Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hyperthyroidism”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources
PubMed1994

The clinical evaluation of patients with subclinical hyperthyroidism and free triiodothyronine (free T3) toxicosis.

PURPOSE: To develop a strategy to identify cases of endogenous subclinical hyperthyroidism and free triiodothyronine (free T3) thyrotoxicosis in otherwise healthy ambulatory patients. PATIENTS AND METHODS: In a retrospective study we reviewed the records of ambulatory patients who had thyroid stimulating hormone (TSH) levels determined between October 1, 1991 and August 31, 1992. Each patient also had a simultaneous free thyroxine (free T4) measurement. Patients were excluded from consideration if they had active, concurrent non-thyroidal illness, psychiatric disease, known hypothalamic/pituitary lesions, were under treatment for hyper- or hypothyroidism, were on drugs known to affect TSH levels, or were pregnant. Patients without exclusions were diagnosed with free T3 toxicosis if they had: (1) a markedly subnormal TSH level (less than or equal to 0.1 mU/L), (2) a normal free T4, (3) a normal total T3, (4) evidence of a primary thyroid abnormality (e.g., autonomous function on a thyroid scan), and (5) an elevated free T3 level by tracer equilibrium dialysis. Patients meeting conditions 1-4, but with normal free T3 levels, were considered to have subclinical hyperthyroidism. RESULTS: One thousand twenty-five patients had TSH and simultaneous free T4 determinations, and 148 of these had markedly subnormal TSH but normal free T4 levels. Three patients met the criteria for free T3 toxicosis and three had subclinical hyperthyroidism. All six patients had either multinodular glands or a single nodule on thyroid exam. Four patients were treated with radioactive iodine or surgery, resulting in reversal of the TSH suppression in three cases. CONCLUSION: Apparently healthy ambulatory patients with subnormal TSH levels should be worked up with measurements of free T4 and total T3. If these are normal, a T3 level (by tracer equilibrium dialysis) be obtained to distinguish subclinical hyperthyroidism from overt free T3 toxicosis. A thyroid scan and radioiodine uptake measurement can be obtained to substantiate the diagnosis. Some patients with these conditions will benefit from treatment.

Adult↗
PubMed1988

Ketone-body metabolism in hyperthyroid rats: reduced activity of D-3-hydroxybutyrate dehydrogenase in both liver and heart and of succinyl-coenzyme A: 3-oxoacid coenzyme A-transferase in heart.

The specific activity of D-3-hydroxybutyrate dehydrogenase is reduced by about a third in liver and heart mitochondria of hyperthyroid rats. State 3 respiration is also reduced in isolated mitochondria from the same animals when DL-3-hydroxybutyrate is the substrate. Determination of the kinetic parameters of the membrane-bound D-3-hydroxybutyrate dehydrogenase in liver of hyperthyroid rats reveals a decreased in maximal velocity (Vmax). The Michaelis and dissociation constants of NAD+ and D-3-hydroxybutyrate are also significantly influenced, thus indicating that both the affinity and the binding of this enzyme toward its substrates are affected. In hyperthyroid rats a significant ketone-body increase is found in both liver and heart: in blood, an almost doubled concentration can be measured. At the same time, in heart mitochondria of these animals the activity of succinyl-coenzyme A: 3-oxoacid coenzyme A-transferase is significantly reduced. The decrease in both D-3-hydroxybutyrate dehydrogenase and 3-oxoacid coenzyme A-transferase associated with the increase in ketone bodies supports the suggestion that there is a lower utilization of these compounds by peripheral tissues. In the blood of hyperthyroid rats a higher D-3-hydroxybutyrate/acteoacetate ratio is also found, probably resulting from a selective utilization of the two compounds in this pathological state.

Acyl Coenzyme A↗
PubMed1983

Effect of hyperthyroidism on lipogenesis in brown adipose tissue of young rats.

Fatty acid synthetic capacity, investigated both in subcellular fractions and in vivo, is very active in brown adipose tissue of room temperature-acclimated rats. In hyperthyroid animals this tissue, analogously to the liver, exhibits an increased activity of acetyl-CoA carboxylase, fatty acid synthetase and microsomal fatty acid chain elongation, this last mechanism remaining unaffected in mitochondria. An enhancement of reducing capacities of a group of cytoplasmic NADP-dependent enzymes has also been observed in brown adipose tissue of hyperthyroid rats, probably due to a greater use of NADPH in lipogenesis under these conditions. An increase in palmitate oxidation and in polyenoic fatty acids was observed in mitochondria of brown adipose tissue from hyperthyroid animals. The latter increase is related to the importance of these compounds in the regulation of membrane fluidity and probably to an increased resistance to cold in the hyperthyroid state.

Adipose Tissue, Brown↗
PubMed1986

Atrial natriuretic polypeptide in atria and plasma in experimental hyperthyroidism and hypothyroidism.

To investigate the involvement of thyroid hormone on the release of atrial natriuretic polypeptide (ANP), we have measured immunoreactive ANP in the atria and plasma of experimental hyperthyroid and hypothyroid rats. Plasma ANP was higher (p less than 0.05) in hyperthyroid rats and was lower (p less than 0.05) in hypothyroid rats than in euthyroid rats. ANP content and concentration in the atria were lower (p less than 0.01) in hyperthyroid rats than in hypothyroid rats. An inverse correlation was found between the plasma ANP and ANP concentration in the atria (n = 15, r = 0.60, p less than 0.01). The results indicate an increased systemic release of ANP from the atria in hyperthyroidism and a decreased systemic release in hypothyroidism.

Animals↗
PubMed1995

Influence of hyperthyroidism on lindane-induced hepatotoxicity in the rat.

Parameters related to hepatic oxidative stress, cell injury, phagocytic activity, and liver histology were studied in control rats and in animals subjected to L-3,3',5-triiodothyronine (T3) and/or lindane administration. Hyperthyroidism elicited a calorigenic response and increased rates of hepatic O2 uptake, which were not modified by lindane treatment. T3 diminished serum lindane levels as well as those in the liver and adipose tissue, whereas lindane enhanced serum T3 levels in animals given T3. Compared with control rats, lindane significantly increased the rate of formation of thiobarbituric acid reactants (TBARS) by the liver, with no changes in either the reduced glutathione (GSH) content, the TBARS/GSH ratio as indicator of oxidative stress, or in the fractional rates of lactate dehydrogenase (LDH) and GSH efflux from perfused livers as integrity parameters. Hyperthyroidism induced GSH depletion in the liver, with a significant enhancement in the TBARS formation, the TBARS/GSH ratio, and in the fractional LDH and GSH efflux. These parameters were increased further by joint T3 and lindane administration in a magnitude exceeding the sum of the effects produced by the separate treatments. In addition, hyperthyroidism led to Kupffer cell hyperplasia and significant increases in serum glutamate oxalacetate transaminase (GOT) and in hepatic zymosan-induced chemiluminescence, while liver myeloperoxidase (MPO) activity was found unchanged, compared with controls. Rats treated with lindane presented normal liver histology, with no changes in biochemical parameters related to cell injury. The joint administration of T3 and lindane, however, elicited a marked elevation in serum GOT and glutamate pyruvate transaminase (GPT), concomitantly with extensive liver necrosis and the presence of granulomas containing lymphocytes, Kupffer cells and polymorphonuclear leukocytes (PMN). In this condition, hepatic zymosan-induced light emission and MPO activity were enhanced over control values. It is concluded that hyperthyroidism increases the susceptibility of the liver to the toxic effects of lindane, which seems to be accomplished by potentiation of the hepatic oxidative stress status. The latter effect may be conditioned by an enhanced phagocytic respiratory burst activity due to the observed Kupffer cell hyperplasia and PMN infiltration, in addition to the increased production of reactive oxygen species in parenchymal cells.

Alanine Transaminase↗
PubMed1989

Increased acylphosphatase levels in erythrocytes from hyperthyroid patients.

Acylphosphatase activity and content were measured in erythrocytes from hyperthyroid patients and healthy controls. In addition, the soluble enzymes glucose-6-phosphate dehydrogenase, hexokinase, and the membrane bound (Na+ + K+)-ATPase and Ca2+-ATPase were assayed. Our results confirmed previous studies indicating a decrease of (Na+ + K+)-ATPase and an increase of Ca2+-ATPase activity in hyperthyroid erythrocytes. While glucose-6-phosphate dehydrogenase was not significantly changed, hexokinase and acylphosphatase activities were significantly higher in the hyperthyroid group. Both activities and content of acylphosphatase returned to normal levels in erythrocytes from treated patients, when they were euthyroid. These findings suggest that an excess of thyroid hormones may stimulate acylphosphatase biosynthesis in erythroid cells and indicate a potential clinical usefulness of this enzyme in hyperthyroidism.

Acid Anhydride Hydrolases↗
PubMed1992

Increased serum concentration of type IV collagen peptide and type III collagen peptide in hyperthyroidism.

Serum concentration of type IV collagen peptide, the 7S domain of type IV collagen (type IV collagen 7S) and the amino terminal propeptide of type III procollagen (type III procollagen peptide) is thought to be a useful marker of progressive liver disease. In the present study, serum levels of these collagens in patients with thyroidal diseases with normal liver function were assayed. Increased levels in the hyperthyroid state and relatively decreased levels in the hypothyroid state were observed. The increased levels in hyperthyroidism was most prominent in type IV collagen peptide. The increased level became normal in the subsidence of hyperthyroidism by treatment with anti-thyroid drug. A positive correlation between serum type IV collagen peptide levels and serum thyroid hormone levels such as T4, T3, free T4 and free T3 was observed. These facts show that serum type IV collagen peptide may be influenced by not only liver disease but also serum thyroid hormone levels. Type IV collagen peptide may provide a useful biochemical marker of hyperthyroid state.

Collagen↗
PubMed1995

Nature of respiratory stimulation in hyperthyroidism: the redox behaviour of cytochrome c.

Hyperthyroid mitochondria show an increased Km and Vmax in the high affinity phase of cytochrome oxidase kinetics. During inhibitor titrations, cytochrome c shows a different redox behaviour in hyperthyroid with respect to protonophore-treated euthyroid mitochondria. The observations are discussed in terms of a different regulation of electron input and output into the respiratory chain during slip and leak types of uncoupling. In hyperthyroid mitochondria during inhibitor titrations, the pattern of the relationship between uncoupler-induced extra-respiration and membrane potential is highly non-linear. The complex nature of the respiratory stimulation in hyperthyroid mitochondria is discussed.

Animals↗
PubMed1991

Distribution of myosin heavy chain mRNA in normal and hyperthyroid heart.

Hyperthyroid treatment produces rapid cardiac cell hypertrophy with all subcellular components increasing in an orderly manner. We compare normal and hyperthyroid tissue in order to relate changes in distribution of myosin mRNA during rapid assembly of myofibrils. At the light microscopic level, in situ hybridization of the ventricular cells shows myosin heavy chain mRNA to be distributed in a spoke-like pattern radiating from the nucleus. Electron microscopy provides the higher resolution necessary to determine mRNA distribution with respect to adjacent sarcomeric and cytoskeletal structures. Papillary muscles were removed from hyperthyroid and normal rabbits, aldehyde fixed, and embedded in LR white. Biotinated riboprobe transcribed from 0.5 kb in the coding region of terminal portion of the rod of alpha-myosin was hybridized and detected by immunocytochemical methods using 5 nm immunoglobulin G gold conjugates. Electron microscopy in situ hybridization runs with same-sense and anti-sense riboprobes were processed and ten micrographs randomly taken from each. Specific cytoplasmic densities of myosin mRNA were calculated by counting clusters of five or more gold particles over respective tissue components after subtraction of background counts. For both normal myocytes and hyperthyroid myocytes, the density of myosin mRNA was about 15 times higher in the cytoskeletal-rich inter-myofibrillar space than in the myofibrils. About half of the myosin mRNA in this inter-myofibrillar region is found within 10 nm of the peripheral filament, but no excess sarcomeric accumulation was seen beside the A-Band. It appears that most of the myosin is translated from mRNA within the inter-myofibrillar space along the entire length of the myofibril periphery. The emerging myosin heavy chain is not directly anchored to the thick filaments in either normal or rapidly growing cardiac cells.

Animals↗
PubMed1986

Alteration in activities of Na,K, ATPase, sugar transport, and insulin receptors in erythrocytes from hyperthyroid patients.

To investigate the selectivity of the reduction in Na,K, ATPase activity in erythrocytes from patients with hyperthyroidism, we have assessed cytochalasin B-sensitive galactose uptake and insulin receptors as well as Na,K, ATPase-mediated rubidium uptake in erythrocytes from 11 patients with hyperthyroidism, 5 patients after treatment and 11 normal controls. There was a significant reduction in the Vmax values for rubidium uptake and the number of insulin receptors (23% and 20% below control, respectively), whereas there was a significant increase in the Vmax and Km values for galactose uptake (49% and 30% above control) and also in the average affinity of insulin receptors. The alterations both in rubidium and galactose transport activities were reversible with effective treatment of hyperthyroidism. The magnitude of alterations in the Vmax for rubidium uptake correlated inversely (r = -0.537 P less than 0.01, n = 16) and the Vmax and Km for galactose uptake correlated positively (r = 0.597 P less than 0.02 and r = 0.553 P less than 0.05, respectively) with serum T4 level. No correlation was found between the number of insulin receptors and serum IRI or T4 levels. These results suggest that the reduction in Na,K, ATPase activity observed in erythrocytes from hyperthyroid patients is not selective to this enzyme, but rather a reflection of widespread alterations of erythrocyte cell-surface proteins.

3-O-Methylglucose↗
PubMed1986

Correlation between insulin clearance and insulin responsiveness: studies in normal, obese, hyperthyroid, and Cushing's syndrome patients.

Insulin clearance and secretion determine the plasma insulin concentration. To elucidate the significance of these parameters in man, we employed the euglycemic insulin clamp technique to measure insulin sensitivity, insulin responsiveness, and insulin clearance, and we calculated the basal insulin delivery rate. In 27 patients (six normal, six obese, ten hyperthyroid, and five with Cushing's syndrome), insulin was infused at rates of 0.3, 1, 3, or 10 mU/Kg/min, and insulin concentration and glucose utilization were measured. C-peptide concentrations were measured before and during insulin infusion and decreased significantly, indicating a reduction of endogenous insulin secretion to 62% of basal in normals and a similar reduction in the other groups. Maximal responsiveness to insulin was a glucose utilization rate of 450 +/- 20 mg/min/m2 in normals, unchanged in obese, 42% increased in hyperthyroid, and 34% decreased in Cushing's syndrome patients. Sensitivity to insulin was decreased in all three abnormal groups. Insulin clearance rates were 1,050 +/- 80 mL/min/m2 for normals, not significantly changed in obese, 45% increased in hyperthyroid, and 33% decreased in Cushing's syndrome patients. All three abnormal groups showed hyperinsulinemia compared to normal. The basal insulin delivery rates were calculated as 7.0 +/- 0.3 mU/min/m2, with a threefold increase in obese and in hyperthyroid and no significant change in Cushing's syndrome patients. Insulin clearance correlated well with insulin responsiveness (r = .65, P less than 0.001), but poorly with insulin sensitivity (r = .36).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Alpha 2- and beta-adrenergic receptor binding and action in gluteal adipocytes from patients with hypothyroidism and hyperthyroidism.

The alpha 2- and beta-adrenergic receptor activities have been investigated in human adipocytes in relation to thyroid status. Adipocytes from 11 hypothyroid and 18 hyperthyroid were compared with 19 euthyroid (normal) subjects. The lipolytic and cAMP responses to isoproterenol and epinephrine were greatly enhanced in adipocytes from hyperthyroid subjects (P less than .01) and impaired in adipocytes from hypothyroid subjects (P less than .05). However, the antilipolytic effect of clonidine (alpha 2-agonist) and the effect of clonidine on cAMP were similar in all three groups. The alpha 2- and beta-receptor numbers were both slightly increased in hyperthyroidism, but the ratio between the alpha 2- and beta-receptors was unchanged in relation to normal subjects. On the other hand, the adrenergic binding to adipocyte membranes from hypothyroid subjects was reduced, and the beta-receptor binding was reduced even much more (50%) than the alpha 2-receptor binding (20%, P less than .01). Thus, the alpha 2- and beta-receptor ratio was almost doubled in hypothyroid adipocytes (P less than .01). The antagonist affinity against the adrenergic receptors (determined by propranolol and yohimbine, respectively) was unchanged in the three groups. Agonist binding determined in intact adipocytes revealed unaltered affinity of clonidine for the alpha 2-receptor in the three groups. In hyperthyroidism, though, there was enhanced affinity of isoproterenol in competition with the beta-receptor (P less than .05). It is concluded that the inhibitory alpha 2-receptor pathway functions normally in all groups, indicating that the alpha 2-receptors and the alpha 2-receptor-mediated pathway in human adipocytes are relatively unaffected by thyroid hormones.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1990

Erythrocyte zinc in hyperthyroidism: reflection of integrated thyroid hormone levels over the previous few months.

Red blood cell (RBC) zinc (Zn) concentration was measured by atomic absorption spectrophotometry in 28 healthy volunteers, in 46 patients with hyperthyroidism, and in 6 patients with hypothyroidism. The mean (+/- SD) RBC Zn concentration in euthyroid controls was 11.4 +/- 1.5 mg/L RBC, and the normal range defined as the mean +/- 2 SD was 8.5 to 14.3 mg/L RBC. The mean RBC Zn in patients with hyperthyroidism was decreased to 6.4 +/- 1.6 mg/L RBC, and 43 (93%) had low values. The mean RBC Zn in patients with hypothyroidism was not different from that in the controls. There was a significant negative correlation between the concentrations of RBC Zn and those of both plasma thyroxine (T4; r = -0.73) and plasma 3,5,3'-triiodothyronine (T3; r = -0.70). After the treatment of 17 hyperthyroid patients with antithyroid drugs, both mean plasma T4 and T3 levels became normal within 4 weeks, but the normalization of RBC Zn lagged about 2 months behind them. The RBC Zn levels significantly correlated with both the plasma T4 and T3 levels obtained 0, 4, 8, and 12 weeks prior to the RBC sampling, and the highest correlation was observed between the RBC Zn levels and plasma T4 and T3 levels measured 8 weeks previously. These data suggest that RBC Zn concentration in hyperthyroid patients reflects a patient's mean thyroid hormone level over the preceding several months as glycosylated hemoglobin level does in diabetic patients.

Adult↗
PubMed1995

Increased plasma levels of endothelin-1 in patients with hyperthyroidism.

Plasma concentrations of endothelin-1 (ET-1) were measured in 25 hyperthyroid subjects, 15 hypothyroid subjects, and 21 age-matched normal controls. In hyperthyroid patients, plasma concentrations of ET-1 were significantly higher than in the control group (P < .0001) and in hypothyroid patients (P < .0001). In contrast, no differences were found between hypothyroid patients and controls. Plasma levels of ET-1 were similarly elevated as in patients with Graves' disease and those with toxic adenoma. No correlations were found between plasma ET-1 levels, thyroid hormones, and thyrotropin (TSH) in hyperthyroid, hypothyroid, and euthyroid groups. The results of our study clearly indicate that in hyperthyroidism, circulating levels of ET-1 are strongly increased, although the pathogenesis of the increase is unclear.

Adult↗
PubMed1975

Estrogen metabolism in hyperthyroidism and in cirrhosis of the liver.

Estrogen metabolism was studied in spontaneous hyperthyroidism (Graves disease) and in alcoholic cirrhosis of the liver. The plasma concentration of estradiol-17beta (PCE2) was increased in men with hyperthyroidism. Although the metabolic clearance rate of estradiol-17beta (MCRE2) was reduced, the production rate (PR) of the steroid was increased above normal. The MCRE2 was also decreased in women with hyperthyroidism but the PCE2 and PRE2 was unchanged from normal. The conversion ratio of estradiol-17beta (CRE2E1) was increased in both hyperthyroid men and women. The PCE2 was significantly increased in men with cirrhosis of the liver. The MCRE2 was normal and this resulted in an increase in the PRE2 in this disorder. The CRE2E1 was significantly higher than normal. The plasma concentration of estrone (E1) was elevated in men with both disorders.

Adult↗
PubMed1978

Experimental hyperthyroidism in rats suppresses in vitro prostaglandin metabolism in lung and kidney.

Metabolism of prostaglandin (PG) F2alpha and PGE2 was depressed 40--62% in 100,000 g cytoplasmic supernatants of lungs and kidneys prepared from rats made hyperthyroid by 18 daily L(-) thyroxine injections (200microgram, s--c). These hyperthyroid rats had elevated serum thyroxine levels, cardiac hypertrophy and thyroid atrophy. There were no differences in soluble protein concentrations, NAD+ utilisation by endogenous enzymes and substrates, or in the NAD+ dependence of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) between the supernatants prepared from hyperthyroid rats and saline-injected controls. Thyroxine did not inhibit PG metabolism in vitro up to 260 micrometer. These results suggest that thyroxine specifically decreases intracellular levels of PG-metabolising enzymes, especially of the rate-limiting 15-PGDH. Metabolism of PGF2alpha and PGE2 by 15-PGDH was faster in smaller rats and declined with increasing animal weight. These studies imply that some of the clinical features of hyperthyroidism in man might be caused by deficiencies in PG metabolism.

Animals↗
PubMed1986

The relationship of anxiety and depression to symptoms of hyperthyroidism using operational criteria.

Twenty-six females and seven males with newly diagnosed, untreated hyperthyroidism were administered a structured questionnaire designed to identify anxiety and depression using operational criteria. By DSM III criteria, 10 patients were found to have depression and 15 anxiety. The number of anxiety symptoms paralleled the number of hyperthyroid symptoms whereas depressive symptoms did not. Prior history of psychiatric disease and family history of psychiatric disease did not predict anxiety or depression in patients with hyperthyroidism. The number with depression and anxiety was felt to be artificially inflated by the concurrent presence of somatic thyroid symptoms. Psychiatric practitioners should be careful to exclude patients with hyperthyroidism before a primary psychiatric diagnosis is made.

Adult↗
PubMed1990

Effects of cimaterol on muscle protein metabolism and its actions in hypothyroid and hyperthyroid rats.

Objectives were to examine mechanisms underlying anabolic actions of cimaterol in skeletal muscle and to evaluate cimaterol's actions in hypothyroid and hyperthyroid rats. In the first study growing rats were fed either a control diet or a diet containing cimaterol for 10 days. In a second study sham-thyroidectomized and thyroidectomized (Tx) rats were assigned to one of 5 treatments: control (sham-Tx), Tx, Tx supplemented with cimaterol, Tx injected with triiodothyronine (T3), and Tx rats injected with T3 and supplemented with cimaterol. Effects of treatments on growth, muscle weights and urinary NT-methylhistidine (NMH) excretion were evaluated in both trials. Muscle was also collected for determinations of DNA, RNA, protein and activities of several proteolytic enzymes. Cimaterol caused muscle hypertrophy and increased urinary NMH excretion. Hence, anabolic actions of cimaterol may result from an increase in myofibrillar protein synthesis which exceeds changes in myofibrillar protein degradation. Urinary NMH excretion was reduced by thyroidectomy and increased in hyperthyroid rats and both hypothyroidism and hyperthyroidism were characterized by myopathy. Cimaterol increased muscle weights in hypothyroid but not in hyperthyroid rats. Therefore, cimaterol's anabolic properties are thyroid hormone-independent and antagonized by excess thyroid hormone. Anabolic actions of cimaterol in hypothyroid rat muscle were attributed to an action on protein synthesis because urinary NMH excretion was not affected by cimaterol but muscle RNA concentration was increased. Activities of cathepsins B, D and L and neutral proteinase were dose-related to thyroid status, however, were unrelated to cimaterol-dependent perturbations in NMH excretion. Control of muscle protein balance by thyroid hormones may involve regulation of these enzymes; however, control of muscle protein degradation by cimaterol is likely directed towards other proteolytic mechanisms or to mechanisms which alter susceptibility of myofibrillar proteins to degradation.

Adrenergic beta-Agonists↗