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PubMed2001

Influence of short-time application of a low sodium diet on blood pressure in patients with hyperthyroidism or hypothyroidism during therapy.

Hyperthyroidism or hypothyroidism are commonly associated with altered blood pressure (BP). Restriction of sodium in the diet produces a decrease in BP in some individuals. It is also well known that hormones other than thyroid affect BP. The present study was designed to evaluate the influence of a low sodium diet on BP in patients with hyperthyroidism or hypothyroidism during therapy. The occurrence of salt-sensitive or salt-nonsensitive BP was compared with hormonal levels (plasma renin activity, aldosterone, atrial natriuretic peptide, and arginine vasopressin). Patients with hyperthyroidism (75 subjects) were investigated before the initiation of treatment, 2 weeks after the treatment, and after the attainment of euthyroid state. Patients with hypothyroidism (31 subjects) were studied before the treatment and in the euthyroid state. Control values were obtained from 37 healthy individuals. Blood pressure, changes of plasma volume, serum aldosterone, atrial natriuretic peptide, vasopressin levels, and plasma renin activity were measured in all investigated subjects after application of a normal sodium diet and after 3 days on a low sodium diet. Elevated systolic BP was found in patients with hyperthyroidism and hypothyroidism. Mean arterial BP was higher only in the untreated hypothyroid patients. The high incidence of salt-sensitive BP was found only in untreated hypothyroid patients. Also in hypothyroid patients the application of a low sodium diet led to a lower increase in plasma renin activity in subjects with salt-sensitive BP than in individuals with salt-resistant BP. Therefore, different mechanisms are responsible for BP elevation in patients with hyperthyroidism or hypothyroidism.

Adolescent↗
PubMed2002

[Hyperemesis in the first trimester of pregnancy: role of biological hyperthyroidism and fetal sex].

OBJECTIVES: Our objectives were to link hyperemesis gravidarum with biochemical hyperthyroidism and hormonal modification (HCG and estradiol) and to test the hypothesis that biological abnormalities (ionogram and liver enzyme) are more often reported in hyperemesis gravidarum with biochemical hyperthyroidism. STUDY DESIGN: Thirty three patients admitted in "Hôpital Jeanne de Flandre" with hyperemesis gravidarum were studied prospectively. RESULTS: Twenty-two patients (66.7%) had biochemical hyperthyroïdsm (suppressed thyroid stimulating hormone or increased triiodothyronine index or tetraiodothyronine index). Hyperthyroid patients were more likely than euthyroid patients to have abnormal electrolyte levels (16/22 [72.7%] vs 3/1 [27.3%], P < 0.02) or increased liver enzyme levels (8/22 [36.4%] vs 3/11 [27.3%]). The severity of hyperemesis was found to vary directly with the degree of hyperthyroidism. We report a female predominance among the offspring of mothers with hyperemesis gravidarum. CONCLUSION: Our results are suggestive of the involvement of hyperthyroidism and fetal sex in the pathogenesis of hyperemesis gravidarum. Also these hypothesis are not clearly understood, human chorionic gonadotrophin occurred in the two mechanisms.

Adult↗
PubMed2005

Unstable angina with normal coronary angiography in hyperthyroidism: a case report.

Hyperthyroidism is associated with an increase in myocardial oxygen consumption that, due to an imbalance of oxygen demand and supply, can cause angina. However, subclinical hyperthyroidism rarely presents as chest pain in the resting state. Herein, we present a case of subclinical hyperthyroidism involving a 58-year-old male who complained of frequent chest tightness and typical electrocardiographic changes while in a resting state. Coronary angiography showed no significant lesion. Laboratory data showed that the patient suffered from hyperthyroidism, for which he was successfully treated with anti-thyroid agents. We are reminded that typical chest pain might be the first symptom of hyperthyroidism.

Angina, Unstable↗
PubMed1999

[Is there a need for treatment in subclinical hypo- and hyperthyroidism?].

Subclinical thyroid dysfunction is characterized by normal levels of thyroid hormones but abnormal values of thyrotropin (TSH) in an asymptomatic individual. Subclinical hypothyroidism is a common disorder with a prevalence of about 7 to 8% in women (most frequently in females over 50 years), and about 3% in men. It is characterized by elevated serum TSH in the presence of normal concentrations of serum thyroxine. Patients with TSH levels about 12 mU/L (and with positive antithyroidal antibodies) have the highest risk for developing overt hypothyroidism. Therefore, these patients will require L-thyroxine treatment. In patients with TSH < 12 mU/L, the indication for therapy depends on the etiology, on risk factors and concomitant diseases (e.g. strumectomy, coronary heart disease, depression, infertility). Subclinical hyperthyroidism (TSH suppression syndrome) is characterized by normal thyroid hormone concentrations but diminished serum TSH. Most frequently, this disorder is caused by exogenous L-thyroxine treatment. The endogenous form of subclinical hyperthyroidism mainly caused by nodular goiter has a prevalence of up to 20% in patients with large goiters. In patients with subclinical hyperthyroidism, there is an increased risk for development of atrial fibrillation and for a decrease in bone mass in postmenopausal women. In the majority of patients measurable TSH levels can be detected before or after stimulation with TRH. This formally excludes overt hyperthyroidism in such patients. Frequently, there is no need for treatment but follow-up is important. However, in patients with subclinical hyperthyroidism associated with atrial fibrillation a therapy with antithyroid drugs, beta-blockers or radioiodine must be considered.

Diagnosis, Differential↗
PubMed1999

[Surgery for hyperthyroidism].

The concept of therapy for hyperthyroidism combines endocrinology, nuclear medicine and surgery. For selection of the treatment of choice, pathophysiology as well as individual aspects are considered. Surgical therapy is mainly concerned with treatment of functional autonomy, Grave's disease and iodine-excess-related hyperthyroidism based on either autonomous or Grave's disease. For each of these three main groups of hyperthyroidism exist differentiated surgical concepts based on the underlying thyroid disease and its course: The various forms of functional autonomy, solitary autonomous nodules, multifocal autonomy or disseminated autonomy are dealt with selective enucleation-resection, functionally and morphologically oriented resection and extensive resection with little remaining thyroid tissue of about 5-6 ml, respectively. For Grave's disease extensive resections with thyroid-tissue remainders of about 2-4 ml or tatal thyroidectomy are established; the latter demonstrating in cases of concomittant endocrine ophthalmopathy the most convincing results. In cases of iodine-related hyperthyroidism the concept of early and radical surgical treatment, following stabilization of the patient in a reasonably short amount of time shows best results and is thus favored. In these cases, contrary to all other forms of hyperthyroidism, establishment of preoperative euthyroid metabolism is not mandatory.

Humans↗
PubMed2002

Evaluation of the role of peroxisome-proliferator-activated receptor alpha in the regulation of cardiac pyruvate dehydrogenase kinase 4 protein expression in response to starvation, high-fat feeding and hyperthyroidism.

Inactivation of cardiac pyruvate dehydrogenase complex (PDC) after prolonged starvation and in response to hyperthyroidism is associated with enhanced protein expression of pyruvate dehydrogenase kinase (PDK) isoform 4. The present study examined the potential role of peroxisome-proliferator-activated receptor alpha (PPARalpha) in adaptive modification of cardiac PDK4 protein expression after starvation and in hyperthyroidism. PDK4 protein expression was analysed by immunoblotting in homogenates of hearts from fed or 48 h-starved rats, rats rendered hyperthyroid by subcutaneous injection of tri-iodothyronine and a subgroup of euthyroid rats maintained on a high-fat/low-carbohydrate diet, with or without treatment with the PPARalpha agonist WY14,643. In addition, PDK4 protein expression was analysed in hearts from fed, 24 h-starved or 6 h-refed wild-type or PPARalpha-null mice. PPARalpha activation by WY14,643 in vivo over the timescale of the response to starvation failed to up-regulate cardiac PDK4 protein expression in rats maintained on standard diet (WY14,643, 1.1-fold increase; starvation, 1.8-fold increase) or influence the cardiac PDK4 response to starvation. By contrast, PPARalpha activation by WY14,643 in vivo significantly enhanced cardiac PDK4 protein expression in rats maintained on a high-fat diet, which itself increased cardiac PDK4 protein expression. PPARalpha deficiency did not abolish up-regulation of cardiac PDK4 protein expression in response to starvation (2.9-fold increases in both wild-type and PPARalpha-null mice). Starvation and hyperthyroidism exerted additive effects on cardiac PDK4 protein expression, but PPARalpha activation by WY14,643 did not influence the response of cardiac PDK4 protein expression to hyperthyroidism in either the fed or starved state. Our data support the hypothesis that cardiac PDK4 protein expression is regulated, at least in part, by a fatty acid-dependent, PPARalpha-independent mechanism and strongly implicate a fall in insulin in either initiating or facilitating the response of cardiac PDK4 protein expression to starvation.

Animals↗
PubMed1992

Mechanisms regulating cardiac fuel selection in hyperthyroidism.

Starvation (48 h) decreases fructose 2,6-bisphosphate (Fru-2,6-P2) concentrations and the ratio of free to acylated carnitine in hearts of euthyroid rats. These decreases, which are indicative of increased lipid fuel oxidation, are accompanied by decreased rates of glucose uptake and phosphorylation, assessed by using radioactive 2-deoxyglucose. Cardiac concentrations of acylated carnitines were increased at the expense of free carnitine even in the fed state in response to experimental hyperthyroidism, but neither Fru-2,6-P2 concentrations nor rates of glucose utilization were suppressed. Starvation (48 h) did not further increase the proportion of acylated carnitine in the heart in hyperthyroidism, and suppression of Fru-2,6-P2 concentrations and glucose utilization rates by starvation was attenuated. Although glucose utilization rates were decreased, starvation did not decrease immunoreactive GLUT 4 protein concentrations. Furthermore, although hyperthyroidism was associated with a statistically significant (30-40%) increase in relative abundance of GLUT 4 mRNA, the amount of GLUT 4 protein was not increased by hyperthyroidism in either the fed or the starved state. The results demonstrate a significant effect of hyperthyroidism to enhance cardiac glucose utilization in starvation by a mechanism which does not involve changes in GLUT 4 expression but may be secondary to changes in glucose-lipid interactions at the tissue level.

Animals↗
PubMed1981

Total body potassium in relation to thyroid hormones and hyperthyroidism.

1. Body weight and total body potassium were measured in 23 hyperthyroid patients before and at various stages during treatment and in 19 athyreotic patients who were being treated with high-dose L-thyroxine. 2. In the hyperthyroid patients the total body potassium rose by 23 +/- 2.8% (SEM) within a few weeks of restoring the blood thyroid hormone levels to normal. The body potassium values after treatment were close to that expected in these individuals if they were healthy indicating that a considerable loss of body potassium is usual in hyperthyroidism. 3. The gain of total body potassium in hyperthyroidism averaged 71 +/- 8 mmol for each kg of body weight gained (compared with muscle potassium concentration of about 92 mmol/kg). In contrast, weight loss produced by dietary treatment of obesity caused very little change of body potassium (maximum averaged was 14 +/- 4 mmol/kg wt. loss). 4. Among the patients with hyperthyroidism, the greatest muscular weakness was present in those with the greatest body potassium loss and these patients regained a large amount of potassium relative to weight on recovery. 5. Total body potassium changes were closely related to total plasma tri-iodothyronine concentrations but unrelated to the thyroxine levels.

Adult↗
PubMed1994

Pressure-diuresis-natriuresis response in hyperthyroid and hypothyroid rats.

1. Renal responses to changes in renal perfusion pressure were studied in anaesthetized hyperthyroid (thyroxine, 300 micrograms day-1 kg-1) and hypothyroid (methimazole, 0.03% via drinking water) rats to determine whether an abnormality in the pressure-diuresis-natriuresis phenomenon is involved in the resetting of kidney function in these disorders. 2. There were no significant differences between control and hypothyroid rats with respect to the relationships between renal perfusion pressure and absolute or fractional water and sodium excretion. However, in hyperthyroid rats the pressure-diuresis-natriuresis mechanism was impaired. 3. Renal blood flow and glomerular filtration rate were well autoregulated and there were no differences between control and hypothyroid rats at every level of renal perfusion pressure. A significantly lower glomerular filtration rate was observed in hyperthyroid rats when data were expressed per gram kidney weight, but glomerular filtration rate was similar to that of control rats when normalized by body weight. 4. The shift in the pressure-diuresis-natriuresis response of hyperthyroid rats is mainly due to an increase in tubular reabsorption. Blunting of the renal pressure-diuresis-natriuresis mechanism in hyperthyroid rats may represent the functional resetting of the kidney necessary for sustained hypertension. However, a normal pressure-natriuresis response was observed in hypothyroid rats, in which blood pressure was markedly reduced.

Animals↗
PubMed1998

Elevated numbers of reticulated platelets in hyperthyroidism: direct evidence for an increase of thrombopoiesis.

We studied thrombopoietic activity in hyperthyroidism by determination of reticulated platelet counts. At the time of hyperthyroidism 14/15 patients had higher reticulated platelets than after achievement of euthyroidism (P<0.001). There was no difference in peripheral platelet counts and mean platelet volumes at the time of hyperthyroidism when compared to euthyroidism. Three patients had pan- and auto-reactive platelet antibodies during hyperthyroidism. These antibodies were directed against GPIIb/IIIa in two patients and against GPIb/IX in one patient. Our findings provide direct evidence that hyperthyroidism is associated with increased platelet production, as reflected by an increase in reticulated platelets.

Adult↗
PubMed2001

Weight gain following treatment of hyperthyroidism.

OBJECTIVE: Patients frequently express concern that treating hyperthyroidism will lead to excessive weight gain. This study aimed to determine the extent of, and risk factors for, weight gain in an unselected group of hyperthyroid patients. DESIGN AND SUBJECTS: We investigated 162 consecutive hyperthyroid patients followed for at least 6 months. Height, weight, clinical features, biochemistry and management were recorded at each clinic visit. RESULTS: Documented weight gain was 5.42 +/- 0.46 kg (mean +/- SE) and increase in BMI was 8.49 +/- 0.71%, over a mean 24.2 +/- 1.6 months. Pre-existing obesity, Graves' disease causing hyperthyroidism, weight loss before presentation and length of follow-up each independently predicted weight gain. Patients treated with thionamides or radioiodine gained a similar amount of weight (thionamides, n = 87, 5.16 +/- 0.63 kg vs. radioiodine, n = 62, 4.75 +/- 0.57 kg, P = 0.645), but patients who underwent thyroidectomy (n = 13) gained more weight (10.27 +/- 2.56 kg vs. others, P = 0.007). Development of hypothyroidism (even transiently) was associated with weight gain (never hypothyroid, n = 102, 4.57 +/- 0.52 kg, transiently hypothyroid, n = 29, 5.37 +/- 0.85 kg, on T4, n = 31, 8.06 +/- 1.42 kg, P = 0.014). This difference remained after correcting for length of follow-up. In the whole cohort, weight increased by 3.95 +/- 0.40 kg at 1 year (n = 144) to 9.91 +/- 1.62 kg after 4 years (n = 27) (P = 0.008), representing a mean weight gain of 3.66 +/- 0.44 kg/year. CONCLUSION: We have demonstrated marked weight gain after treatment of hyperthyroidism. Pre-existing obesity, a diagnosis of Graves' disease and prior weight loss independently predicted weight gain and weight continued to rise with time. Patients who became hypothyroid, despite T4 replacement, gained most weight.

Adolescent↗
PubMed2006

Hyperthyroidism and the kidney.

Hyperthyroidism and chronic renal failure (CRF) are both common diseases of older cats. Hyperthyroidism increases GFR by a variety of physiologic effects. Chronic renal failure can suppress total T4 concentrations in cats with concurrent hyperthyroidism, and free T4 is not a useful distinguishing test. Medical therapy (ie, methimazole) is recommended in cats with pre-existing CRF. Overt renal failure occurs in approximately 30% of cats treated for hyperthyroidism. It usually occurs within one month of treatment and tends to remain mild and stable over time. There is no practical way to predict which cats will develop CRF after treatment of hyperthyroidism, although GFR measurement does seem useful.

Animals↗
PubMed2002

Hyperthyroidism and pulmonary hypertension.

In recent years, many authors have described several cases revealing an association between hyperthyroidism and pulmonary hypertension (PH). This observational study was designed to evaluate the incidence of PH in hyperthyroidism and was set in a department of internal medicine and pulmonary diseases with an out-patients department of endocrinology. Thirty-four patients, 25 women and nine men, with a mean age of 38 +/- 15 SD years participated. Twenty had Graves' disease and 14 had a nodular goitre. The patients were divided into two equally matched groups: those with a recently diagnosed hyperthyroidism, taking no drugs (group 1; n = 17) and those in a euthyroid state taking methimazole (group 2; n= 17). Transthoracic Doppler echocardiography was performed and systolic pulmonary artery pressurements of (PAPs) was determined by the tricuspid regurgitation method using the Bernoulli equation. Measurements of triiodothyronine, tetraiodothyronine, free thyroxine (Ft4), thyroid-stimulating hormone (TSH) and antithyroglobulin and antimicrosomal antibodies were also taken. We found a mild PH in seven patients of group 1 and in none of group 2. The mean +/- SD systolic pulmonaryartery pressurewas 28.88 +/- 6.41 in group 1 and 22.53 +/- 1.84 ingroup 2 (P<0.0001). A correlation was found between the TSH value and PAPs (r = -082;P < 0.001) and Ft4 and PAPs (r = 0 85; P < 0.001) in group 1. These findings indicate the presence of a frequent association between PH and hyperthyroidism. We suggest that hyperthyroidism be included in the differential diagnosis of PH.

Adult↗
PubMed1975

Experimental hyperthyroidism in dogs. Evaluation and effects on blood sugar, serum insulin and free fatty acids during glibenclamide infusion test.

The effects of hyperthyroidism on the BS, serum IRI and FFA responses to HB 419 were studied. Hyperthyroidism, induced by l-thyroxine administration, caused an increase in body temperature, respiratory rate, BS, serum FFA and PBI basal levels. Fasting serum cholesterol was reduced, and body weight, basal metabolic and heart rates, as well as basal serum insulin level failed to be affected. The hypoglycaemic response to HB 419 was moderately facilitated by hyperthyroidism, despite of inducing an impairment in the insulin secretory response. Serum FFA profile, similarly shaped in hyperthyroid dogs and in euthyroid controls, was shifted upwards by hyperthyroid condition. Results are discussed.

Animals↗
PubMed1978

Urinary cyclic AMP in hyperthyroidism.

Urinary cyclic AMP was studied in 22 female and in 6 male hyperthyroid normocalcemic patients and in 3 hyperthyroid hypercalcemic men. Cyclic AMP/creatinine ratios were elevated both in female (4.12 +/- 0.26 mumoles/gm creatinine) and male (3.92 +/- 0.41 mumoles/gm creatinine) hyperthyroid normocalcemic patients as compared with normal female and male controls (2.85 +/- 0.20 and 2.54 +/- 0.14 mumoles/gm creatinine, respectively). However, there was no difference in the 24-hour urinary cyclic AMP excretion of both hyperthyroid and normal subjects. The hyperthyroid hypercalcemic men excreted less (2.47 +/- 0.19) mumoles/24 hr) cyclic AMP/24 hr than the normal male controls. In the thirteen female patients, studied when euthyroid, the cyclic AMP/creatinine ratio was normalised.

Adult↗
PubMed1989

Effect of acute hyperthyroidism on insulin removal in the rats.

The aim of this work was to study secretion and removal of insulin in hyperthyroidism. The experiments were carried out on two groups of male Wistar rats: control and hyperthyroid. Acute hyperthyyreosis was induced by administration of L-thyroxine (Fluka A.G.) 0.8 mg/kg for 21 days. Each group was divided into three subgroups: fed, fasted 24 h, fasted 24 h-treated with glucose. The insulin concentration was determined in the portal and aortal blood and a difference between the two concentrations was considered as reflecting insulin removal. The plasma insulin concentrations in both vessels of fed as well fasted hyperthyroid group were higher from the respective values in the control one. The removal of the hormone in the fed rats was similar in the both groups. Fasting reduced insulin removal only in the control group. Treatment of the fasted rats with glucose abolishes this difference. The liver glycogen content was similar in the two fasted groups but the blood glucose level was higher in the hyperthyroid than in the control rats. The latter factor could account for the difference in insulin removal between the two groups. It is concluded that hyperthyroidism increases insulin secretion but does not affect its removal.

Animals↗
PubMed1996

Constitutively activating TSH receptor mutations as the cause of toxic thyroid adenoma, multinodular toxic goiter and autosomal dominant non autoimmune hyperthyroidism.

cAMP stimulates both the growth and differentiated thyroid function of the thyroid gland. In toxic nodules the clinical observation of hyperthyroidism together with TSH independent growth of the hot nodule suggests a chronic activation of the cAMP cascade. Somatic mutations in a gene of the cAMP regulatory cascade leading to constitutive activation of this cascade in toxic nodules were first detected in the G protein Gs alpha. Thereafter constitutively activating TSH receptor mutations were identified in 20-80% of toxic thyroid nodules and in 3 of 6 toxic multinodular goiters. Constitutively activating TSH receptor germline mutations are expected to lead to toxic hyperplasia. Sequencing of the TSH receptor gene in families with hereditary non autoimmune hyperthyroidism led to the identification of constitutively activating TSH receptor mutations in 7 families. Moreover, sporadic TSH receptor germline mutations have been identified in 3 children with severe congenital nonautoimmune hyperthyroidism. Therefore, in cases of clustering of non autoimmune hyperthyroidism in families and in cases of sporadic congenital hyperthyroidism with thyroid hyperplasia and no evidence for an autoimmune etiology a search for TSH receptor gene mutations is necessary to appropriately direct the therapy of these patients.

Adenoma↗
PubMed1999

Evaluation of procollagen III peptide as a marker of tissue hyperthyroidism in long-term treated women with TSH suppressive doses of thyroxine.

Increased serum concentrations of the aminoterminal propeptide of collagen III (PIIINP) are found in overt hyperthyroidism. Thus, measurement of serum PIIINP might be useful as an early marker of tissue hyperthyroidism in patients with TSH suppressive thyroxine treatment. In a prospective study we evaluated female patients followed in the thyroid outpatient clinic. Serum PIIINP concentrations were analysed in three groups: patients with TSH suppressive thyroxine treatment for more than 6 months (n = 33, TSH < 0.1 mU/l), patients with thyroxine substitution for hypothyroidism for more than 6 months (n = 20, TSH 0.2-4.0 mU/l) and spontaneous hyperthyroid patients (n = 8, TSH < 0.03 mU/l, increased freeT4 and/or T3). Beside TSH, thyroid hormones and serum PIIINP we measured serum SHBG and a clinical score. Hyperthyroid patients had clearly elevated serum PIIINP and SHBG values and a higher clinical score when compared with other study groups (p < 0.001). Patients with TSH suppressive thyroxine treatment had higher fT4 and T3 concentrations than the thyroxine substitution group (fT4 22 +/- 4.8 pmol/l vs. 17 +/- 2.6 pmol/l, T3 2.2 +/- 0.4 nmol/l vs. 1.8 +/- 0.3 nmol/l, p < 0.001) and also elevated serum SHBG values (77.6 +/- 27.5 nmol/l vs. 58.4 +/- 18 nmol/l, p < 0.01). However, serum PIIINP concentrations and the clinical score were very similar in both thyroxine treated groups (PIIINP in TSH suppression group 3.0 +/- 0.67 microg/l vs. 2.8 +/- 0.65 microg/l in the substitution group, clinical score 2 +/- 1.8 pts. vs. 1.7 +/- 1.5 pts. p = n.s.). In conclusion, serum PIIINP is not a reliable early marker for detection of tissue hyperthyroidism in long-term thyroxine treated women with suppressed TSH.

Adult↗