Untreated Hyperthyroidism Research Articles

Hunger–Satiety Signals in Patients with Graves' Thyrotoxicosis Before, During, and After Long-Term Pharmacological Treatment

Patients with Graves' thyrotoxicosis lose weight despite increased appetite and food intake, thus suggesting a disturbed balance between energy intake and expenditure. Underlying mechanisms are not fully elucidated. The objective of this study was to investigate whether hormonal factors, known to affect hunger/satiety, change significantly over time as pharmacological treatment turns hyperthyroidism into euthyroidism. For that purpose 11 patients with Graves' thyrotoxicosis were given thiamazole and l-thyroxine for 18-20 mo. They were investigated on three occasions: Test 1: before pharmacological therapy; Test 2: during medication; Test 3: a few months after conclusion of the pharmacological treatment. Sixteen healthy subjects were also investigated for comparison. The participants were fasted overnight. Blood samples for determination of plasma glucose and serum concentrations of free T3 and T4, TSH, albumin, cortisol, insulin, GH, IGF-1, IGFBP-1, leptin, and ghrelin were drawn in the morning from an antecubital vein. Laboratory data obtained in test 1 were statistically compared with those in tests 2 and 3. The study showed that the free T3 level declined from 42.8 +/- 4.3 pmol/L in test 1 to 6.0 +/- 0.8 pmol/L in test 2 (85 +/- 2% decline), and 5.5 +/- 0.3 pmol/L in test 3 (86 +/- 2% decline). The free T4 level fell concomitantly from 65.2 +/- 4.8 to 16.6 +/- 1.7 and 14.4 +/- 1.2 pmol/L. The glucose level was significantly higher during hyperthyroidism (test 1) than during euthyroidism (tests 2 and 3), whereas cortisol, insulin, GH, IGF-1, and leptin levels were similar. The IGFBP-1 level was initially high (48.8 +/- 8.5 microg/L in test 1), but with a relative decline in free T3 of 85 +/- 2% (test 2) the IGFBP-1 level declined by 34 +/- 13%, and with a free T3 decline of 86 +/- 2% (test 3) the binding protein fell by 39 +/- 29%. This brought about increased IGF-1 bioavailability as reflected by a rising IGF-1/IGFBP-1 ratio from 5.1 +/- 1.1 to 13.8 +/- 2.9 (p < 0.01). The ghrelin level was low (2454 +/- 304 ng/L) in test 1. It increased to 3127 +/- 397 ng/L in test 2 (p < 0.05), and to 3348 +/- 279 ng/L in test 3 (p < 0.01). Both ghrelin secretion and IGF-1 bioavailability are low in patients with untreated thyrotoxicosis, but increase markedly as pharmacotherapy makes them euthyroid. These metabolic changes may be caused by the transition of hyperthyroidism into euthyroidism rather than by the pharmacotherapy per se, since the metabolic changes prevailed also in the posttreatment period.

Bone mineral density in hyperthyroidism.

To investigate whether previous hyperthyroidism is a cause of permanent secondary osteoporosis. In this cross-sectional study, 164 women with untreated or previously treated overt and symptomatic hyperthyroidism were examined 0-31 years after the initial episode of hyperthyroidism and its treatment, and were compared with a control group of 79 age-matched women without previous history of hyperthyroidism. Subjects with current or previous metabolic bone disease, any antiresorptive treatment for osteoporosis or treatments and habits known to affect bone metabolism were excluded. The age of the first manifestation of the disease, the age at the measurement of bone mineral density (BMD) at the spine and femoral neck and the interval between diagnosis and treatment of hyperthyroidism and BMD measurement were recorded and the Z-scores and T-scores of BMD were analysed. Untreated hyperthyroidism and hyperthyroidism up to 3 years after its diagnosis and treatment were associated with decreased BMD. Three or more years after the first episode of the disease the mean Z-score at both skeletal sites was near zero and not different from the controls. The age at which hyperthyroidism was manifested for the first time had no effect on the final outcome. Women affected at a young age (13-30 years) had a more pronounced loss of BMD when examined untreated or early (< 3 years) after diagnosis, but a BMD significantly above zero if examined later (> 3 years). Older women (aged 51-70 years) showed a similar pattern, although the differences were not significant. Middle-aged subjects (31-50 years) had the smallest loss of BMD during the first 3 years. Analysis of T-scores of former hyperthyroid women aged > or = 51 years showed no significantly different relative risk (RR) for osteoporosis in comparison with the controls. However, the study was not powered enough to give meaningful RR results. Overt symptomatic hyperthyroidism is associated with decreased BMD during the first 3 years after diagnosis and treatment of the disease. After this interval, former hyperthyroid women have a Z-score near zero and not different from women without a history of the disease, apparently because of recovery of the bone density lost early during the course of the disease. Symptomatic hyperthyroidism does not seem to be a cause of long-lasting osteoporosis, and the age of the patient during the first episode is irrelevant.

Hyperthyroidism, bone mineral, and fracture risk--a meta-analysis.

This study examined changes in bone mineral and fracture risk after treatment for hyperthyroidism in a meta-analysis. The PubMed and EMBASE were searched using the MESH terms "hyperthyroidism," "bone mineral density" (BMD), and "fracture," resulting in retrieval of 289 references. Twenty references describing BMD and five describing fracture risk were included in the meta-analysis. BMD was significantly decreased in patients with untreated hyperthyroidism. Upon treatment BMD increased significantly and reversed to normal levels with a temporary increase above normal levels 1-4 years after diagnosis. The risk of hip fractures increased significantly with age at diagnosis of hyperthyroidism. The hip fracture risk after diagnosis predicted from studies on BMD was close to that observed in clinical studies comparing fracture risk in hyperthyroid patients with normal controls. Thus BMD is significantly decreased and fracture risk increased in untreated hyperthyroidism. Upon normalization of the hyperthyroid state BMD return to normal even though no specific antiosteoporotic measures are taken other than normalizing the hyperthyroid state.

Depression and Anxiety in Hyperthyroidism

Background Our objective was to determine symptomatology of depression and anxiety in patients with untreated hyperthyroidism and compare with euthyroid patients. Methods Thirty-two patients with hyperthyroidism (high free T3 and free T4, and suppressed TSH) and 30 euthyroid (normal free T3, free T4, and TSH) controls attending the Endocrinology Out-Patient Department at Celal Bayar University Hospital in Manisa, Turkey were included in the study. Hormonal screening was performed by immunoassay and hemagglutination method. For psychiatric assessment, Hospital Anxiety and Depression Scale [HAD], Hamilton Depression Rating Scale [HAM-D], and Hamilton Anxiety Rating Scale [HAM-A] were used. There was no difference between the two groups in terms of demographic features. Results Total scores obtained both from HAM-D and HAM-A were significantly greater in the hyperthyroidism group than that of the euthyroid group ( p <0.05); there was no difference in terms of HAD. When compared in terms of symptomatology, early insomnia (HAM-D#6), work and activities (HAM-D#7), psychic anxiety (HAM-D#10), weight loss (HAM-D#16), insomnia (HAM-A#4), and cardiovascular symptoms (HAM-A#8) were significantly more frequent in the hyperthyroidism group. By Wilks lambda discriminant analysis, psychomotor agitation (HAM-D#9), weight loss (HAM-D#16), and insomnia (HAM-A#4) were found as the discriminating symptoms for the hyperthyroidism group, whereas somatic anxiety (HAM-A#11) and loss of interest (HAD#14) were distinguishing symptoms of the euthyroidism group. Conclusions Hyperthyroidism and syndromal depression–anxiety have overlapping features that can cause misdiagnosis during acute phase. For differential diagnosis, one should follow-up patients with hyperthyroidism with specific hormonal treatment and evaluate persisting symptoms thereafter. In addition to specific symptoms of hyperthyroidism, psychomotor retardation, guilt, muscle pain, energy loss, and fatigue seem to appear more frequently in patients with comorbid depression and hyperthyroidism; thus, presence of these symptoms should be a warning sign to nonpsychiatric professionals for the need for psychiatric consultation.

The effects of thyrotoxicosis and its treatment on central arterial stiffness.

To assess central arterial stiffness in thyrotoxicosis using the technique of pulse wave analysis. Case control study designed to determine the effect of thyrotoxicosis on central arterial stiffness and at 6 months after radioiodine treatment. Twenty (18 women and 2 men) thyrotoxic patients and 20 age- and sex-matched controls were studied at baseline. Thyrotoxic patients were re-studied at 6 months following treatment of thyrotoxicosis with 555 MBq (131)I with no additional therapy for the six-month period. Using the sphygmocor apparatus, peripheral pressure waveforms were recorded non-invasively from the radial artery and central pressure waveforms were generated from these. Indices of arterial stiffness, central augmentation index (AI), augmentation of central arterial pressure (AG) and central blood pressures were derived. AI corrected for heart rate (AIc) was calculated. Thyrotoxic patients recorded a significantly lower AI (means+/-s.e.m.) compared with controls (15.0+/-2.1 vs 28.0+/-2.1%; P<0.0005) even when corrected for differences in heart rate AIc (20.0+/-2.1 vs 28.0+/-2.1%; P<0.005) as well as AG (6.0+/-0.8 vs 10.0+/-1.1 mmHg; P<0.002) but higher pulse pressure (58.0+/-3.5 vs 47.0+/-2.0 mmHg; P<0.02). At 6 months following treatment, a significant rise in AIc (27.0+/-1.8 vs 20.0+/-2.1%; P<0.005) and AG (11.0+/-1.0 vs 6.0+/-0.8 mmHg; P<0.005) was noted. Lipid profiles were comparable between the groups. These data suggested that subjects with untreated thyrotoxicosis have a decreased augmentation of central arterial pressure or lowered central arterial stiffness that would not appear to contribute to any excess cardiovascular risk in that condition.

Osteopenia and Osteoporosis in Two Children with Graves’ Disease

Osteopenia and Osteoporosis in Two Children with Graves’ Disease

The prevalence and clinical significance of blocking thyrotropin receptor antibodies in untreated hyperthyroid Graves' disease.

The goal of this study was to evaluate the clinical significance of the blocking thyrotropin receptor antibodies (TSHRAb) in Graves' disease. The amount of blocking and stimulating TSHRAb were measured in 200 patients with untreated hyperthyroid Graves' disease using several cell lines carrying different TSHR chimera. Stimulating TSHRAb were measured in Chinese hamster ovary (CHO) cells with wild-type human TSHR (CHO-hTSHR) or a TSHR chimera with residues 90-165 (Mc2) or 8-165 (Mc1+2) substituted by equivalent residues of rat luteinizing hormone/chorionic gonadotrophin (LH/CG) receptor or in FRTL-5 cells. Blocking TSHRAb were measured in Mc2 cells. The activities of different TSHRAb were assessed and clinical features were compared to patients who were positive or negative for blocking TSHRAb antibodies. Blocking TSHRAbs were detected in 18.5% of patients (37/200) with hyperthyroid Graves' disease. Patients with blocking antibodies had significantly lower mean stimulating TSHRAb activities than those without blocking antibodies in wild-type CHO-hTSHR cells (301 +/- 179 vs. 446% +/- 537%, p = 0.005). Mean stimulating TSHRAb activities measured by FRTL-5, Mc1+2, or Mc2 cells and mean thyrotropin receptor inhibitor immunoglobulin (TBII) activities were not different between the two groups. The patients with blocking antibodies were not different from those without blocking antibodies in age, gender ratio, initial serum free thyroxine (T4) levels, or goiter size. However, the prevalence of exophthalmos was higher (35.1% vs. 17.5%, p = 0.024) in the patients with blocking antibodies than those without. In summary, the presence of blocking TSHRAb is not rare in patients with hyperthyroid Graves' disease when measured with chimeric receptor expressing cells. Blocking TSHRAb in Graves' sera do not strongly antagonize the action of stimulating TSHRAb in vivo, but could be a major factor responsible for underestimation of stimulating TSHRAb activities measured by CHO-hTSHR. The association of blocking TSHRAb with ophthalmopathy suggests that the TSHRAb repertoire of Graves' patients is different in those who do and who do not have ophthalmopathy.

Causes of anorexia in untreated hyperthyroidism: a prospective study

Seventeen consecutive patients (mean (SD) 46 (11) years) with untreated hyperthyroidism and anorexia and 29 patients (35 (9) years) with untreated hyperthyroidism without anorexia were studied. The study was conducted...

Serum Levels of Adhesion Molecules in Children and Adolescents with Immune and Non-immune Thyroid Diseases

Serum levels of sICAM-1, sVCAM-1 and sP-selectin were determined in patients with Graves' disease before and after 8 weeks and 24 months of methimazole therapy, in levothyroxine suppressed patients with non-toxic nodular goiter, and in a group of healthy controls, to elucidate the relationship to circulating antithyroid antibodies and possible role of soluble adhesion molecules as markers of inflammatory activity. sICAM-1, sVCAM-1, and sP-selectin in patients with untreated hyperthyroidism were markedly elevated compared with controls. After 8 weeks of methimazole treatment, the concentrations of these molecules dropped, but were still significantly higher than in healthy children. In patients with clinical and biochemical remission after 24 months of therapy, sICAM-1 values were on the verge of significance, but still higher than in the control group, whereas serum levels of sVCAM-1 and sP-selectin had normalized. Slightly higher serum sICAM-1 values were observed in patients with non-toxic nodular goiter compared with healthy children.

Grey scale thyroid ultrasonography in the evaluation of patients with Graves' disease.

Graves’ disease is a genetically induced autoimmune disorder characterized by hyperthyroidism due to circulating thyroid stimulating hormone (TSH) receptor autoantibodies (TRAb) with thyroid stimulating activity (1). Graves’ disease is the most common cause of hyperthyroidism, which has an estimated prevalence in iodine sufficient areas of 20/1000 females and 2.3/ 1000 males (2). It is most common in females between the ages of 20 and 50 years, but it may occur at any age. The laboratory diagnosis of Graves’ disease is based on the finding of high serum thyroid hormone and undetectable serum TSH concentrations associated with circulating thyroglobulin and thyroperoxidase antibodies. TRAb is detectable in almost 90% of patients, but usually it is not needed for the diagnosis. Radioisotope scan of the thyroid shows a diffuse and homogeneous radionuclide uptake. Treatment strategies for Graves’ hyperthyroidism include medical therapy with antithyroid drugs (ATD) or thyroid ablation with 131 I or surgery. ATD, mainly thionamides, inhibit thyroid hormone synthesis by blocking iodine organification catalysed by thyroid peroxidase. Treatment of Graves’ disease with thionamides is mainly performed in Europe and in Japan, while in the USA and Canada radioiodine is commonly preferred as the first choice treatment (3). Many studies have been undertaken to find parameters which help predict the clinical outcome of Graves’ hyperthyroidism after ATD withdrawal. Among them, TRAb measurement at the end of an ATD course was found to be the most predictive (4, 5). After its introduction into clinical practice in the late sixties, thyroid ultrasonography (US) proved to be very effective in the diagnostic approach to thyroid diseases, the anatomical location of the gland being advantageous for this technique. The most widely used application of thyroid US is identification and characterization of thyroid nodules (6). Rapid improvements in the development of US equipment have made available real-time high frequency transducers (7.5‐ 10 MHz) with high resolution, which allow a more precise definition of the echostructure of the thyroid tissue. In addition, recently developed color Doppler technology allows determination of the blood flow through the gland, offering the possibility of recording objective measurements, such as the peak systolic velocity of the blood flow at the level of thyroid arterial vessels (i.e. inferior thyroid artery). Using these techniques, thyroid blood flow has been shown to be correlated with the thyroid status in patients with Graves’ disease, being markedly increased in 17/18 patients with untreated active hyperthyroidism and less clearly increased in treated patients. In patients with Hashimoto’s thyroiditis, the thyroid blood flow was not correlated to thyroid status or treatment and was never markedly increased (7). Color Doppler sonography was also shown to be useful in distinguishing cases of destructive thyrotoxicosis by amiodarone (i.e. amiodarone thyrotoxicosis type 2), characterized by a low thyroid blood flow, from cases in which thyroid hyperfunction also occurs (i.e. amiodarone thyrotoxicosis type 1), characterized by an increased thyroid

Stress echocardiography in hyperthyroidism.

Exertion symptoms occur frequently in subjects with hyperthyroidism. Using stress echocardiography, exercise capacity and global left ventricular function can be assessed noninvasively. To evaluate stress-induced changes in cardiovascular function, 42 patients with untreated thyrotoxicosis were examined using exercise echocardiography. Studies were performed during hyperthyroidism, after treatment with propranolol, and after restoration of euthyroidism. Twenty-two healthy subjects served as controls. Ergometry was performed with patients in a semisupine position using a continuous ramp protocol starting at 20 watts/min. In contrast to control and euthyroidism, the change in end-systolic volume index from rest to maximal exercise was lower in hyperthyroidism. At rest, the stroke volume index, ejection fraction, and cardiac index were significantly increased in hyperthyroidism, but exhibited a blunted response to exercise, which normalized after restoration of euthyroidism. Propranolol treatment also led to a significant increase of delta (delta) stroke volume index. Maximal work load and delta heart rate were markedly lower in hyper- vs. euthyroidism. Compared to the control value, systemic vascular resistance was lowered by 36% in hyperthyroidism at rest, but no further decline was noted at maximal exercise. The delta stroke volume index, delta ejection fraction, delta heart rate, and maximal work load were significantly reduced in severe hyperthyroidism. Negative correlations between free T3 and diastolic blood pressure, maximal work load, delta heart rate, and delta ejection fraction were noted. Thus, in hyperthyroidism, stress echocardiography revealed impaired chronotropic, contractile, and vasodilatatory cardiovascular reserves, which were reversible when euthyroidism was restored.

Myocardial damage does not occur in untreated hyperthyroidism unless associated with congestive heart failure

Even in the absence of underlying cardiac disease, hyperthyroidism has seldom been reported to be associated with left ventricular dysfunction and congestive heart failure. The left ventricular function invariably improves with achievement of euthyroid status. Anecdotal autopsy reports have suggested that myocardial necrosis associated with hyperthyroidism may be responsible for congestive heart failure. This study prospectively evaluates the role of myocardial necrosis in untreated hyperthyroidism by imaging with Indium-111 antimyosin antibody. Thirteen consecutive patients (7 men and 6 women, mean age 36 ± 11 years) with hyperthyroidism and Graves' disease (10 patients), subacute thyroiditis (2 patients), or multinodular goiter (1 patient) formed the basis of the study. The T4 levels ranged from 33 to 183 pmol/L (mean 103 ± 47 pmol/L) and cardiac output from 5.47 to 11.0 L/min (mean 7.17 ± 1.75 L/min). Two patients had clinical congestive heart failure and mildly depressed left ventricular ejection fraction. Both patients had scintigraphic evidence of myocardial damage with abnormal antimyosin scans. In the remaining 11 patients with normal left ventricular ejection fraction, no antimyosin uptake was observed. The reevaluation of two patients with abnormal initial scans 6 to 8 months after treatment revealed euthyroid status, resolution of antimyosin uptake, and normalization of left ventricular function. This study indicates that myocardial necrosis may be detected in a small proportion of patients with hyperthyroidism, which could contribute to left ventricular systolic dysfunction. (Am Heart J 1997;134:1133-7.)

Circulating telopeptide type I is a peripheral marker of thyroid hormone action in hyperthyroidism and during levothyroxine suppressive therapy.

The aim of the present investigation was to evaluate the clinical performance of serum carboxy-terminal-1-telopeptide (ICTP), a new marker of bone resorption, in identifying peripheral overexposure to thyroid hormones, as compared with serum osteocalcin (OC) and serum sex hormone binding globulin (SHBG). Serum ICTP, SHBG, and OC were assayed by specific radioassays in three study groups. Group 1: 50 perimenopausal women on long-term levothyroxine (LT4) suppressive treatment; group 2: 29 women with untreated hyperthyroidism; group 3: 36 normal euthyroid women matched with group 1 patients for age, alcohol, smoking habits, and lifestyle. Serum concentrations of SHBG, ICTP, and OC were markedly increased in hyperthyroid patients, whereas only serum ICTP was slightly but significantly increased in LT4 treated patients. Serum ICTP had higher diagnostic value for hyperthyroidism when compared with SHBG and to OC (sensitivity: 100%, 71%, 55%; accuracy: 97%, 88%, and 76%, respectively). In group 1, increased serum ICTP was observed in 30 of 50 patients, whereas increased SHBG and OC were found only in 11 of 50 (p < .001). Serum free thyroid hormone concentrations correlated with circulating ICTP and SHBG, and the correlation with serum OC was of lower significance. In conclusion, serum ICTP is a sensitive and reliable marker of peripheral thyroid hormone activity at the bone level; its clinical performance is higher than OC and even better than SHBG. Thus, serum ICTP is better than other peripheral markers in monitoring LT4 suppressive therapy in patients at increased risk for osteoporosis such as perimenopausal women.

Bioelectrical impedance assessment of body composition in thyroid disease.

To assess the metabolic effects of thyroid disease, body composition was determined by bioimpedance analysis (BIA) in 72 patients with untreated hyperthyroidism (mean age 48.7 +/- 1.9 years) and 26 patients with untreated hypothyroidism (63.8 +/- 3.4 years). Bioelectrical whole body resistance (R) and reactance (Xc) were used for computerized calculation of lean body mass (LBM), body cell mass (BCM), extracellular mass (ECM) and body fat (BF). Compared with age- and sex-matched healthy controls the most sensitive parameter indicating excess thyroid hormone was the ECM/BCM ratio which was markedly elevated in all hyperthyroid subjects. ECM/BCM alteration resulted from marked depletion of BCM with concomitant expansion of ECM. BCM change is thought to be predominantly due to a loss of muscle mass while ECM rise may reflect an increase in extracellular fluids. In contrast, hypothyroidism was characterized by an increase in BF besides a relatively unaffected LBM component. Serum parameters of thyroid function (tri-iodothyronine (T3), free thyroxine, TSH) did not correlate with the determinants of body composition except for a slight inverse relationship between the phase angle (Xc/Rx180 degrees/pi) and T3 concentration in Graves' disease patients. We conclude that hyperthyroidism is primarily accompanied by quantitative as well as qualitative changes in the lean body while considerable fat increase is the most important feature of hypothyroidism. Severity of body composition derangement cannot be predicted from the degree of thyroid dysfunction. BIA could become a useful tool which allows objective determination of even subtle metabolic manifestations of thyroid disease and should, therefore, complement conventional clinical and biochemical assessment.

Effects of thyroid status on pituitary gonadotropin and testicular reserve in men.

This investigation was conducted to evaluate the effect of thyroid dysfunction on the pituitary-gonadal axis. Ten men with Graves' disease and 5 hypothyroid patients were studied; 10 normal males were studied as a control group. In untreated conditions hyperthyroidism was associated with a normal serum-free testosterone concentration, an increased serum of 17OHP levels, a reduced testosterone response to hCG stimulation, and a hyperresponse of LH to GnRH. These abnormalities reverted after normalization of high FT4 serum levels. Untreated hypothyroid men showed a normal hormone sex response to hCG, but the LH responst to GnRH was reduced, with a tendency to improve after T4 supplementation. There was a strong and significant negative correlation between FT4 and testosterone response, expressed as an area under the curve, and a positive correlation with LH response to GnRH. Despite normal basal free testosterone concentrations, 70% of hyperthyroid and 60% of hypothyroid patients had complaints of decreased libido. The results suggest that thyroid hormones play an important dual pituitary-gonadal effect that is reflected by an impairment of testicular testosterone synthesis associated to hyperresponse to LH in hyperthyroidism and a defective LH response to GnRH in hypothyroidism.

Study of calcium homeostasis in feline hyperthyroidism.

Thirty cats with untreated hyperthyroidism were blood sampled and their calcium homeostatic mechanisms and renal function assessed. The results were compared with those obtained from 38 age-matched control cats. The hyperthyroid group of cats were found to have significantly lower blood ionised calcium and plasma creatinine concentrations and significantly higher plasma phosphate and parathyroid hormone concentrations. Hyperparathyroidism occurred in 77 per cent of hyperthyroid cats, with parathyroid hormone concentrations reaching up to 19 times the upper limit of the normal range. The aetiology, significance and reversibility of hyperparathyroidism in feline hyperthyroidism remains to be established but could have important implications for both bone strength and renal function.

Hyperthyroidism During Pregnancy: Nursing Care Issues

Untreated hyperthyroidism during pregnancy is associated with a high incidence of maternal and fetal complications. The perinatal nurse needs knowledge of the pathophysiology of this condition to implement a care plan. Antithyroid medications are used to restore the patient's normal thyroid function. Ongoing evaluation of clinical and laboratory data assists the nurse in recognizing the development and implementation of interventions for complications, such as thyroid crisis and heart failure, in the pregnant patient.

Bone mass, bone turnover, calcium homeostasis, and body composition in surgically and radioiodine-treated former hyperthyroid patients.

Untreated hyperthyroidism is characterized by increased bone turnover with loss of bone and bone mineral. The aim of the present investigation was to evaluate the reversibility of these changes by measuring bone mass, bone turnover, and calcium homeostasis in surgically treated former hyperthyroid patients who had been euthyroid for at least 6 years. Sixty euthyroid former hyperthyroid patients and 94 normal sex- and age-matched controls participated. Heights and body weights and composition were similar in the two groups. In the thyroxine substituted patients (n = 27) both serum T4 and serum free T4-index (S-FT4I) were increased (p < 0.001) compared to the normal controls as well as the nonsubstituted patients. In the nonsubstituted patients. In the nonsubstituted patients (n = 33), serum TSH was increased (p < 0.001) compared to the normal controls. No significant differences were observed between substituted and nonsubstituted patients and normal controls with respect to serum T3, serum free T3-index (S-FT3I), or regional or total bone mineral content (BMC) and density (BMD) values. Serum levels of calcium, phosphate, magnesium, intact PTH, and renal excretion of calcium were unchanged. However, serum levels of 1,25-dihydroxy- and 25-hydroxyvitamin D were reduced. Urinary excretion of hydroxyproline was increased by 16% (p < 0.05), but serum cross-linked carboxy-terminal teleopeptide of type I collagen (ICTP) was decreased by 11% (p < 0.01). Urinary excretion of collagen cross-links was normal. Serum levels of osteocalcin, carboxy-terminal propeptide of human type I procollagen (PICP), and total and bone alkaline phosphatase were all normal. In conclusion, surgically treated former hyperthyroid patients have normal bone mass, bone turnover, and calcium homeostasis in spite of minor variations in thyroid hormones and vitamin D metabolites.

Refractory atrial fibrillation in an emergency surgical patient: a sign of untreated thyrotoxicosis.

Refractory atrial fibrillation in an emergency surgical patient: a sign of untreated thyrotoxicosis.

Refractory atrial fibrillation in an emergency surgical patient: a sign of untreated thyrotoxicosis

Refractory atrial fibrillation in an emergency surgical patient: a sign of untreated thyrotoxicosis