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At least 19 recordsLinked to original sources
PubMed1997

Bone loss in hyperthyroid patients and in former hyperthyroid patients controlled on medical therapy: influence of aetiology and menopause.

OBJECTIVE: The effect of hyperthyroidism on osteoporosis risk and its reversal after control of hyperthyroidism remains somewhat controversial. We assessed the values of bone mineral density in hyperthyroid patients and in former hyperthyroid patients euthyroid on medical therapy, as well as the influence of aetiology and menopause upon bone mass. DESIGN: The values of bone mineral density in hyperthyroid patients (active) and former hyperthyroid patients euthyroid on medical therapy (controlled), were compared, together with data from our control group and from the Spanish reference population. We also compared the values of bone mineral density in patients with Graves' disease with those in patients with toxic nodular goitre and assessed the influence of the menopause. PATIENTS: We studied 127 consecutive hyperthyroid patients (age 41 +/- 16 years; 110 females, 17 males; 102 Graves' disease and 25 toxic nodular goitre); 78 were active (group A) and 49 controlled on medical therapy (carbimazole, mean time of euthyroidism 7.5 +/- 9.1 months; group B). We also studied 43 healthy subjects (age 40 +/- 14 years; 41 females, two males; group C). MEASUREMENTS: Bone mineral density was assessed by dual X-ray absorptiometry at lumbar spine (L2-L4), femoral neck and Ward's triangle. Data were expressed as g/cm2 and as a Z score (SD vs Spanish reference population adjusted by age and sex). Blood was obtained to measure the levels of free T4, TSH and TSH receptor antibody. RESULTS: Patients with active hyperthyroidism showed a generalized reduction in axial bone mineral density in comparison with both the control group and the reference population, whereas former hyperthyroid patients showed partial recovery of bone mass in lumbar spine and Ward's triangle. Mean Z scores at lumbar spine, femoral neck and Ward's triangle were: -0.92, -0.79 and -0.89 in group A; -0.74, -0.23 and -0.44 in group B and 0.18, 0.09 and 0.36 in group C, respectively. No differences were found between bone mineral density values from patients with Graves' disease and those with toxic nodular goitre, nor between pre and postmenopausal hyperthyroid women once adjusted by age and sex. CONCLUSIONS: Our data suggest that hyperthyroid patients show a generalized reduction of bone mass in the axial skeleton and that only partial recovery is present in former hyperthyroid patients after a mean of 7.5 months of biochemical euthyroidism. This recovery is insufficient to normalize the bone density in lumbar spine and Ward's triangle, although femoral bone mass was not different from that of the control group. The extent and degree of hyperthyroid bone disease surpass the effects of the menopause on the bone mass. The aetiology of hyperthyroidism does not seem to play any role in the severity of hyperthyroid bone disease.

Absorptiometry, Photon↗
PubMed1998

Hyperthyroidism in early infancy: pathogenesis, clinical features and diagnosis with a focus on neonatal hyperthyroidism.

Neonatal hyperthyroidism has mostly been described in the context of maternal Graves' disease. It has been estimated that about 0.2% of pregnant women have Graves' disease; however only 1% of the children born to these women are described as having hyperthyroidism. In most of the cases, the disease is due to maternal antibodies transferred from the mother into the fetal compartment, which stimulate the fetal thyroid by binding to the thyrotropin (TSH) receptor. In this form of neonatal hyperthyroidism, thyrotoxicosis disappears with the clearance of the maternal antibodies and usually signs disappear during the first 4 months of life. Rare forms of persistent, nonimmune neonatal hyperthyroidism are explained by molecular abnormalities of the TSH receptor. Prematurity is frequent, as well as hypotrophia. Tachycardia, goiter, hyperexcitability, poor weight gain, hepatomegaly and/or splenomegaly, stare and/or eyelid retraction are among the most frequent neonatal thyrotoxicosis clinical signs. Diagnosis is based on the determination of the blood level of thyroxine (T4), triiodothyronine (T3), and TSH. Even if these levels are normal in the cord blood, tests should be repeated 3 to 10 days later to detect possible delayed appearance of the disorder. These parameters should be interpreted according to the age of the neonate. To confirm the immune nature of this hyperthyroidism, thyroid-stimulating immunoglobulins (TSI) should be determined. The TSI determination is crucial in identifying nonimmune causes of neonatal hyperthyroidism: in this neonatal hyperthyroidism, TSI are not detected, either by radioreceptor assay and/or by functional assay, and molecular studies are needed to identify the mutation. Mutation of the TSH receptor leading to its constitutive activation and to neonatal hyperthyroidism have been described. Germline mutations are found in hereditary hyperthyroidism; de novo germline mutations can cause sporadic congenital hyperthyroidism.

Autoantibodies↗
PubMed1985

[Hyperthyroidism and mitral valve prolapse: comparative two-dimensional echocardiography study of a hyperthyroid and a control population totalling 104 patients].

Recent studies seem to demonstrate a higher incidence of mitral valve prolapse in hyperthyroid patients. A complete cardiological check-up including 2D echocardiography was performed in 52 hyperthyroid patients and 52 control subjects. In the hyperthyroid population, mitral valve prolapse was diagnosed 3 times, 5,8 p. 100 of cases. These 3 subjects were female; hyperthyroidism was nodular in 2 cases: Grave's disease was only present in 1 case. Hyperthyroidism was very active at the time of the echocardiographic study in those 3 patients. In the control group, mitral valve prolapse was observed in 4 cases (7.7 p. 100). These 4 patients were all female. The results of this study do not show a higher incidence of mitral valve prolapse in the hyperthyroid population than in the control group. Grave's disease was not more prevalent in hyperthyroid patients with mitral valve prolapse. On the other hand, there were significantly more female patients with MVP in both the hyperthyroid and control populations.

Echocardiography↗
PubMedDate not supplied

Hyperthyroidism and pregnancy. II. Thyroid function in normal pregnancy and in pregnancy associated with hyperthyroidism.

Starting from the diagnostic difficulties when hyperthyroidism is associated with pregnancy, PBI, total T4 and free thyroxin, triiodothyronine (T3), rT3, TBG, TSH and LATS were assayed in a group of euthyroid pregnant women (136) more or less equally distributed between month 2 and 9 of pregnancy; the same tests were applied to 14 pregnant hyperthyroid women (month 2-3), the latter also undergiving a test for urinary elimination of catecholamines. The results were referred to the normal values of techniques employed. The work presents the alterations in the thyroid status parameters when pregnancy is associated with hyperthyroidism, as against normal pregnancy, pointing out the need for performing a complex set of assays "in vitro" in order to establish correctly the diagnosis of hyperthyroidism in pregnancy and apply the right therapy at the right moment. Increased T3 and free T4 levels in hyperthyroidism referred to an increased TBG level in euthyroid pregnancy are considered as discriminators.

Female↗
PubMedDate not supplied

Researches on neuro-muscular functional parameters in experimentally hyperthyroidized rats and in human hyperthyroidism.

The authors have determined the neuro-muscular functional parameters of conductibility and excitability in normal and hyperthyroidized rats. The determination of hyperthyroidization and of the neuro-muscular functional parameters was accomplished by utilizing an own experimental model. The data obtained in rats were compared with those established by authors in normals and in patients suffering from hyperthyroidism. It resulted clearly that in rats hyperthyroidization disturbs particularly the conductibility of motor fibres while in man hyperthyroidism modified especially the excitability of motor fibres.

Animals↗
PubMedDate not supplied

Experimental hyperthyroidism IV. Myocardial muscle mechanics and oxygen consumption in euand hyperthyroidism.

Myocardial mechanics and oxygen consumption were studied in right ventricular papillary muscles taken from cats pretreated with cristalline L-thyroxine (1 mg/kg/day, i.p.) 8-18 days prior to the examination. Isotonic afterloaded and isometric contractions were employed. Oxygen consumption was determined polarographically. Data obtained were compared with control studies on papillary muscles taken from euthyroid cats. In isotonic afterloaded contractions the extent of shortening was nearly identical in both groups. However, maximum rate of isometric tension development and velocity of isotonic shortening were considerably increased in hyperthyroid myocardium. Myocardial oxygen consumption was significantly increased in hyperthyroidism, primarily due to an increased maximum rate of isometric tension development and-to a lesser extent-to increased isotonic contraction velocity. In isometric contractions maximum tension development (preload near Lmax) was similar in both groups. However, maximum rate of isometric tension development was markedly increased in hyperthyroidism. A close and linear relationship was found between maximum rate of isometric tension development (isometric contraction) and myocardial oxygen consumption. The results demonstrate increases of velocity factors of myocardial performance in experimental hyperthyroidism. Myocardial oxygen consumption is significantly increased. This increase in oxygen consumption quantitatively has its mechanical equivalent in increased isometric contraction velocity and, to a small amount, in increased isotonic contraction velocity.

Animals↗
PubMed1985

Metabolism of coronary vasculature in euthyroid, hyperthyroid and recovering hyperthyroid rats: a histochemical study.

Coronary arteries and arterioles from normal rats, from rats made hyperthyroid by administration of desiccated thyroid for 10 weeks, and from hyperthyroid rats which were then fed normal control diets for 10 weeks, were examined histochemically to determine the activity of key metabolic pathways. The primary aims of this study were to determine if the alterations in particular enzyme and substrate activities that occur in thyrotoxic rat myocardium, arteries and arterioles were reversible and would return to normal levels following cessation of the hyperthyroid state. Our results suggest that hyperthyroid rats, even after 10 weeks on the normal diet, still show some compromise in arteriolar aerobic metabolism in favor of anaerobic pathways, while coronary arteries still demonstrate little glucose-6-phosphate dehydrogenase activity. Myocardial metabolic activity approximates that of normal control animals by the end of the 10th week on the normal diet.

Animals↗
PubMed1986

Hyperthyroidism and the heart: study of left ventricular function in preclinical hyperthyroidism.

To study the response of the target organs to minor increments of thyroid hormone levels, left ventricular ejection fraction (LVEF) the primary indicator of left ventricular function, was measured in patients with preclinical hyperthyroidism and the results were compared with those obtained in euthyroid subjects and in patients with toxic adenoma. In euthyroid subjects and in patients with preclinical hyperthyroidism LVEF in response to exercise involving an isometric static work load revealed a minor increase, whereas in manifest hyperthyroidism (toxic adenoma) an opposite response with an impairment of left ventricular functional capacity was found. The results showed that the pituitary responds more sensitively to minor changes in the circulating thyroid hormone levels than does the heart and indicated that the typical hyperthyroid heart changes associated with the evolution of toxic adenoma develop gradually.

Adenoma↗
PubMedDate not supplied

[Neonatal hyperthyroidism caused by TSH receptor antibodies in maternal autoimmune hyperthyroidism].

Between July 1993 and December 1994 five term infants of mothers with Graves' disease were hospitalised at the Frühgeburtenstation of the Univ.-Frauenklinik Graz. Four Mothers had elevated TSH-receptor-antibody (TRAb)--levels during pregnancy, one had normalised TRAb-titers. In one case hyperthyroidism was first diagnosed during pregnancy. Three newborns had elevated TRAb-titers; in one of them thyrotoxicosis was diagnosed clinically and biochemically at the second day of life, one newborn had mild hyperthyroidism with tachycardia at the end of the first week of life and one newborn was asymptomatic by immediately initiated therapy. The two other newborns had normal thyroid hormone and antibody levels and no symptoms or signs of hyperthyroidism. The cases are reported and discussed in detail and our overall approach to diagnosis and treatment of neonatal hyperthyroidism in case of maternal Graves' disease will be given.

Autoantibodies↗
PubMed1996

Primary hyperthyroidism and associated hyperparathyroidism in a patient with myotonic dystrophy: Steinert with hyperthyroidism and hyperparathyroidism.

A patient with myotonic dystrophy and associated primary hyperthyroidism and hyperparathyroidism is described; this association has not been reported previously, to the authors' knowledge. The patient also suffered from hypergonadotropic hypogonadism and hyperinsulinism with insulin resistance. The etiology of hyperthyroidism and hyperparathyroidism is not clear. At surgery, a parathyroid adenoma was extirpated, and a subtotal thyroidectomy was performed. Postoperative course was unremarkable, with consistently normal serum calcium levels but persistently elevated serum parathyroid hormone concentrations. The possibility that the patient had a residual hyperparathyroidism could not be eliminated. Thyroid function was normal. After surgery, the patient reported subjective improvement in his muscle strength. The authors conclude that both diseases-- hyperthyroidism and hyperparathyroidism--exert a negative effect on the myotonic dystrophy and that an early recognition of these two diseases is crucial for the favorable evolution of the patient.

Adenoma↗
PubMed1982

A case report on disequilibrium hypercalcemia in hyperthyroidism. Comparison of calcium metabolism with other patients with hyperthyroidism.

The patient, a 30-year-old woman, was admitted to Itoh Hospital in February, 1979 for hyperthyroidism. She had a history of pyelonephritis and recurrent urinary tract infection. Laboratory data on admission revealed overt hyperthyroidism (T3: 405 ng/dl, T4: 22.5 micrograms/dl and T3U: 57.--%), severe hypercalcemia of 12.6 mg/dl and hypercalciuria. The PSP excretion and GFR were both decreased. Serum c-PTH was nondetectable. As the thyroid function improved, there was a gradual decrease and later normalization of plasma calcium, phosphate and urinary calcium excretion. When subtotal thyroidectomy was performed on October 19, 1979, hypertrophy of the parathyroid gland was not demonstrated. In comparison with 98 other hyperthyroid patients, the pathogenesis of hypercalcemia was discussed. In conclusion, hypercalcemia in the patient, T. Y., was regarded as a kind of disequilibrium hypercalcemia which resulted from a combination of increased bone turnover and decreased calcium excretion by the kidney.

Adult↗
PubMed1976

DNA-synthesis of lymphocytes in hyperthyroid and euthyroid subjects. Effect of 131I therapy on hyperthyroidism.

The DNA-synthesis of human lymphoid cells as estimated by the measurement of thymidine incorporation in vitro was investigated in healthy controls and in patients with various thyroid disorders before and after therapy. Hyperthyroid patients treated with 131I and surgery (euthyroid at initial blood sampling before surgery), patients with atoxic nodular goitre treated by surgery and healthy untreated control individuals comprised the material. The synthesis of DNA in lymphocytes was higher in hyperthyroid patients in comparison with euthyroid individuals, and decreased subsequent to 131I therapy in the hyperthyroid patients. No decrease was recorded in the other groups of patients. No evidence suggesting a change in the lymphocyte reactivity to thyroglobulin was found in any of the patient groups.

Adult↗
PubMed1976

[Analysis of radio-isotope tests "in vivo" and "in vitro" in the diagnosis of hyperthyroidism. Statistical study of parameters obtained from routine investigations in normal and hyperthyroid subjects (author's transl].

Considering recent progress which permits routine direct estimation of circulating iodinated hormones, classical investigations based on plasma iodine fractions (PBI 127, BEI 127, 127 IH) must be considered out of date for the routine diagnosis of hyperthyroidism. The best possible approach for the detection of hyperthyroidism by radio-isotope tests in vitro consists of associating a determination of the free thyroxine index and tri-iodothyronine. Certain types of hyperthyroidism, mainly in the goup of toxic adenomas, escape this detection in vitro, and justify the use of conventional in vivo tests whenever this diagnosis is suspected.

Electronic Data Processing↗
PubMed1994

[Lithium therapy and hyperthyroidism: disease caused or facilitated by lithium? Review of the literature apropos of a case of hyperthyroidism preceded by transient hypothyroidism].

A case of hyperthyroidism occurring in a 68 year old man receiving lithium carbonate (1 g/day) for 5 years is reported. The clinical history of the patient, treated for bipolar affective disorder, was remarkable for transient hypothyroidism followed several months later by tremor, increased free thyroxine and triiodothyronine, and decreased TSH levels which led to lithium withdrawal. Two months later, clinical and biological signs were unchanged, Tc99m-scan displayed a homogeneous and increased isotope uptake. In this setting, high levels of autoantibodies against TSH-receptor, and grade I exophthalmos and slightly ocular muscle enlargement at CT-scan favored the diagnosis of Graves' disease (perhaps facilitated by lithium therapy). Carbimazole treatment was effective in controlling hyperthyroidism. Review of the literature disclosed 44 cases of hyperthyroidism occurring in lithium-treated patients. Most of these cases concerned specific thyroid diseases, particularly with an autoimmune mechanism. There is also evidence for an actual role of lithium in increasing intrathyroid iodide pool and for an impact of lithium on the immune system. Thus, the hypothesis that lithium may trigger the development of an autoimmune thyroid disease in predisposed patients deserves further investigation.

Aged↗
PubMedDate not supplied

[Characteristics of the water-electrolyte regulation in experimental hyperthyroidization and hyperthyroidism].

In experiments on rats the effect of hyperthyroidization (induced by thyroidin, 1-thyroxin) and hyperthyrosis (induced by TSH, cold exposure) on volume natriuresis was studied. As revealed, after expansion of extracellular space natriuresis increased under hyperthyroidization and hyperthyrosis, and was much higher than in control rats. Natriuresis elevation in response to increased volume of extracellular fluid in rats under hyperthyroidization resulted from the rise of natriuretic factor in the blood.

Animals↗
PubMed1990

Similarity and dissimilarity between clinical and laboratory findings, especially anti-thyrotropin receptor antibody in ophthalmic Graves' disease without persistent hyperthyroidism and hyperthyroid Graves' disease.

The aim of this study was to investigate thyroid states, significance of anti-TSH receptor antibodies and the clinical courses of patients with euthyroid Graves' ophthalmopathy. The clinical and laboratory finding of 30 patients with euthyroid Graves' ophthalmopathy were briefly as follows: 1) normal sized thyroid or small goiter; 2) negative or weakly positive thyrotropin binding inhibitor immunoglobulin (TBII); 3) normal thyroid [99 m-Tc] pertechnetate uptake; and 4) frequent observations of low serum TSH values. Besides TBII, thyroid stimulating antibody (TSAb) was measured under low salt and isotonic conditions using FRTL-5 rat thyroid cells. Both TBII and TSAb titers were lower in euthyroid Graves' ophthalmopathy than in hyperthyroid Graves' disease. Serum TSH levels frequently became low in patients considered as euthyroid upon the first examination as well as in Graves' patients in remission, reflecting preceding or mild hyperthyroidism. In follow-up studies, these patients with mildly elevated thyroid hormone levels and low TSH levels seldom reached a state of persistent hyperthyroidism, when TBII was negative or only weakly positive.

Adult↗
PubMed1987

The decrease in non-specific suppressor T lymphocytes in female hyperthyroid Graves' disease is secondary to the hyperthyroidism.

There has recently been considerable interest generated in the significance of changes in the peripheral blood T lymphocyte subsets in patients with autoimmune thyroid disease. Previously, monoclonal antibodies that recognized T cells (Leu 1+ cells), T helper/inducer cells (Leu 3a+ cells), and T suppressor/cytotoxic cells (Leu 2a+ cells), have been used to enumerate these subsets. Using 2 new monoclonal antibodies (anti-Leu-8 and anti-Leu-15), in addition to the above 3 antibodies, and 2-colour flow cytometry, we have enumerated the total T, T helper/inducer, T suppressor/cytotoxic, T helper (Leu 3a+8-), T inducer (Leu 3a+8+), T suppressor (Leu 2a+15+), and T cytotoxic (Leu 2a+15-) cells in 22 patients with hyperthyroid Graves' disease, 38 patients with 131I-treated Graves' disease and 10 patients with Hashimoto's thyroiditis. All patients and controls were female. We found that hyperthyroid patients with Graves' disease had significantly lower T suppressor/cytotoxic cells (p less than 0.05) than did controls, and that this was mainly due to a decrease in T suppressor cells (p less than 0.01). Furthermore, patients with severe hyperthyroidism had a more significant decrease in T suppressor/cytotoxic (p less than 0.001) and T suppressor (p less than 0.001) cells, and an increase in the T helper/inducer:T suppressor/cytotoxic (p less than 0.01) and T helper:T suppressor (p less than 0.01) cell ratios. Patients who were euthyroid more than 1 year after 131I therapy for Graves' disease had normal T cell subsets and ratios, whether or not TSH receptor antibody or other thyroid auto-antibody titres were elevated. Ten females with Hashimoto's thyroiditis also had normal T cell subsets.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗