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PubMed1992

Subclinical hyperthyroidism: physical and mental state of patients.

We investigated whether subclinical hyperthyroidism [subnormal basal thyroid-stimulating hormone (TSH) level, attenuated TSH response to thyrotropin-releasing hormone (TRH) stimulation, peripheral thyroid hormones within normal range] is accompanied by physical and mental changes. Thirty-five subclinically hyperthyroid patients (27 female, 8 male) were compared with 60 overtly hyperthyroid patients (51 female, 9 male) and with 28 euthyroid control patients (18 female, 10 male) with respect to physical symptoms, affective state, short-term memory, ability to concentrate and psychomotor performance. Patients with subclinical hyperthyroidism ranged between the other two groups. The major difference between controls and subclinically hyperthyroid patients was an increase in frequency of nervous symptoms and symptoms due to an increase of metabolic rate and thermal regulation changes. The major differences between subclinically hyperthyroid and overtly hyperthyroid patients were psychomotor impairment and symptoms of increased metabolic rate. Self-ratings of affective state tended to be similar in patients with subclinical and overt hyperthyroidism. The ability to concentrate and short-term memory were not impaired in any group. Symptoms in patients with subclinical hyperthyroidism probably result from central changes which lead to attenuated TSH responses to TRH, or from elevated but still normal thyroxine levels, which possibly enhance the effect of catecholamines.

Adult↗
PubMed1983

Characterization of hyperthyroidism enhancement of halothane-induced hepatotoxicity.

Administration of anesthetic doses of halothane to hyperthyroid male rats results in the development of hepatic necrosis. The severity of the hepatic lesion was dependent on the dose of triiodothyronine (T3) and the length of time it was administered. Pretreatment of rats with iodinated metabolites of thyroxin which do not induce hyperthyroidism did not result in any signs of hepatotoxicity after halothane exposure. The administration of halothane to hyperthyroid female rats or mice of either sex did not result in the development of any overt hepatotoxicity. Likewise, hyperthyroidism did not enhance the hepatotoxicity of another hepatotoxin bromobenzene. The in vitro enzymatic activities associated with cytochrome P-450-dependent metabolism and glutathione S-transferase conjugation activity were markedly altered in hyperthyroid rats. Cytochrome P-450 levels, aminopyrine N-demethylase activity, glutathione levels and glutathione S-transferase activity were all significantly lower in hyperthyroid rats. However, other enzyme activities were stimulated by T3 pretreatment; aniline hydroxylase activity was increased by 45% and cytochrome c reductase activity was increased by 54% in hyperthyroid rats. Glutathione levels were also reduced significantly in hyperthyroid male rats. Maximal changes in both the cytochrome P-450 system and in the glutathione detoxification system were required before halothane demonstrated its hepatotoxic effects. Thus, a new balance between cytochrome P-450-dependent bioactivation and glutathione conjugation of halothane may be necessary for the exaggerated hepatotoxicity of halothane seen in hyperthyroid male rats.

Alanine Transaminase↗
PubMed1983

Mechanisms of enhanced phosphorylase activation in the hyperthyroid rat heart.

Enhanced phosphorylase activation in hearts from hyperthyroid animals has been well documented. To elucidate the mechanisms responsible for the enhanced phosphorylase a formation, hearts from euthyroid and hyperthyroid rats were perfused by the Langendorff method with calcium (3.75 mM), isoproterenol, dibutryl cAMP and trifluoperazine, an inhibitor of calcium-calmodulin dependent enzymes. Comparative biochemical analyses revealed increased phosphorylase a formation in hearts from both euthyroid and hyperthyroid animals following exposure to calcium, dibutryl cAMP and isoproterenol. Hearts from hyperthyroid rats had an increased sensitivity to threshold concentrations of isoproterenol for both cAMP formation and phosphorylase b to a conversion. At higher concentrations of isoproterenol (10(-8) M and 3 x 10(-8) M), no significant differences in cAMP formation were noted between euthyroid and hyperthyroid animals in spite of persistently increased phosphorylase a levels in the hyperthyroid state. Trifluroperazine had no effect on basal phosphorylase a levels but significantly inhibited phosphorylase a formation in both groups following calcium or isoproterenol stimulation. However, enhanced phosphorylase a formation was still present in the hearts from hyperthyroid rats following trifluoperazine preperfusion. Determinations of phosphorylase kinase activity revealed a specific activity in the hyperthyroid animals twice that of the euthyroid controls. At least two mechanisms, an increased sensitivity to beta-adrenergic agents and increased cardiac phosphorylase kinase activity, may mediate the enhanced phosphorylase a formation found in hearts from hyperthyroid rats.

Animals↗
PubMed1994

Enhanced cytochrome oxidase activity and modification of lipids in heart mitochondria from hyperthyroid rats.

In order to further investigate the mechanism regulating the control of mitochondrial respiration by thyroid hormones, the effect of the hyperthyroidism on the kinetic characteristics of cytochrome c oxidase in rat heart mitochondria was studied. Mitochondrial preparations from both control and hyperthyroid rats had equivalent Km values for cytochrome c, while the maximal activity of cytochrome oxidase was significantly increased (by around 30%) in mitochondrial preparation from hyperthyroid rats. This enhanced activity of cytochrome oxidase was associated to a parallel increase in mitochondrial State 3 respiration. The hormone treatment resulted in a decrease in the flux control coefficient of the oxidase. The enhanced activity of cytochrome oxidase in hyperthyroid rats does not appear to be dependent on an increase in the mass of this enzyme complex in that the heme aa3 content was equivalent in both hyperthyroid and control preparations. The Arrhenius plot characteristics differ for cytochrome oxidase activity in mitochondria from hyperthyroid rats as compared with control rats in that the breakpoint of the biphasic plot is shifted to a lower temperature. Cardiolipin content was significantly increased in mitochondrial preparations from hyperthyroid rats, while there were no significant alterations in the fatty acid composition of cardiolipin of control and hyperthyroid preparations. The results support the conclusion that the enhanced cytochrome oxidase activity in heart mitochondrial preparations from hyperthyroid rats is due to a specific increase in the content of cardiolipin.

Animals↗
PubMed1987

Short-term hyperthyroidism modulates adenosine receptors and catalytic activity of adenylate cyclase in adipocytes.

The effects of short-term hyperthyroidism in vivo on the status of the components of the fat-cell hormone-sensitive adenylate cyclase were investigated. The number of beta-adrenergic receptors was elevated by about 25% in membranes of fat-cells isolated from hyperthyroid rats as compared with euthyroid rats, but their affinity for radioligand was unchanged. Membranes of hyperthyroid-rat fat-cells displayed less than 65% of the normal complement of receptors for [3H]cyclohexyladenosine. The affinity of the receptors for this ligand was normal. In contrast with the marked increase in the amounts of the alpha-subunits of the guanine nucleotide-binding proteins Gi (Mr 41,000) and Go (Mr 39,000) observed in the hypothyroid state [Malbon, Rapiejko & Mangano (1985) J. Biol. Chem. 260, 2558-2564], the amounts of alpha-Gi, alpha-Go as well as alpha-Gs subunits [Mr 42,000 (major) and 46,000/48,000 (minor)] were not changed by hyperthyroidism. Adenylate cyclase activity in response to forskolin, guanosine 5'-[gamma-thio]triphosphate or isoprenaline, in contrast, was decreased by 30-50% in fat-cell membranes from hyperthyroid rats. Fat-cells isolated from hyperthyroid rats accumulated cyclic AMP to less than 50% of the extent in their euthyroid counterparts in the presence of adenosine deaminase and either adrenaline or forskolin, suggesting a decrease in the amount or activity of the catalytic subunit of adenylate cyclase. In the absence of exogenous adenosine deaminase, cyclic AMP accumulation in response to adrenaline was elevated rather than decreased in fat-cells from hyperthyroid rats. The inhibitory influence of adenosine is apparently limited in the hyperthyroid state by the decreased complement of inhibitory R-site purinergic receptors in these fat-cells. Short-term hyperthyroidism modulates the fat-cell adenylate cyclase system at the receptor level (beta-receptor number increased, R-site purinergic-receptor number decreased) and the catalytic subunit of adenylate cyclase.

Adenylyl Cyclases↗
PubMed1997

Effect of hyperthyroidism on the in vitro metabolism and covalent binding of 1,1-dichloroethylene in rat liver microsomes.

Hyperthyroidism potentiates the in vivo hepatotoxicity of 1,1-dicholoroethylene (DCE) in rats, with a concomitant increase in [14C]-DCE covalent binding. The enhanced injury produced in hyperthyroid livers by DCE could be due to alterations in either the bioactivation or detoxication phases of DCE metabolism. Previous in vitro studies suggested that hyperthyroidism did not potentiate DCE hepatotoxicity by increasing DCE oxidation to intermediates which were able to covalently bind. Several factors, however, that could contribute to the magnitude of DCE bioactivation or covalent binding were not examined. Our objectives were to characterize the effects of hyperthyroidism in male Sprague-Dawley rats on: (1) covalent binding of [14C]-DCE to microsomes and other subcellular fractions, (2) microsomal mixed-function oxidase (MFO) and glutathione S-transferase (GST) activities, and (3) inactivation of microsomal enzyme activities by presumptive DCE reactive intermediates. Hyperthyroid (HYPERT) and euthyroid (EUT) rats received 3 s.c. injections of thyroxine (100 micrograms/100 g) or vehicle, respectively, at 48-h intervals; microsomes and other subcellular fractions were isolated from HYPERT and EUT livers 24 h after the last injection. [14C]-DCE-derived covalent binding was consistently greater in EUT than HYPERT microsomes. The absence of NADH, and the addition of low concentrations (0.1 and 0.5 mM), but not higher concentrations (> 1 mM), of glutathione (GSH) diminished covalent binding to a greater extent in HYPERT than EUT microsomes. Covalent binding in mitochondrial, nuclear, and cytosolic fractions of EUT and HYPERT livers was equivalent. Regression analysis of covalent binding to liver cell fractions from both EUT and HYPERT rats showed a significant correlation with P-450 content. Hyperthyroidism decreased microsomal, but not mitochondrial, cytochrome P-450 content, and MFO activities for 7-ethoxycoumarin and benzphermine were similarly decreased. Hyperthyroidism also diminished microsomal GST activity, and altered GST kinetics for both GSH and 1-chloro-2,4-dinitrobenzene (CDNB). The magnitude of inactivation of MFO and GST activities in the presence of DCE (presumably by DCE reactive intermediates) was comparable between EUT and HYPERT microsomes. When covalent binding was standardized to cytochrome P-450 concentrations in microsomes and mitochondria, HYPERT fractions exhibited slightly greater covalent binding than EUT fractions, suggesting that hyperthyroidism does not reduce the capacity of P-450 hemoproteins to bioactive DCE. Thus, potentiation of DCE hepatotoxicity by hyperthyroidism may be predominantly due to diminished Phase II constituents, and major increases in reactive intermediate/conjugates that covalently bind to and impair critical cellular molecules.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1997

Hyperthyroidism in McCune-Albright syndrome with a review of thyroid abnormalities sixty years after the first report.

We present a patient with hyperthyroidism associated with McCune-Albright syndrome (MAS). MAS is a sporadic genetic disease characterized by polyostotic fibrous dysplasia, cafe au lait cutaneous spots and endocrinopathies (peripheral precocious puberty, thyroidopathies, acromegaly, etc.). It is caused by an activating mutation of the gene for the Gs alpha membrane-associated protein, which mediates the thyrotropin (TSH)-induced and other hormone-induced activation of adenylyl cyclase. A 13-month-old girl was diagnosed with MAS. Precocious puberty was treated initially with testolactone and later with oophorectomy. Subclinical hyperthyroidism was detected biochemically at birth, and 10 months later, it became clinically evident, albeit mild, with absence of goiter. A concomitant liver dysfunction precluded treatment with thionamides and she was sporadically treated with beta-blockers. The combination of increased free thyroxine (T4) and triiodothyronine (T3) with low plasma thyrotropin (TSH) levels in the absence of thyroid-stimulating autoantibodies persisted until the age of 6 years, when she was referred to our unit. Hyperthyroidism was then clinically evident with cardiac hyperactivity, and it was cured with administration of radioiodine (131I). Thyroid disease is the second most common endocrinopathy associated with MAS, and since 1936, 63 cases of thyroidopathies have been described, including 19 nodular (14 with and 5 without hyperthyroidism) and 23 diffuse (20 with and 3 without hyperthyroidism) goiters, and 18 cases of hyperthyroidism without goiter. The previously described somatic activating mutation of the gs alpha gene in the ovaries, the liver and the peripheral blood of our patient, in the absence of stigmata, autoimmunity might be incriminated for the secretory and mitotic activation of the thyroid gland. We suggest the treatment of choice of hyperthyroidism in MAS patients should be 131I administration because: (a) hyperthyroidism is very likely to recur after withdrawal of antithyroid medication; (b) the morbidity of these patients is elevated; (c) oophorectomized patients do not need to be advised to avoid procreation during the months after 131I administration; and (d) finally, even in the usual cases of hyperthyroidism in childhood, 131I treatment is becoming more popular worldwide.

Child↗
PubMed1989

Hyperthyroid adult rat cardiomyocytes. II. Single cell electrophysiology and free calcium transients.

The effects of hyperthyroidism on electrophysiological properties and intracellular free calcium transients in single adult rat cardiomyocytes were studied using conventional microelectrodes and time-resolved single cell fura-2 fluorescence microscopy. Under control conditions, resting membrane potentials and triggered action potentials were not different in euthyroid and hyperthyroid myocytes. Calcium transients produced by electrical stimulation, however, were markedly abbreviated in hyperthyroid myocytes. During a train of stimuli, the duration of the calcium transients at half peak amplitude (half time) was 124 +/- 14 ms at the fifth beat in hyperthyroid cells vs. 287 +/- 35 ms in euthyroid cells. Isoproterenol (1 microM) prolonged time to 50% repolarization (APD50) of the action potentials and increased the peak calcium transients in both euthyroid and hyperthyroid myocytes. It also shortened the half time of the calcium transients in euthyroid myocytes but had little effect on the half time in hyperthyroid cells. These data are consistent with the electrophysiology and mechanical performance in intact euthyroid and hyperthyroid cardiac tissues, and the intrinsic changes in hyperthyroid tissues can therefore be illustrated in single ventricular myocytes. Furthermore, the results suggest that alterations in intracellular calcium handling by sarcoplasmic reticulum may account for contractile changes of the heart induced by hyperthyroidism.

Action Potentials↗
PubMed1997

The influence of hyperthyroidism on vasoconstrictor and vasodilator responses in isolated coronary and renal resistance arteries.

The influence of hyperthyroidism on the functional vascular responsiveness of isolated coronary and renal resistance vessels was investigated. Hyperthyroidism was established by feeding rats for 1 and 4 weeks with 5 mg/kg L-thyroxine (T4)-containing rat chow. Preparations of either coronary or renal resistance vessels were mounted in an isometric wire myograph. Subsequently, concentration-effect curves were determined for the effects of 5-hydroxytryptamine (5-HT), 9,11-dideoxy-11alpha,9alpha-epoxymethanoprostaglandin F2alpha (U46619) and isoproterenol in coronary vessels, and for those of methoxamine, U46619 and isoproterenol in renal vessel preparations. Our results indicate that hyperthyroidism does not induce major changes in the sensitivity of both coronary and renal resistance vessels towards 5-HT, U46619 and methoxamine. A clearly sensitizing influence of acute hyperthyroidism (1 week of T4 treatment) was found for isoproterenol-induced relaxant responses, whereas hyperthyroidism for 4 weeks did not influence the responses mediated by isoproterenol in coronary resistance arteries. Furthermore, the isoproterenol-induced relaxation in renal arteries was not influenced by the chronic hyperthyroid state of the animal. The present results indicate that in acute hyperthyroidism beta-adrenoceptor-mediated vasodilation is increased. However, in chronic hyperthyroidism changes in responsiveness to vasoconstrictor or vasodilator agents of coronary and renal resistance arteries appear not to play a major role. The influence of hyperthyroidism on the functional response of resistance arteries appears to be both tissue and time dependent.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1990

Decreased contractile efficiency and increased nonmechanical energy cost in hyperthyroid rabbit heart. Relation between O2 consumption and systolic pressure-volume area or force-time integral.

Both systolic pressure-volume area (PVA) and force-time integral (FTI) have been used as measures of oxygen consumption per beat (VO2) in the isolated left ventricle. The reciprocal of the slope of the VO2-PVA relation has been considered to reflect the chemomechanical energy transduction efficiency of the contractile machinery (contractile efficiency), whereas its VO2 intercept consists of energy cost of excitation-contraction coupling and basal metabolism. To examine whether the increase in myosin isoform V1/V3 ratio in hyperthyroid rabbits decreases contractile efficiency and to determine overall mechanisms of higher oxygen consumption in hyperthyroid hearts, the VO2-PVA and VO2-FTI relations as well as the end-systolic pressure-volume relation were assessed in cross-circulated, isovolumically beating hearts isolated from normal, hyperthyroid, and hypothyroid rabbits. Normalized initial slopes of the rising limb of the curvilinearly fitted end-systolic pressure-volume relation (E'max, ventricular contractility index) were similar for normal and hyperthyroid groups. However, the slopes and VO2 intercepts of the VO2-PVA and VO2-FTI relations were greater in hyperthyroid hearts than in normal hearts. Accordingly, in the hyperthyroid hearts, the contractile efficiency (27 +/- 6%) was lower and left ventricular VO2 for excitation-contraction coupling (0.028 +/- 0.004 ml O2/beat/100 g) was higher than in normal hearts (40 +/- 4% and 0.021 +/- 0.005 ml O2/beat/100 g, respectively). This decreased contractile efficiency in the hyperthyroid hearts was attributable to myosin isoform alteration rather than to increased beta-adrenoceptors because isoproterenol did not affect the slope of the VO2-PVA relation in all groups. In contrast, the slope of the VO2-FTI relation was significantly increased by isoproterenol in all groups. Neither the VO2-PVA nor the VO2-FTI relations in hypothyroid hearts were different from those in normal hearts except for significantly lower VO2 for basal metabolism. We conclude that in hyperthyroid rabbits, the left ventricle has decreased contractile efficiency and increased energy cost of excitation-contraction coupling and that the decreased contractile efficiency in hyperthyroid hearts is probably due to the increased V1/V3 ratio of the myosin isoform component. In addition, this study demonstrates that the VO2-PVA and VO2-FTI relations dissociate depending on the intervention, even in the same isovolumic contraction mode.

Animals↗
PubMed1988

A multicompartmental model for iodide, thyroxine, and triiodothyronine metabolism in normal and spontaneously hyperthyroid cats.

A comprehensive multicompartmental kinetic model was developed to account for the distribution and metabolism of simultaneously injected radioactive iodide (iodide*), T3 (T3*), and T4 (T4*) in six normal and seven spontaneously hyperthyroid cats. Data from plasma samples (analyzed by HPLC), urine, feces, and thyroid accumulation were incorporated into the model. The submodels for iodide*, T3*, and T4* all included both a fast and a slow exchange compartment connecting with the plasma compartment. The best-fit iodide* model also included a delay compartment, presumed to be pooling of gastrosalivary secretions. This delay was 62% longer in the hyperthyroid cats than in the euthyroid cats. Unexpectedly, all of the exchange parameters for both T4 and T3 were significantly slowed in hyperthyroidism, possibly because the hyperthyroid cats were older. None of the plasma equivalent volumes of the exchange compartments of iodide*, T3*, or T4* was significantly different in the hyperthyroid cats, although the plasma equivalent volume of the fast T4 exchange compartments were reduced. Secretion of recycled T4* from the thyroid into the plasma T4* compartment was essential to model fit, but its quantity could not be uniquely identified in the absence of multiple thyroid data points. Thyroid secretion of T3* was not detectable. Comparing the fast and slow compartments, there was a shift of T4* deiodination into the fast exchange compartment in hyperthyroidism. Total body mean residence times (MRTs) of iodide* and T3* were not affected by hyperthyroidism, but mean T4* MRT was decreased 23%. Total fractional T4 to T3 conversion was unchanged in hyperthyroidism, although the amount of T3 produced by this route was increased nearly 5-fold because of higher concentrations of donor stable T4. Analysis of the data indicates that the increased overall T4* turnover (decreased MRT) in hyperthyroidism is due to increased losses through pathways other than T3 formation. Conjugation, with subsequent deiodination, is proposed as one possibly important pathway. Results of this multicompartmental analysis are compared with those of noncompartmental analysis of the same data and with results of similar model analyses in other species.

Animals↗
PubMed1985

Hyperthyroidism influences the distribution and apolipoprotein A composition of the high density lipoproteins in man.

Hyperthyroidism has a different influence on the major high density lipoprotein (HDL) components cholesterol, apoprotein (apo) A-I, and apo A-II. To characterize in greater detail the alterations induced by hyperthyroidism within the HDL subclasses, we investigated HDL distribution and composition in 11 hyperthyroid women before and during treatment. The plasma concentrations of total cholesterol, HDL cholesterol, phospholipids, apo A-I, and apo B were decreased when the patients were hyperthyroid compared with the values during treatment. Apo A-II and apo C-III levels were only slightly lower in the hyperthyroid state. Triglyceride and apo E concentrations did not change significantly during therapy. Analysis of lipoprotein subclasses separated by isopycnic ultracentrifugation revealed 1) marked decreases in low density lipoprotein (LDL) cholesterol, phospholipids, and apo B; 2) less pronounced reductions in the very low density lipoprotein (VLDL) lipid and apo B concentrations; and 3) a consistent decrease in the HDL2b (density, 1.063-1.100 g/ml) fraction in the hyperthyroid patients. The reduction in HDL2b mass was associated with lower concentrations of HDL2b cholesterol, phospholipids, and apo A-I. The HDL2b apo A-II levels remained constant during treatment. Hyperthyroidism, therefore, modified the apo A composition of the HDL2b particles and resulted in a decreased molar apo A-I to apo A-II ratio within HDL2b. Further analysis of HDL particles differing in their apo A composition; i.e. HDL particles containing apo A-I only [(A-I)HDL] or containing both apo A-I and A-II [(A-I + A-II)HDL], by immunological procedures suggested that hyperthyroidism influenced the apo A content of HDL2b mainly by changing the proportions of (A-I)HDL and (A-I + A-II)HDL and the amount of apo A-I associated with (A-I)HDL. Treatment reversed the preferential decrease in (A-I)HDL within the HDL2b subclass. The particle sizes within HDL subfractions, measured by polyacrylamide gradient gel electrophoresis, were similar in the untreated and treated patients. Consequently, the decreased mass of apo A-I and lipids within HDL2b in the hyperthyroid patients could be attributed to a reduced number of identically sized particles within this fraction. These data demonstrate that the thyroid hormones are important regulators of HDL metabolism through their influence on the concentration and distribution of apo A-I.

Adolescent↗
PubMed1988

Peripheral and hepatic insulin antagonism in hyperthyroidism.

Eight hyperthyroid and eight normal subjects underwent 2-h oral glucose tolerance tests (OGTT) and euglycemic clamp studies to assess the presence of peripheral and hepatic insulin antagonism in hyperthyroidism. Although the mean total glucose area during the OGTT was similar in the hyperthyroid patients and normal subjects [16.4 +/- 0.8 (+/- SE) vs. 15.8 +/- 0.7 mmol/L.h], the mean insulin area was significantly elevated in the hyperthyroid group (1413 +/- 136 vs. 1004 +/- 122 pmol/L.h; P less than 0.05). Basal hepatic glucose production was measured during the second hour of a primed [3-3H]glucose infusion. A two-insulin dose euglycemic clamp study with [3-3H]glucose and somatostatin (500 micrograms/h) was carried out during the next 6 h. The insulin infusion rate was 0.05 mU/kg.min during the third, fourth, and fifth hours and 0.60 mU/kg.min during the sixth, seventh, and eighth hours. Hepatic glucose production and glucose utilization were measured during the final 0.5 h of each clamp period. Serum C-peptide concentrations were measured in the initial sample and in the last sample of each clamp period. The mean equilibrium serum insulin concentrations were similar in both groups during the final 0.5 h of the low (90 +/- 8 vs. 79 +/- 6 pmol/L) and high (367 +/- 11 vs. 367 +/- 15 pmol/L) insulin infusion rates. Basal serum C-peptide levels were significantly increased in the hyperthyroid patients (596 +/- 17 vs. 487 +/- 43 pmol/L; P less than 0.05) but were suppressed equally in both groups at the end of both clamp periods. The MCRs of insulin were similar in the hyperthyroid and normal subjects during the low (6.7 +/- 1.1 vs. 5.6 +/- 0.5 mL/kg.min) and high (11.9 +/- 0.4 vs. 12.1 +/- 0.5 mL/kg.mm) insulin infusion rates. Glucose production was significantly increased in the hyperthyroid patients during the basal state (17.6 +/- 0.9 vs. 11.5 +/- 0.5 mumol/kg.min; P less than 0.001) and remained elevated during the final 0.5 h of the low (12.1 +/- 1.1 vs. 5.9 +/- 1.7; P less than 0.01) and high (3.2 +/- 1.2 vs. 0.5 +/- 0.3; P less than 0.05) insulin infusion rates. Peripheral insulin action, assessed by Bergman's sensitivity index, was significantly decreased in the hyperthyroid patients (7.4 +/- 2.2 vs. 15.6 +/- 2.1 L/kg min-1/pmol/L; P less than 0.02). In conclusion, hyperthyroidism is characterized by 1) hyperinsulinemia after oral glucose loading, 2) increased basal hepatic glucose production, 3) impairment of insulin-mediated suppression of hepatic glucose production, and 4) antagonism to insulin-stimulated peripheral glucose utilization.

Adult↗
PubMed1984

T3-hyperthyroidism caused by enhanced and shifted T4-conversion.

Radioactivities of endogenously labelled thyroid hormones following in vivo application of 131 I and extraction from serial blood samples, show that T4 secretion is enhanced in T3-hyperthyroidism as it is in T4-T3-hyperthyroidism. In an extreme case of T3-hyperthyroidism with serum concentrations (SC) of T3 nearly equal to T4 (1000 ng/dl and 1800 ng/dl, respectively) tracer studies revealed a very short half life of T4 when compared to T3 (21.8 and 20.2 hrs., respectively). In 110 cases with both types of hyperthyroidism, regression analysis showed that T3/T4 ratio as an indicator of T4 conversion, as well as T3/rT3 ratio as an indicator of the direction of the conversion, are related to T4SC (r = -0.84 and -0.72, respectively, p less than 0.001). T3-hyperthyroidism is described by high values of these ratios. For the definition of T3-hyperthyroidism it is suggested that both T4 and rT3SC are within the normal range (T4 less than or equal to 11.5 micrograms/dl, rT3 less than or equal to 43.0 ng/dl) and according to this definition, T3/rT3 is higher than in T4-T3-hyperthyroidism and in an undefined group (24.8 +/- 4.5 vs. 6.3 +/- 0.4 or 7.5 +/- 0.4, respectively). By means of the ratios the undefined group may be allocated to T4-T3-hyperthyroidism. The T3/rT3 ratio is value of greater than 10 has a frequency of 88% in thus defined T3-hyperthyroidism and a ratio of less than or equal to 10 is found in 90% of the other cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Granulocytes↗
PubMed1995

Radioiodine therapy compared in patients with toxic nodular or Graves' hyperthyroidism.

In view of uncertainty regarding the most appropriate radioiodine dose for patients with hyperthyroidism due to toxic nodular disease or Graves' disease, we prospectively studied outcome in patients with these disorders given a single 5 mCi (185 MBq) dose of radioiodine. We studied 103 patients receiving their first radioiodine dose; 44 with toxic nodular hyperthyroidism and 59 with Graves' hyperthyroidism. Thyroid status (off anti-thyroid drug therapy) at 6 and 12 months after radioiodine was related to diagnosis, use of carbimazole before or after radioiodine, and physical and biochemical findings. At 6 months, persistent hyperthyroidism was less frequent in toxic nodular disease than in Graves' disease (34.1% vs. 55.9%, p < 0.05); hypothyroidism was also less frequent (11.4% vs. 27.1%, p < 0.05). Those with persistent hyperthyroidism at 6 months were given a second (10 mCi, 370 MBq) dose of radioiodine. At 12 months after the first dose, 80.6% of the group with toxic nodular hyperthyroidism were either euthyroid or hypothyroid, and 74.5% of those with Graves' disease were euthyroid or hypothyroid, the rate of hypothyroidism again being less in toxic nodular disease (19.4% vs. 58.8%, p < 0.05). Logistic regression and stepwise discriminant analysis demonstrated that 'cure' (euthyroidism or hypothyroidism) at 6 months was related to serum free T4 at presentation (p < 0.001) and administration of carbimazole before or after radioiodine (p < 0.001) (severe hyperthyroidism and carbimazole increasing the likelihood of persistent hyperthyroidism) but was not related to the diagnosis of toxic nodular or Graves' hyperthyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

[31P-magnetic resonance spectroscopy: impaired energy metabolism in latent hyperthyroidism].

31Phosphorus magnetic resonance spectroscopy allows an in vivo examination of energy metabolism. The present study was designed to evaluate whether in patients with latent hyperthyroidism alterations of muscle energy metabolism could be found similar to those observed in patients with overt hyperthyroidism. In 10 patients with overt hyperthyroidism before therapy and 20 with latent hyperthyroidism (also without therapy) and in 24 healthy volunteers magnetic resonance spectroscopy of the calf muscle was performed within a 1.5-Tesla magnet. Muscle concentrations of phosphocreatine, inorganic phosphate, and ATP were quantified compared to an external standard solution of K2HPO4. In the patients with overt hyperthyroidism and with latent hyperthyroidism a significant decrease of phosphocreatine was found. Further, the ATP concentration in patients with latent and manifest hyperthyroidism tended towards lower values. There were no significant differences in the decrease of phosphocreatine and ATP between both patient groups. Therefore, this study for the first time shows that alterations of energy metabolism in latent hyperthyroidism can be measured and that they are similar to those observed in overt hyperthyroidism.

Adult↗
PubMed1997

Pharmacokinetics of propranolol in healthy cats during euthyroid and hyperthyroid states.

OBJECTIVE: To examine the pharmacokinetic profile of propranolol in cats before and during experimentally induced hyperthyroidism. ANIMALS: 8 conditioned, random-source, young adult, female cats. PROCEDURE: Propranolol was administered i.v. as a single bolus and 72 hours later by mouth. Thereafter, the cats were dosed for 5 weeks with L-thyroxine (50 micrograms/kg of body weight, s.c., once daily) to induce hyperthyroidism (serum thyroxine concentration, 217 +/- 17 nmol/L). Blood samples were obtained at appropriate intervals before and during hyperthyroidism and were analyzed for plasma propranolol concentration by use of high-performance liquid chromatography. RESULTS: In all cats, a two-compartment model best described the control and hyperthyroid intravenous data. The change in thyroid status from euthyroid to hyperthyroid caused a significant (P < 0.05), but small reduction in propranolol area under the curve (19,932 +/- 7,900 min.micrograms/L vs 15,911 +/- 1,400 min.micrograms/L) after i.v. administration. In contrast, after oral administration during the hyperthyroid state, a twofold increase (P < 0.05) in propranolol area under the curve (105,430 +/- 57,600 min.micrograms/L vs 226,811 +/- 112,000 min.micrograms/L) and peak serum propranolol concentration (651 +/- 247 micrograms/L vs 1191 +/- 590 micrograms/L) were attributed to significant (P < 0.05) increase in propranolol bioavailability caused by increased fractional absorption (57 +/- 28% vs 137 +/- 73%) and decreased total body clearance (58 +/- 27 ml/min/kg vs 30 +/- 19 ml/min/kg). Mean arrival time after oral dosing was significantly lengthened by hyperthyroidism (100 +/- 38 minutes vs 157 +/- 71 minutes). CLINICAL RELEVANCE: Hyperthyroidism-induced changes in propranolol pharmacokinetics may signal the need to reduce doses of propranolol when they are orally administered to hyperthyroid cats.

Administration, Oral↗
PubMed1998

[Atrial fibrillation and hyperthyroidism. The results of a retrospective study].

BACKGROUND: To examine the prevalence of atrial fibrillation (AF) in cardiopathic patients with hyperthyroidism. METHODS: The data concerning the patients had been derived from registers of the Laboratory of Radioimmunoassay where cardiopathic patients' blood samples were referred from the Cardiology Unit to evaluate thyroid function, consecutively from January 1992 to December 1997. Of the 443 patients, 303 (68.4%) were classified as being euthyroid, 23 (5.2%) hypothyroid, 117 (26.4%) hyperthyroid. Thyroid function was diagnosed clinically and confirmed by serum TSH and free thyroid hormone (FT3, FT4), levels. RESULTS: Among hyperthyroid patients, the more frequent arrhythmia was AF (54.7%). After excluding from the study those hyperthyroid patients with rheumatic disease, hypertension, myocardial infarction, 37 hyperthyroid patients were selected; 18 (48.6%), (mean age 63.4 +/- 10.8 yrs), showed sinus rhythm and 19 (51.4%), (mean age 66.0 +/- 12.1 yrs), showed AF. FT3 and FT4 were higher in patients with AF than in those without AF, whereas TSH was not significantly different between the groups. Left ventricular (LV) mass index was significantly increased in hyperthyroid women with AF compared with hyperthyroid women without AF (109.80 +/- 22.33 g/m2 vs 84.50 +/- 6.20 g/m2; p < 0.005). A significant correlation was found between FT3 levels and LV mass index in the hyperthyroid women with and without AF (r = 0.77; p < 0.001). CONCLUSIONS: In this study the prevalence of AF is 51.4% in hyperthyroid patients. FT3 is higher in patients with AF than in those without AF. Finally, the correlation between FT3 and LV mass index suggests that cardiac hypertrophy is associated with thyroid hyperfunction.

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