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PubMed1982

Altered developmental changes of neuromuscular junction in hypo- and hyperthyroid rats.

1. Effects of thyroid hormone on the development of neuromuscular junctions (n.m.j.s.) were investigated electrophysiologically in the diaphragms (sternal region) of normal, hypo- and hyperthyroid rats from the age of birth (day 0) to day 35.2. Hypothyroidism in new-born rats was induced either by daily administration of propylthiouracil to mothers or by subcutaneous injection of 150 muCi (131)I on day 1. Hyperthyroidism was induced by daily injection of thyroxine.3. In normal rats up to day 10, muscle fibres were innervated polyneuronally. By day 20, multiple innervation was eliminated and muscle fibres received only a single input. In hypothyroid rats elimination of polyneuronal innervation was retarded by 5-8 days, while in hyperthyroid rats the elimination was accelerated by 2-3 days.4. The frequency of miniature end-plate potentials (m.e.p.p.s) in normal rats increased from one per 40 sec on days 0-5 to 1/sec on days 25-35. The m.e.p.p. frequency in hypothyroid rats was 25-65% of that in normal rats of the same age. In hyperthyroid rats the m.e.p.p. frequency was normal up to day 18 but subnormal afterwards. The duration of m.e.p.p. measured on day 22-23 was slower in hypothyroid rats and faster in hyperthyroid rats, relative to m.e.p.ps in normal rats.5. The sensitivity to acetylcholine (ACh) at extrajunctional regions in normal rats was about 100 mV/nC at birth and declined to 1 mV/nC by day 26. In hypothyroid rats, the ACh sensitivity was as high as 30 mV/nC on day 26; in hyperthyroid rats, ACh sensitivity on day 26 was undetectable.6. With pairs of nerve stimuli (applied at a 50 msec interval), the second end-plate potential was facilitated until day 10 and depressed after day 16 in normal rats. This shift from facilitation to depression during development was not altered in either hypo-or hyperthyroid rats.7. It is concluded that the lack and excess of thyroid hormone retards and facilitates the development of n.m.j.s. respectively. Possible mechanisms for this altered development are discussed.

Acetylcholine↗

PubMed1979

Effect of hypoxia on mechanical properties of hyperthyroid cat papillary muscle.

It has been previously established that hyperthyroid myocardium exhibits increased performance under well-oxygenated conditions. To date, it is not known whether hyperthyroid cardiac muscle can maintain this increased performance during hypoxia. The responses of isolated right ventricular papillary muscles from hyperthyroid and euthyroid kittens to hypoxia were compared under isometric conditions at 31 degrees C. Under well-oxygenated conditions, the hyperthyroid cardiac muscle exhibited both an increased contractility and an accelerated rate of relaxation. A similar degree of acute hypoxic stress for 15 min resulted in a greater decrease in contractility in the hyperthyroid compared with the euthyroid papillary muscle as indicated by a greater fall in both peak tension development (2.2 +/- 0.25 from 4.2 +/- 0.2 vs. 0.9 +/- 0.15 from 3.2 +/- 0.4 g/mm2, P less than 0.01) and +dT/dt (12.9 +/- 2.3 from 25 +/- 3 vs. 4.0 +/- 0.6 from 14 +/- 1 g-s-1-mm-2, P less than 0.01). In addition, compared with the euthyroid data, hypoxia resulted in impaired myocardial relaxation in the hyperthyroid cardiac muscle. Thus, the hyperthyroid compared with the euthyroid papillary muscle exhibits both a greater decrease in contractility and an impairment of myocardial relaxation during hypoxia, indicating a greater susceptibility to a given hypoxic stress.

Animals↗

PubMed1987

Effects of beta-blocking agents on urinary excretion of 3-methylhistidine during experimental hyperthyroidism in rats.

Beta-blocking agents are increasingly used as preoperative treatment of hyperthyroid patients. Relatively little is known about the effects of these drugs on metabolic alterations in hyperthyroidism. The aim of this investigation was to study the effects of two different beta-blocking agents on the urinary excretion of 3-methylhistidine (3-MH) during experimental hyperthyroidism in rats. Experimental hyperthyroidism was induced by daily intraperitoneal injections of triiodothyronine (T3; 100 micrograms/100 g body weight) for 3 days. Control animals were injected with corresponding volumes of solvent. Groups of rats received food enriched with metoprolol (8.8 mmol/kg of diet) or propranolol (3.3 mmol/kg of diet) or food without additions. Urinary 3-MH excretion was increased by about 40% during experimental hyperthyroidism. A similar increase of 3-MH excretion was found in animals receiving T3 + metoprolol, whereas the excretion of 3-MH was reduced to control level in hyperthyroid rats receiving propranolol. No effects of metoprolol or propranolol on 3-MH excretion were found in control animals. Although the source of 3-MH cannot be exactly defined, the present results indicate that increased proteolysis in skeletal muscle and/or other tissues during experimental hyperthyroidism was reduced by propranolol.

Adrenergic beta-Antagonists↗

PubMed1992

Effect of arginine on the GHRH-stimulated GH secretion in patients with hyperthyroidism.

Patients with hyperthyroidism have reduced GH responses to pharmacological stimuli and reduced spontaneous nocturnal GH secretion. The stimulatory effect of arginine on GH secretion has been suggested to depend on a decrease in hypothalamic somatostatin tone. The aim of our study was to evaluate the effects of arginine on the GH-releasing hormone (GHRH)-stimulated GH secretion in patients with hyperthyroidism. Six hyperthyroid patients with recent diagnosis of Graves' disease [mean age +/- SEM, 39.2 +/- 1.4 years; body mass index (BMI) 22 +/- 0.4 kg/m2] and 6 healthy nonobese volunteers (4 males, 2 females; mean age +/- SEM, 35 +/- 3.5 years) underwent two experimental trials at no less than 7-day intervals: GHRH (100 micrograms, i.v.)-induced GH secretion was evaluated after 30 min i.v. infusion of saline (100 ml) or arginine (30 g) in 100 ml of saline. Hyperthyroid patients showed blunted GH peaks after GHRH (13.2 +/- 2.9 micrograms/l) as compared with normal subjects (23.8 +/- 3.9 micrograms/l, p < 0.05). GH peaks after GHRH were only slightly enhanced by arginine in hyperthyroid subjects (17.6 +/- 2.9 micrograms/l), whereas, in normal subjects, the enhancement was clear cut (36.6 +/- 4.4 micrograms/l; p < 0.05). GH values after arginine + GHRH were still lower in hyperthyroid patients with respect to normal subjects. Our data demonstrate that arginine enhances but does not normalize the GH response to GHRH in patients with hyperthyroidism when compared with normal subjects. We hypothesize that hyperthyroxinemia may decrease GH secretion, both increasing somatostatin tone and acting directly at the pituitary level.

Adult↗

PubMed1982

Elevation of serum angiotensin-converting enzyme activity in patients with hyperthyroidism.

The activity of serum angiotensin-converting enzyme (S-ACE) was determined spectrophotometrically in 45 patients with hyperthyroidism (30 untreated and 15 treated and euthyroid patients), 14 patients with hypothyroidism, and 135 normotensive healthy subjects. S-ACE was significantly higher in the patients with untreated hyperthyroidism (51.6 +/- 1.9 less than SE greater than nmol.min/ml) than in the healthy controls (28.6 +/- 0.6 nmol.min/ml; P less than 0.001). On the other hand, S-ACE was found to be within the normal range in patients with hypothyroidism (23.2 +/- 1.3 nmol.min/ml). In patients with hyperthyroidism, S-ACE gradually fell into the normal range as the thyroid function became normalized, and there were significant positive correlations between S-ACE and the plasma T3 or T4 concentration (r = 0.60 and P less than 0.001; r = 0.61 and P less than 0.001, respectively ). S-ACE had no definite relation to blood pressure, serum glutamic oxaloacetic acid transaminase, or glutamic pyruvic acid transaminase. When the physicochemical characteristics of the enzyme in the sera of hyperthyroidism patients were compared with those in sarcoidosis patients, similar peak activities of S-ACE on gel chromatography and identical Michaelis constants were obtained; the effects of ethyldiaminetetraacetic acid, SQ14225, and pH on the enzymatic reaction were also similar in both diseases. Thus, hyperthyroidism is considered to be one of the diseases in which S-ACE is elevated. The elevation of S-ACE might be directly or indirectly related to the hyperthyroid state. In addition, it is suggested that the enzyme characteristics are identical in hyperthyroidism and sarcoidosis.

Adolescent↗

PubMed1984

Glucose metabolism in experimental hyperthyroidism: intact in vivo sensitivity to insulin with abnormal binding and increased glucose turnover.

The characteristics of the dose response of insulin on the glucose turnover rate and erythrocyte insulin binding parameters were determined in five normal men before and during experimentally induced hyperthyroidism [L-T4 (2 micrograms kg-1 day-1) for 4 weeks with additional L-T3 (1 microgram kg-1 day-1) for the following 3 weeks]. Hyperthyroidism was characterized by significant rises in T3 from 1.92 +/- 0.17 (+/- SEM) to 3.66 +/- 0.17 nmol/liter (P less than 0.01) and resting metabolic rate from 39 +/- 0.7 to 48 +/- 1 watt/m2 (P less than 0.001). While the subjects received a diet adapted to the metabolic rate, blood glucose rose from 3.8 +/- 0.07 to 4.46 +/- 0.11 mmol/liter (P less than 0.05) without a significant change in plasma insulin. During the insulin dose-response study, glucose infusion rates were unaltered by hyperthyroidism, and neither the maximum effect nor the sensitivity to insulin was altered. Glucose turnover rate, measured using [6,6-2H2]glucose as tracer, was determined in the basal state and during the 0.4 mU kg-1 min-1 insulin infusion. In the basal state, it was significantly increased by hyperthyroidism (control, 2.3 +/- 0.1; hyperthyroidism, 3.7 +/- 0.1 mg kg-1 min-1). During the insulin infusion, hepatic glucose production was totally suppressed before T4 and T3 treatment, but was 0.96 +/- 0.39 mg kg-1 min-1 during T4 and T3 treatment. A marked decrease in the insulin binding affinity to erythrocytes was found without a change in the insulin receptor number. In conclusion, glucose metabolism in experimental hyperthyroidism is characterized by 1) increases in basal glucose production and utilization; 2) antagonism between the effect of insulin and hyperthyroidism at the hepatic level; and 3) lack of peripheral insulin resistance in spite of marked alteration in erythrocyte insulin binding affinity.

Adult↗

PubMed1987

Plasma atriopeptin concentrations in hyperthyroidism, euthyroidism, and hypothyroidism: studies in man and rat.

Atriopeptin (AP) is a polypeptide produced by atrial myocytes that is capable of inducing diuresis, natriuresis, and vasodilatation. Because thyroid dysfunction is known to be associated with alterations in both renal function and vasomotor control, we investigate the possible effects of varying thyroid function on AP in humans and rats. Plasma AP concentrations were determined in hyperthyroid and hypothyroid patients and normal subjects. Plasma AP was also measured in some patients after the iv infusion of 1 L 150 mmol/L NaCl and after treatment of hyperthyroidism or hypothyroidism. Plasma and atrial AP concentrations were measured in hyperthyroid, euthyroid, and hypothyroid rats. Plasma AP concentrations did not differ in the hyperthyroid (n = 22), euthyroid (n = 45), and hypothyroid (n = 16) subjects [47.1 +/- 18.2 (mean +/- SD), 45.1 +/- 28.9, and 42.4 +/- 20.0 pg/mL, respectively]. After NaCl infusion, mean plasma AP concentrations did not increase significantly in any of the three groups. Treatment of hyperthyroidism and hypothyroidism did not result in a significant change in plasma AP levels. In contrast, plasma AP concentrations were significantly higher in T4-treated (hyperthyroid) rats than in either euthyroid or propylthiouracil-treated (hypothyroid) rats [621 +/- 17 vs. 266 +/- 41 (P less than 0.01) and 210 +/- 28 pg/mL (P less than 0.001), respectively], whereas atrial AP contents were similar in the three groups of rats. We conclude that hyperthyroidism and hypothyroidism in man are not associated with significantly altered plasma AP concentrations. The higher plasma AP levels in T4-treated rats may reflect the relatively shorter duration or greater severity of thyroid dysfunction or thyroid hormone-induced myocardial hypertrophy in the animals.

Adult↗

PubMed1990

Peripheral glucose metabolism in human hyperthyroidism.

The present study was designed to determine the effect of spontaneous hyperthyroidism on the forearm muscle glucose uptake and oxidation during the postabsorptive state and after an oral glucose challenge. Ten normal subjects and 11 hyperthyroid patients were studied after an overnight fast (12-14 h) and for 3 h after ingestion of 75 g glucose. Peripheral glucose metabolism was analyzed by the forearm technique to estimate muscle exchange of substrate combined with indirect calorimetry. Increased forearm glucose uptake was observed in the hyperthyroid patients compared to that in the normal subjects (1286 +/- 212 vs. 677 +/- 88 mumol/100 mL forearm.3 h) with enhanced glucose oxidation (443 +/- 40 vs. 147 +/- 29 mumol/100 mL forearm.3 h). Nonoxidative glucose metabolism was also greater in hyperthyroid patients than in normal subjects (842 +/- 234 vs. 529 +/- 90 mumol/100 mL forearm.3 h). Basal serum FFA levels were significantly higher in hyperthyroid than in normal subjects (0.252 +/- 0.025 vs. 0.182 +/- 0.022 g/L), as were the basal lipid oxidation rates in the forearm muscles of the thyrotoxic individuals (0.290 +/- 0.066 vs. 0.088 +/- 0.016 mg/100 mL forearm.min). After glucose ingestion, serum FFA levels and lipid oxidation rates declined significantly to equivalent values in both groups of subjects, and the similar basal insulin concentrations increased to significantly higher levels in the hyperthyroid patients. In conclusion, spontaneous human hyperthyroidism increases glucose uptake by the forearm muscles in the postabsorptive state and during an oral glucose challenge, with augmented fluxes of glucose through the oxidative and nonoxidative pathways.

Administration, Oral↗

PubMed1988

Suppressed plasma prolactin response to thyrotropin-releasing hormone in hyperthyroidism reproduced by thyroxine but not by triiodothyronine administration to normal subjects.

In 10 hyperthyroid women studied in the follicular phase of the menstrual cycle, basal plasma PRL was normal, but PRL release after TRH was significantly suppressed compared with that in 11 control women. The suppressed PRL response to TRH was not explained by changes in serum estradiol or sex hormone-binding globulin. It recovered after treatment of hyperthyroidism. When normal women were treated with T4 (0.5 mg daily for 6 to 10 days), their mean serum free T4 level increased to about 70% of that in the hyperthyroid patients, whereas their serum free T3 levels increased to a lesser degree. During T4 administration, these women had PRL changes similar to those of the hyperthyroid patients. When the normal women took T3 (60-120 micrograms for 6 to 8 days), their serum free T3 increased to almost the level of the hyperthyroid patients, but the TRH stimulated PRL release remained close to the control level. The PRL increase after dopaminergic blockade with metoclopramide was significantly suppressed in hyperthyroid patients, and they had no PRL response to TRH after pretreatment with metoclopramide. In conclusion, the PRL changes in hyperthyroidism were reproduced by administration of T4, but not by administration of T3 to healthy women. The site of action is suggested to be pituitary, but additional hypothalamic effects cannot be excluded.

Adult↗

PubMed1986

Delayed puberty caused by hyperthyroidism in ram lambs is not a result of suppression in body growth.

Over a period of 8 weeks ram lambs (16 weeks old) were made hyperthyroidal (serum thyroxine approximately equal to 150 ng/ml, compared with control approximately equal to 48 ng/ml) by daily subcutaneous injections of thyroxine or maintained at a constant body weight by restriction of the feed intake. Hyperthyroidal and restricted-intake lambs remained at a constant body weight during the period of treatment whilst control rams gained body weight. Testicular growth was normal in restricted-intake lambs but was suppressed in hyperthyroidal animals. Hyperthyroidism, but not feed restriction, was also associated with decrease in LH pulse frequency (1.3 +/- 0.3/12 h compared with controls 4.8 +/- 0.9/12 h. Hyperthyroidal lambs showed normal LH responses to exogenous LHRH. After cessation of treatment testicular growth continued to be suppressed for up to 16 weeks in previously hyperthyroidic rams; thereafter testes began to increase in size but at 30 weeks after treatment were still smaller than those of control rams. It is concluded that elevated thyroxine concentrations directly influence sexual maturation in ram lambs through actions at hypothalamic and/or higher brain centres which control LH secretion. Transient hyperthyroidism during sexual maturation may cause permanent impairment of sexual development.

Animals↗

PubMedDate not supplied

Decreased serum C-peptide/insulin molar ratios after oral glucose ingestion in hyperthyroid patients.

Since C-peptide/immunoreactive insulin (IRI) molar ratios may reflect hepatic extraction of insulin, we measured simultaneous serum glucose, IRI, and C-peptide levels during fasting and 30, 60, 90, 120, and 180 min after 75 g of oral glucose in 10 hyperthyroid patients and 10 age- and weight-matched controls. Mean fasting serum glucose and IRI levels were significantly higher in the hyperthyroid versus control subjects (glucose: 4.9 +/- 0.3 mmol/L versus 4.36 +/- 0.11 mmol/L, P less than 0.01; IRI: 0.10 +/- 0.02 pmol/ml versus 0.05 +/- 0.01 pmol/ml; P less than 0.025). After glucose, mean serum glucose levels were significantly higher in the hyperthyroid versus control subjects at all times studied except for 180 min (P less than 0.01). Mean IRI levels were significantly higher at all times studied including 180 min (P less than 0.01). Mean fasting C-peptide levels were significantly greater in the hyperthyroid patients compared with the controls (1.2 +/- 0.25 pmol/ml versus 0.62 +/- 0.09 pmol/ml; P less than 0.025). After oral glucose, mean C-peptide levels were significantly higher (P less than 0.025) in the hyperthyroid compared with control subjects at 30-60 min but not at 90-180 min. Molar ratios of C-peptide/IRI were significantly lower (P less than 0.05) in the hyperthyroid versus control subjects at all times studied except fasting. In summary, glucose intolerance and hyperinsulinism occur in hyperthyroidism. In addition, C-peptide/IRI molar ratios are reduced after oral glucose ingestion.

Administration, Oral↗

PubMed1988

Increased lipid peroxidation in hyperthyroid patients: suppression by propylthiouracil treatment.

Plasma and urinary levels of thiobarbituric acid reactive substances (TBAR) were determined in 24 hyperthyroid patients, 19 hypothyroid subjects, 35 controls, and 17 hyperthyroid patients before and after propylthiouracil (PTU) treatment (400 mg/day for 2-3 months), as indexes of lipid peroxidation. These measurements were carried out together with t-butyl hydroperoxide (t-BHP)-induced oxygen uptake and visible chemiluminescence in erythrocytes as functional tests related to the antioxigenic capacity of cells. Hyperthyroid patients exhibited increased levels of plasma and urinary TBAR compared to controls. Erythrocyte suspensions from hyperthyroid patients showed, compared to controls, higher rates of oxygen consumption with shorter induction periods upon addition of t-BHP, together with 142% and 75% increases in basal and t-BHP-induced chemiluminescence, respectively. Levels of TBAR in untreated hyperthyroid patients in plasma (16.2 +/- 1.3 pmol/mg of protein) and urine (15.9 +/- 1.5 nmol/mg of creatinine) were decreased after PTU treatment (Plasma, 9.5 +/- 0.7, p less than 10(-4); urine, 7.8 +/- 0.9, P less than 10(-5) to values not significantly different from those of the control group (plasma, 10.3 +/- 0.6; urine, 7.9 +/- 0.7). Compared to control, elevated rates of oxygen uptake induced by t-BHP, basal and t-BHP-induced chemiluminescence in erythrocyte suspensions from untreated hyperthyroid patients were reverted to normal by PTU, while decreased induction period (T0) values were enhanced. Determination of these lipid peroxidative parameters in hypothyroid patients revealed no significant changes over control values, excepted t-BHP-induced chemiluminescence in erythrocytes that was diminished. These data indicate that hyperthyroidism is associated with a pro-oxidant condition characterized by an enhancement in circulating and urinary lipid peroxidative indexes, which is suppressed by PTU treatment. It is suggested that this condition might reflect an oxidative stress at cellular level in tissues which are target for thyroid hormone action with a calorigenic response.

Adult↗

PubMed1992

[Cardiac and plasma catecholamine response to dynamic exercise in hyperthyroidism].

To investigate cardiac and sympathoadrenal responses to dynamic exercise, heart rate, systolic blood pressure, serial plasma norepinephrine (NE) and epinephrine (E) concentrations during multistage treadmill exercise were measured in 24 hyperthyroid patients (mean age; 42 +/- 16) and 24 age-sex matched control subjects. Eleven patients were re-examined in the euthyroid state after antithyroid therapy. Exercise duration was shorter in patient with hyperthyroidism. Also, the heart rates and systolic blood pressures at rest and in the early stage of exercise were significantly higher in hyperthyroidism. NE at rest (normal vs hyperthyroid: 124 +/- 10 vs 80 +/- 7 pg/ml, p < 0.01) and NE at peak exercise (475 +/- 38 vs 310 +/- 38 pg/ml, p < 0.01) were lower in hyperthyroidism. E at rest (22 +/- 2 vs 29 +/- 4 pg/ml, n.s.) did not differ, however, E during the first stage of exercise (30 +/- 3 vs 69 +/- 12 pg/ml, p < 0.01) was higher in hyperthyroidism. Re-examination for the euthyroid state revealed the decreases in the heart rates and systolic blood pressures at rest and in the early stage of exercise, and the normalization of the NE and E response. Thus, patients with hyperthyroidism was in the hyperdynamic cardiac state at rest and during dynamic exercise, which was accounted for by decreased sympathetic nervous activity and increased adrenomedullary responses. These modifications of sympathoadrenal response seemed reversible when patients were controlled by antithyroid therapy.

Adolescent↗

PubMedDate not supplied

[Serum activity of angiotensin-converting enzyme and osteocalcin levels in hyperthyroidism].

This study was carried out in order to investigate serum changes of osteocalcin (BGP) and angiotensin converting enzyme (SACE) activity in a group of patients with hyperthyroidism. We studied 20 hyperthyroid patients (F 14, M 6; age mean 37.5 +/- 16.8 years) and 13 control subjects (F 11, M 2; age mean 40.3 +/- 7.5 years). In both patients and controls we measured: FT3, FT4, T3, T4, TSH, BGP, SACE. Finally, in patients with hyperthyroidism a TRH test and functional investigations were also performed. We observed that mean SACE levels were significantly increased in hyperthyroid patients (32.06 +/- 10.3 nmol/ml/min) in respect to control subjects (14.66 +/- 3.88 nmol/ml/min) (p = 2.02 E-6). Similarly serum BGP levels were significantly increased in hyperthyroid patients (5.94 +/- 2.55 ng/ml) than in control subjects (2.89 +/- 1.58 ng/ml) (p = 5.66 E-4). There was a significant linear correlation between SACE and T4 levels (r = 0.48; p < 0.05), between serum BGP and T4 (r = 0.50; p < 0.02) and furthermore between SACE and BGP (r = 0.57; p < 0.01). In conclusion both serum BGP and SACE levels are increased in patients with hyperthyroidism and are directly correlated between than and with indexes of thyroid function; therefore, they may be regarded as peripheral indexes of hyperthyroidism.

Adult↗

PubMedDate not supplied

Effect of hypoxia and catecholamine stimulation on cardiac performance in the isolated working hyperthyroid rat heart.

The hyperthyroid heart has a greater oxygen demand due to its enhanced contractile state and higher basal metabolic rate. Consequently, it may be more sensitive to conditions of decreased oxygen supply or increased oxygen use. We, therefore, investigated the effect of a restricted oxygen supply (hypoxia) and enhanced oxygen demand (catecholamine stimulation) on cardiac function in the isolated working hyperthyroid heart. Hypoxia was induced by substituting 20% of the oxygen in the perfusate with nitrogen, while catecholamine stimulation was with isoproterenol. Hypoxia caused a 37% drop in cardiac output in the hyperthyroid heart and a 10% decrease in euthyroid hearts. In response to isoproterenol, a dose-dependent increase in heart rate was found in both groups which was greatly augmented in the hyperthyroid hearts by hypoxia. With isoproterenol stimulation under normoxic conditions, euthyroid hearts showed a moderate increase in contractile performance (cardiac output and dP/dtmax), while in hyperthyroid hearts contractile performance declined. Hypoxia exacerbated the decrease in function of the hyperthyroid heart. In conclusion, our results indicate that the hyperthyroid heart is very sensitive to imbalances in the myocardial oxygen supply/demand ratio, especially when demand is increased in the presence of decreased supply.

Animals↗

PubMed1991

Low serum thyrotropin (thyroid-stimulating hormone) in older persons without hyperthyroidism.

We studied a large population (n = 2575) of unselected ambulatory persons older than 60 years to determine the prevalence of a low serum thyroid-stimulating hormone (TSH) level, ie, of less than 0.1 mU/L using a sensitive assay, a level suggestive of hyperthyroidism in younger adults. One hundred one persons (3.9%) had a low serum TSH level. About half of them (51/101) were taking thyroid hormone. Of the remainder, 44 were not hyperthyroid did not become so during up to 4 years of follow-up. Forty-one of the 44 euthyroid persons had a serum thyroxine level of less than 129 nmol/L; repeated testing showed a serum TSH level of more than 0.1 mU/L in the three euthyroid persons with a serum thyroxine level of more than 129 nmol/L. Only six were hyperthyroid or became so during the follow-up period; all had a serum thyroxine level of more than 129 nmol/L. Routine clinical examination was not a sensitive indicator of hyperthyroidism and did not permit discrimination from euthyroidism. A low value of serum TSH alone, while it had high sensitivity and specificity for hyperthyroidism, had a low positive predictive value (12%) for this diagnosis; addition of the thyroxine assay raised the predictive value fivefold to 67%. A low value of serum TSH is far more common in older persons than is hyperthyroidism. Low values in euthyroid persons are accompanied by a clearly normal serum T4 concentration (less than 129 nmol/L) or by a serum TSH level of more than 0.1 mU/L on repeated testing. We recommend measurement of the serum TSH thyroid concentration, using a sensitive assay, as the initial step in testing any older person for possible hyperthyroidism. Measurement of the serum T4 concentration or the free T4 index on the same sample would be needed only in the approximately 2% with a serum TSH level of less than 0.1 mU/L; alternatively, the TSH assay in these could be repeated at a later time.

Aged↗

PubMed1990

[The risk of recurrence following the thyrostatic treatment of immunogenic and nonimmunogenic hyperthyroidism].

Data of 196 patients treated for hyperthyroidism exclusively with antithyroid drugs were analyzed retrospectively concerning the relapse rate within a follow-up period of four years. Patients were subdivided for primary or recurrent disease, and for immunogenic or non-immunogenic hyperthyroidism, respectively. In immunogenic as well as in non-immunogenic hyperthyroidism, the relapse rate was significantly lower for patients with primary disease (35% and 52%, respectively) compared to those with recurrent hyperthyroidism (82%, p less than 0.001 and 83%, p less than 0.001, respectively). In patients with primary disease, clinical, biochemical and scintigraphic parameters were tested with respect to their capability of predicting a relapse. For immunogenic hyperthyroidism the highest relapse rates were observed in young patients and in those with large goitres, whereas for non-immunogenic hyperthyroidism they were highest in old patients, in those with nodular goitres and in those without an increased urinary iodine excretion at the time of diagnosing hyperthyroidism.

Adolescent↗

PubMed1990

[Incidence of autonomy and immune hyperthyroidism before and following preventive use of iodized salt in the Berlin-Brandenburg area].

The incidence of hyperthyroidism was observed in the area of Berlin (1.2 million inhabitants) and in a rural district in the geographical region of the "Mark Brandenburg" (48.115 inhabitants) during the period from 1975 und 1989. This area is characterized with a iodine deficiency grade II (WHO). In 1985 an iodine salt supplementation was introduced by law. The period before iodine salt supplementation 1975-1985 was compared to the period after iodine prophylaxis: there was an increase in hyperthyroidism in the Berlin-area by the ratio 1:3.1 and 1:2.8 (1975-83 compared to 1988 and 1989), in the rural district by 1:1.7 (1980-1985 compared to 1986/87). The ratio autonomy (non immunogenic form) to immunogenic etiology was 1:12 (1977-83), and changed to 1:1.45 in 1988 and 1:16.3 in 1989 after iodine supplementation. The sex ratio male:female was 1:10 before, and 1:6.8 after prophylaxis for hyperthyroidism in total, in autonomy the ratio was observed as 1:12 before and 1:7.7 (1988), 1:4.7 (1989) after supplementation, in immunogenic hyperthyroidism 1:10 unchanged in the early and late period of observation. The increase of hyperthyroidism after iodine prophylaxis correlated well with the consumption of thyrostatic drug Thiamazol (Methimazol) for the whole country. The defined daily dose (DDD)/1000 inhabitants/day increased during the observation time from 0.5 (1984), 0.55 (1985), 0.66 (1986), to 1.47 (1987), 1.26 (1988) and 0.81 (1989). The results are compared and discussed with reports from USA, Iceland, Great Britain, Denmark, Italy and Tasmania. During the period of seven years (1980-87) in the rural district a seasonal dependence of onset in hyperthyroidism was observed in spring time between May and June only in immunogenic hyperthyroidism, despite in thyroidal autonomy the disease began throughout the year without a seasonal peak.

Berlin↗