262 cats with hyperthyroidism.

The efficacy and safety of the antithyroid drug methimazole were evaluated over a 3-year period in 262 cats with hyperthyroidism. In 181 of the cats, methimazole was administered for 7 to 130 days (mean, 27.7 days) as a preoperative preparation for thyroidectomy. The remaining 81 cats were given methimazole for 30 to 1,000 days (mean, 228 days) as sole treatment for the hyperthyroid state. After 2 to 3 weeks of methimazole therapy (10 to 15 mg/d), the mean serum thyroxine (T4) concentration decreased significantly (P less than 0.001) from a pretreatment value of 12.1 micrograms/dl to 2.1 micrograms/dl. The final maintenance dose needed to maintain euthyroidism in the 81 cats that were given methimazole as sole treatment for hyperthyroidism ranged from 2.5 to 20 mg/d (mean, 11.9 mg/d). Clinical side effects developed in 48 (18.3%) cats (usually within the first month of therapy), which included anorexia, vomiting, lethargy, self-induced excoriation of the face and neck, bleeding diathesis, and icterus caused by hepatopathy. Mild hematologic abnormalities developed in 43 (16.4%) cats (usually within the first 2 months of treatment), which included eosinophilia, lymphocytosis, and slight leukopenia. In ten (3.8%) cats, more serious hematologic reactions developed including agranulocytosis and thrombocytopenia (associated with bleeding). These hematologic abnormalities resolved within 1 week after cessation of methimazole treatment. Immunologic abnormalities associated with methimazole treatment included the development of antinuclear antibodies in 52 of 238 (21.8%) cats tested and red cell autoantibodies (as evidenced by positive direct antiglobulin tests) in three of 160 (1.9%) cats tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Radioactive iodine treatment of a functional thyroid carcinoma producing hyperthyroidism in a dog.

Radioactive iodine (131I) was used in the treatment of a 12-year-old female dog with hyperthyroidism resulting from a large, unresectable (and metastatic) thyroid carcinoma associated with signs of severe inspiratory stridor and dyspnea. Hyperthyroidism was diagnosed on the basis of clinical signs (polyuria, polydipsia, polyphagia, weight loss, nervousness) and high basal serum thyroxine (T4) concentrations, as well as thyroid radioiodine kinetic studies that showed a high radioiodine uptake into the thyroid (% thyroid uptake) and markedly increased serum concentrations of protein-bound iodine-131 (PB131I) after 131I tracer injection. Thyroid imaging revealed diffuse radionuclide accumulation by the tumor, which involved both thyroid lobes. The dog was treated with three large doses of radioiodine (131I), ranging from 60 to 75 mCi, given at intervals of 5 to 7 months. The dog became euthyroid, and the size of the tumor decreased by approximately 25% after each 131I treatment, improving the severe inspiratory stridor and dyspnea, but both the hyperthyroid state and breathing difficulty recurred within a few months of each treatment. The dog was euthanatized 5 months after the last treatment because of progressive tracheal compression and pulmonary metastasis.

Animals↗
PubMed2006

Verification of the agreement of two dosimetric methods with radioiodine therapy in hyperthyroid patients.

The aim of this study was to verify the capability of an MIRD formula-based dosimetric method to predict radioiodine kinetics (fraction of administered iodine transferred to the thyroid, U0, and effective clearance rate, lambda(eff)) and absorbed dose after oral therapeutic 131I administration. The method is based on 123I intravenous administration and five subsequent gamma camera measured uptake values determined separately on different structures within the thyroid. Another dosimetric method based on only the 123I 24-h uptake and a fixed lambda(eff) value was also considered. Eighty-nine hyperthyroid patients (10 with Graves' disease and 79 with autonomously functioning nodules) were studied and 132 thyroidal structures were evaluated. The mean time interval between dosimetry and therapy was 20 +/- 10d. Uptake values were measured at 2, 4, 24, 48, and 120 h during dosimetry and at 2, 4, 24, 48, 96, and 168 h during therapy. The value 0.125d(-1) was chosen in the fixed-lambda(eff) method. The planned doses to the target ranged from 120 to 250 Gy depending on the type and severity of hyperthyroidism. The following significant correlations between therapeutic and dosimetric parameters were found: U0(ther)=0.88U0(dos) (r=0.97,p<0.01), lambda(eff)ther = 1.01 lambda(eff)dos (r=0.85,p<0.01), and D(estimated)= 0.85D(planned) (r=0.88, p<0.01). The percent difference between U0(ther) and U0(dos) ranged from -44 to 32% and between lambda(eff)ther and lambda(eff)dos from -32 to 48%. U0(ther) was lower than U0(dos) in 74% of cases: this can be explained by the self-stunning effect of 131I therapeutic activity that produced a dose of about 20 Gy with a maximum dose rate of 0.6 Gy/h over the initial 24-48 h. The differences, deltaD, between the estimated and the planned doses ranged from -42% (-87 Gy) to 32% (59 Gy); in 73% of cases the difference was within +/- 35 Gy. Greater discrepancies were found with the fixed-lambda(eff) method, in which deltaD ranged from -69 to 95% (-202 to 88 Gy, respectively). In hyperthyroid patients, the five uptake value dosimetric method is able to predict with a good agreement the radioiodine kinetics and the dose after the therapeutic administration in about 73% of the analyzed thyroid structures. The fixed-lambda(eff) method is less reliable.

Aged↗
PubMed1985

Raised plasma glutathione S-transferase values in hyperthyroidism and in hypothyroid patients receiving thyroxine replacement: evidence for hepatic damage.

Using plasma glutathione S-transferase measurements hepatocellular integrity was assessed in groups of hyperthyroid and hypothyroid patients before and after treatment. Ten of 14 hyperthyroid patients had clearly raised plasma glutathione S-transferase values at presentation and in each patient treatment with either iodine-131 or carbimazole resulted in a significant fall in glutathione S-transferase. The eight hypothyroid patients had normal glutathione S-transferase values at presentation and all showed a significant increase in these after thyroxine replacement therapy. In three of these patients in whom standard doses of replacement therapy were associated with a raised free thyroxine (T4) concentration but normal total and free triiodothyronine (T3) values glutathione S-transferase was increased. Similar though less consistent changes were seen in the results of standard chemical tests of liver function. It is concluded that hyperthyroidism may produce subclinical liver damage in a high proportion of patients and that this resolves with effective treatment. More important, the data suggest that hypothyroid patients receiving thyroxine replacement therapy may have similar subclinical liver damage. Patients receiving thyroxine should be monitored by the measurement of free, not total hormone concentrations, and in those in whom free T4 is raised the dose of thyroxine should be reduced. It would also be expedient to include periodic biochemical assessment of liver function in patients receiving thyroxine.

Adult↗
PubMed1989

Treatment of amiodarone induced hyperthyroidism with potassium perchlorate and methimazole during amiodarone treatment.

To exploit the antiarrhythmic effect of amiodarone when patients develop the side effect of thyrotoxicosis three patients with hyperthyroidism induced by amiodarone were given simultaneously 1 g potassium perchlorate a day for 40 days and a starting dose of 40 mg methimazole a day while they continued to take amiodarone. As hyperthyroidism might have recurred after potassium perchlorate treatment was stopped the dose of methimazole was not reduced until biochemical hypothyroidism (raised thyroid stimulating hormone concentrations) was achieved. The patients became euthyroid (free triiodothyronine concentration returned to normal values) in two to five weeks and hypothyroid in 10 to 14 weeks. One patient became euthyroid while taking 5 mg methimazole a day and 600 mg amiodarone weekly; the two others required substitution treatment with thyroxine sodium while taking 5 mg methimazole or 50 mg propylthiouracil (because of an allergic reaction to methimazole) and 2100 or 1400 mg amiodarone weekly. Hyperthyroidism induced by amiodarone may be treated with potassium perchlorate and methimazole given simultaneously while treatment with amiodarone is continued.

Aged↗
PubMed1984

Delayed recovery of left ventricular function after antithyroid treatment. Further evidence for reversible abnormalities of contractility in hyperthyroidism.

Sequential measurements of systolic time intervals, left ventricular dimensions, and the derived indices of contractility were undertaken at rest and during isometric exercise in 15 hyperthyroid patients before, during, and after antithyroid treatment. At rest hyperthyroidism was characterised by a shortened pre-ejection period and increased velocity of circumferential shortening of the left ventricle. During isometric exercise, however, the pre-ejection period increased significantly beyond that predicted for normal subjects, and the velocity of circumferential fibre shortening fell by 30%. In contrast, both the pre-ejection period and the velocity of circumferential fibre shortening were unchanged during exercise after a stable euthyroid state had been achieved for at least three months. Comparison between exercise responses and thyroid status during antithyroid treatment showed that a biochemical euthyroid state may be achieved many weeks before normalisation of contractile response to exercise. These findings support the hypothesis of reversible depression of left ventricular function in hyperthyroidism. Responses at rest principally reflect the peripheral actions of thyroid hormone excess.

Adult↗
PubMed1985

Myxoedema followed by TSAb-induced hyperthyroidism: report of 2 cases.

The development of spontaneous hyperthyroidism following primary hypothyroidism is an unusual occurrence. We report two cases of confirmed primary hypothyroidism who subsequently became hyperthyroid. Thyroid stimulating antibodies were present in the sera of both patients during the hyperthyroid state. The significance of this sequence of events is discussed and a possible explanation proposed.

Adult↗
PubMed1986

Iodine-induced hyperthyroidism in a patient with a normal thyroid gland.

Iodine-induced hyperthyroidism can develop even in the presence of an otherwise normal gland. One of the less common sources of iodine is tablets of seaweed, sold over the counter without prescription. We report the case of a 72 year old female who developed clinical and laboratory evidence of hyperthyroidism while ingesting sea-kelp (Vitalia) tablets. Six months after stopping the tablets, the symptoms and laboratory evidence of hyperthyroidism had disappeared. No evidence of pre-existing thyroid disease was found.

Aged↗
PubMed1990

Clinical hyperthyroidism due to non-neoplastic inappropriate thyrotrophin secretion.

We report a case of hyperthyroidism due to inappropriate thyrotrophin (TSH) secretion in a patient with selective pituitary resistance to thyroid hormone action. Symptoms of hyperthyroidism in patients with this disorder are usually mild, implying some peripheral tissue resistance to the metabolic effects of thyroid hormone. Our patient had unusually severe symptoms, including marked weight loss and cardiac arrythmias which required carbimazole and beta-blocker therapy for control. Somatostatin was ineffective in suppressing TSH secretion. The introduction of sensitive thyrotrophin assays should facilitate the accurate diagnosis of TSH-induced hyperthyroidism and avoid inappropriate treatment.

Adult↗
PubMed1984

Airway response to inhaled salbutamol in hyperthyroid and hypothyroid patients before and after treatment.

For many years the development of thyrotoxicosis has been known to cause a deterioration in asthma but the mechanism is unknown. We have studied the effect of thyroid function on airway beta adrenergic responsiveness in 10 hyperthyroid and six hypothyroid subjects before and after treatment of their thyroid disease. Airway adrenergic responsiveness was assessed by measuring specific airway conductance (sGaw) after increasing doses of inhaled salbutamol (10-410 micrograms). After treatment there was no difference in resting FEV1, sGaw, or thoracic gas volume. FVC increased in the hyperthyroid subjects but did not change in the hypothyroid subjects. In the hyperthyroid subjects there was a significant increase in delta sGaw after 35, 60, 110, and 41 micrograms salbutamol; in sGaw after 60, 110, and 410 micrograms salbutamol; and in the area under the salbutamol dose response curve (AUC) after treatment of the thyroid disorder. In the hypothyroid subjects there was a significant reduction in sGaw after 10 and 60 micrograms salbutamol and in the AUC after treatment. When all subjects were considered, there was a negative correlation between the AUC and serum thyroxine values. These findings suggest that an inverse relationship exists between the level of thyroid function and airway beta adrenergic responsiveness.

Adult↗
PubMed1978

Evaluation of oxidative phosphorylation in hearts from euthyroid, hypothyroid, and hyperthyroid rats.

The energy relationships between cytosolic and mitochondrial metabolism were studied in the hearts from euthyroid, hypothyroid, and hyperthyroid rats. Isolated mitochondria showed high respiratory control ratios and impermeability to exogenous NADH. Hypo- and hyperthyroidism, respectively, resulted in lower and higher contents of both cytochromes per mitochondrion and mitochondrial protein per gram of wet weight of heart without changes in the ratio of cytochrome c to cytochrome aa3. In isolated perfused heart, the hyperthyroid state led to an increase in work rate and thereby an elevation of Vo2, which resulted in an increase oxidation-reduction turnover number for the cytochromes. An agreement was found between [ATP]/[ADP][Pi] of cytosolic free adenine nucleotides and the value calculated from a mathematical model of mitochondrial respiration. This implies that mitochondrial respiration is controlled at the cytochrome oxidase reaction and that oxidative phosphorylation in intact tissue is tightly coupled irrespective of thyroid state. It is concluded that thyroid hormone causes an increase in the mitochondrial mass, mitochondrial cytochrome content, and respiratory rate, and consequently expands the capacity of oxidative metabolism without an uncoupling effect on oxidative phosphorylation.

Adenine Nucleotides↗
PubMed2005

Effects of chronic inhibition of inducible nitric oxide synthase in hyperthyroid rats.

We hypothesized that nitric oxide generated by inducible nitric oxide synthase (iNOS) may contribute to the homeostatic role of this agent in hyperthyroidism and may, therefore, participate in long-term control of blood pressure (BP). The effects of chronic iNOS inhibition by oral aminoguanidine (AG) administration on BP and morphological and renal variables in hyperthyroid rats were analyzed. The following four groups (n = 8 each) of male Wistar rats were used: control group and groups treated with AG (50 mg.kg(-1).day(-1), via drinking water), thyroxine (T4, 50 microg.rat(-1).day(-1)), or AG + T4. All treatments were maintained for 3 wk. Tail systolic BP and heart rate (HR) were recorded weekly. Finally, we measured BP (mmHg) and HR in conscious rats and morphological, plasma, and renal variables. T(4) administration produced a small BP (125 +/- 2, P < 0.05) increase vs. control (115 +/- 2) rats. AG administration to normal rats did not modify BP (109 +/- 3) or any other hemodynamic variable. However, coadministration of T4 and AG produced a marked increase in BP (140 +/- 3, P < 0.01 vs. T4). Pulse pressure and HR were increased in both T4- and T4 + AG -treated groups without differences between them. Plasma NOx (micromol/l) were increased in the T4 group (10.02 +/- 0.15, P < 0.05 vs. controls 6.1 +/- 0.10), and AG reduced this variable in T4-treated rats (6.81 +/- 0.14, P < 0.05 vs. T4) but not in normal rats (5.78 +/- 0.20). Renal and ventricular hypertrophy and proteinuria of hyperthyroid rats were unaffected by AG treatment. In conclusion, the results of the present paper indicate that iNOS activity may counterbalance the prohypertensive effects of T4.

Animals↗
PubMed2004

Hyperthyroidism and cation pumps in human skeletal muscle.

Skeletal muscle constitutes the major target organ for the thermogenic action of thyroid hormone. We examined the possible relation between energy expenditure (EE), thyroid status, and the contents of Ca2+-ATPase and Na+-K+-ATPasein human skeletal muscle. Eleven hyperthyroid patients with Graves' disease were studied before and after medical treatment with methimazole and compared with eight healthy subjects. Muscle biopsies were taken from the vastus lateralis muscle, and EE was determined by indirect calorimetry. Before treatment, the patients had two- to fivefold elevated total plasma T3 and 41% elevated EE compared with when euthyroidism had been achieved. In hyperthyroidism, the content of Ca2+-ATPase was increased: (mean +/- SD) 6,555 +/- 604 vs. 5,212 +/- 1,580 pmol/g in euthyroidism (P = 0.04) and 4,523 +/- 1,311 pmol/g in healthy controls (P = 0.0005). The content of Na+-K+-ATPase showed 89% increase in hyperthyroidism: 558 +/- 101 vs. 296 +/- 34 pmol/g (P = 0.0001) in euthyroidism and 278 +/- 52 pmol/g in healthy controls (P < 0.0001). In euthyroidism, the contents of both cation pumps did not differ from those of healthy controls. The Ca2+-ATPase content was significantly correlated to plasma T3 and resting EE. This provides the first evidence that, in human skeletal muscle, the capacity for Ca2+ recycling and active Na+-K+ transport are correlated to EE and thyroid status.

Adult↗
PubMed1992

Skeletal muscle beta-adrenoceptor distribution and responses to isoproterenol in hyperthyroidism.

To determine whether hyperthyroidism selectively increases beta-adrenergic receptor density in vessels or fibers of human skeletal muscle, we characterized beta-receptor distribution autoradiographically in muscle biopsies of 18 subjects aged 26 +/- 1 yr before and after daily administration of 100 micrograms 3,5,3'-triiodothyronine (T3) for 2 wk. To establish whether vascular and metabolic responses to beta-adrenergic stimulation are concomitantly altered, we quantified calf blood flow and plasma concentrations of glucose, lactate, glycerol, free fatty acids (FFA), insulin, and C-peptide during graded-dose isoproterenol infusion in eight of these individuals. Differences in beta-adrenergic receptor density among muscle fiber types and vascular components were highly significant (type I greater than type IIa greater than type IIb muscle fibers, P less than 0.001; and type I muscle fibers greater than resistance arterioles, P less than 0.05). Hyperthyroidism increased beta-adrenergic receptor density in all types of muscle fibers (+31-50%; P less than 0.01) but not in resistance arterioles. There was no change in calf blood flow or plasma glucose, glycerol, FFA, insulin, or C-peptide responses to isoproterenol. A rise in lactate during stages 3 and 4 of isoproterenol infusion (P less than 0.01) was observed before but not after T3 administration. Thus hyperthyroidism increases beta-adrenergic receptor density in fibers but not vessels of human skeletal muscle without increasing either metabolic or vascular responses to selective beta-adrenergic stimulation.

Adult↗