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At least 343 records · Page 19Linked to original sources
PubMed1988

Studies of thyroid function and immune parameters in patients with hyperthyroid Graves' disease in remission.

The natural course of hyperthyroidism due to Graves' disease after discontinuation of antithyroid drug therapy was studied in 184 patients who had been treated with methimazole and whose thyroid function was suppressible with T3 when methimazole was discontinued. The patients were followed after discontinuation of therapy for up to 60 months. Serum T4, free T4 (FT4) and T3 levels, TSH receptor antibody (TRab) and anti-DNA antibody titers, and the percentage of HLA-DR positive lymphocytes in peripheral blood were measured serially. TRab and anti-DNA antibody tests were positive in the majority of patients before treatment and were negative in most at the end of treatment. Twenty-three (12.5%) patients had a recurrence of their hyperthyroidism, which occurred a mean of 20 months after withdrawal of methimazole; they are designated as having overt recurrent hyperthyroidism (group A). In these patients, serum T4, FT4 and T3 concentrations increased rather abruptly to markedly elevated levels in a several-month period and the TRab and anti-DNA antibody titers increased markedly at or shortly after recurrence in the majority. In 9 patients (4.1%), TRH-induced TSH secretion became totally suppressed, indicating the reappearance of thyroidal autonomy; however, the patients did not have any hyperthyroid signs and symptoms (subclinical hyperthyroidism; group B). Their serum T4 and FT4 concentrations fluctuated in the upper normal to slightly supra-normal range, and their serum T3 concentrations remained within the normal range throughout the follow-up period, but their TRab and anti-DNA antibody titers did not appreciably increase. Thus, the time of recurrence could not be precisely determined in group B. In the remainder (152 patients; 83.4%), serum thyroid hormone levels and TRH-induced TSH secretion remained normal, TRab and anti-DNA antibody titers remained negative, and hyperthyroidism did not recur (euthyroid remission; group C). At the time of final examination (in groups B and C) or at the time of recurrence (in group A), the percentage of HLA-DR positive peripheral lymphocytes was 17.9% in group A, 15.9% in group B, and 12.1% in group C. Retrospective analysis of the data indicated that the mean pretreatment TRab titer (percent inhibition of TSH binding) was slightly but not significantly lower in group C (37.8%) compared to those in group A (53.9%) and group B (54.8%). The 3 groups were indistinguishable by all other laboratory data both before treatment and at the time of the T3 suppression test. These data strongly indicate heterogeneity among patients with hyperthyroidism due to Graves' disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2001

Food choice in hyperthyroidism: potential influence of the autonomic nervous system and brain serotonin precursor availability.

We explored energy and macronutrient intake in patients with Graves' hyperthyroidism. We specifically hypothesized that hyperthyroidism is associated with increased appetite for carbohydrates, because of enhanced sympathetic tone and diminished serotonin mediated neurotransmission in the brain. To test this hypothesis, we measured food intake by dietary history and food selected for lunch in the laboratory in 14 patients with Graves' hyperthyroidism. Twenty-four-hour catecholamine excretion was used as a measure of activity of the sympathetic nervous system (SNS) and the plasma [Trp]/[NAA] ratio was measured to estimate (rate limiting) precursor availability for brain 5-hydroxytryptamine synthesis. All measurements were repeated after the subjects had been treated to establish euthyroidism. In addition, the effects of nonselective beta-adrenoceptor blockade upon these parameters were studied to evaluate the influence of beta-adrenergic hyperactivity on food intake. Hyperthyroidism was marked by increased SNS activity and reduced plasma [Trp]/[NAA] ratio. Accordingly, energy intake was considerably and significantly increased in hyper vs. euthyroidism, which was fully attributable to enhanced carbohydrate consumption, as protein and fat intake were not affected. These results suggest that hyperthyroidism alters the neurophysiology of food intake regulation. Increased SNS activity and reduced Trp precursor availability for 5-hydroxytryptamine synthesis in the brain may drive the marked hyperphagia and craving for carbohydrates that appears to characterize hyperthyroid patients. Because propranolol did not affect food intake in hyperthyroidism, the potential effect of catecholamines on food intake might be mediated by alpha-adrenoceptors.

Autonomic Nervous System↗
PubMed2002

High dose of (131)I therapy for the treatment of hyperthyroidism caused by Graves' disease.

Radioactive iodine ((131)I) has become the most widely used therapy for patients with hyperthyroidism caused by Graves' disease in the United States. There remains, however, significant variability among (131)I dosing regimens, and it is clear that most patients ultimately develop hypothyroidism after therapy. To avoid persistent hyperthyroidism, we adopted a high dose (131)I therapy protocol based on measurement of 24-h thyroid (123)I uptake designed to deliver 8 mCi (296 MBq) to the thyroid gland 24 h after (131)I administration. To evaluate the efficacy of this protocol, we reviewed our clinical experience over a 7-yr period. We treated 261 patients (219 women and 42 men) with hyperthyroidism caused by Graves' disease with (131)I [mean dose, 14.6 mCi (540 MBq)] between 1993 and 1999. Before treatment, 207 (79%) had received an antithyroid drug (109 propylthiouracil and 98 methimazole). We determined their thyroid status 1 yr after treatment in relation to age, pretreatment with an antithyroid drug, pretreatment thyroid size, and dose of (131)I retained in the thyroid 24 h after treatment. Among the 261 patients, 225 (86%) were euthyroid or hypothyroid 1 yr after treatment, and 36 patients (14%) had persistent hyperthyroidism and required a second treatment. The patients who had persistent hyperthyroidism were younger (P < 0.01), had larger thyroid glands (P < 0.01), higher pretreatment thyroid (123)I uptake values (P < 0.01), and higher serum T(4) concentrations (P < 0.01) and were more likely to have taken antithyroid medication before administration of (131)I (P = 0.01). Five of these patients developed transient hypothyroidism, followed by thyrotoxicosis. There was an asymptotic, inverse relationship between the retained dose of (131)I at 24 h and persistent hyperthyroidism, revealing a 5-10% failure rate despite delivery of up to 400 microCi (14.8 MBq)/g. A dose of (131)I that results in accumulation of 8 mCi (296 MBq) in the thyroid gland 24 h after administration is an effective treatment for the majority of patients with Graves' hyperthyroidism. Young patients with larger thyroid glands, higher serum T(4) concentrations, and higher 24-h thyroid (123)I uptake values, and those pretreated with antithyroid medication for greater than 4 months are at higher risk for treatment failure. A higher dose of (131)I may be advisable in such patients.

Adult↗
PubMed1990

Effects of methimazole treatment on growth hormone (GH) response to GH-releasing hormone in patients with hyperthyroidism.

In vitro studies have demonstrated that thyroid hormones can enhance basal and stimulated growth hormone secretion by cultured pituitary cells. However, both in man and in the rat the effects of high thyroid hormone levels on GH secretion are unclear. The aim of our study was to test the GH response to human GHRH in hyperthyroid patients and to evaluate the effects on GH secretion of short- and long-term pharmacological decrease of circulating thyroid hormones. We examined 10 hyperthyroid patients with recent diagnosis of Graves' disease. Twelve healthy volunteers served as controls. All subjects received a bolus iv injection of GHRH(1-29)NH2, 100 micrograms. Hyperthyroid patients underwent a GHRH test one and three months after starting antithyroid therapy with methimazole, 10 mg/day po. GH levels at 15, 30, 45, 60 min and GH peak after stimulus were significantly lower in hyperthyroid patients than in normal subjects. The GH peak was also delayed in hyperthyroid patients. After one month of methimazole therapy, most of the hyperthyroid patients had thyroid hormone levels in the normal range, but they did not show significant changes in GH levels after GHRH, and the GH peak was again delayed. After three months of therapy with methimazole, the hyperthyroid patients did not show a further significant decrease in serum thyroid hormone levels. However, mean GH levels from 15 to 60 min were significantly increased compared with the control study. The GH peak after GHRH was also earlier than in the pre-treatment study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Effect of hyperthyroidism and its treatment on bone mineral content.

Patients with hyperthyroidism may develop osteopenia associated with fractures; however, there has been no general agreement on the incidence of osteopenia in hyperthyroidism or the recovery of the mineral loss after treatment of hyperthyroidism. We conducted a longitudinal prospective study on the effect of hyperthyroidism and its treatment on bone mineral content (BMC) using photon absorptiometry. We observed that both young and older hyperthyroid patients showed a significantly decreased baseline BMC compared with age- and sex-matched controls. We also observed a slight recovery of BMC in hyperthyroid patients at the two-year interval after a euthyroid state had been achieved. However, the BMC was still much lower than that of controls, and we did not find any significant restoration of BMC following "cure" of hyperthyroidism.

Adult↗
PubMedDate not supplied

Cancer mortality following treatment for adult hyperthyroidism. Cooperative Thyrotoxicosis Therapy Follow-up Study Group.

CONTEXT: High-dose iodine 131 is the treatment of choice in the United States for most adults with hyperthyroid disease. Although there is little evidence to link therapeutic (131)I to the development of cancer, its extensive medical use indicates the need for additional evaluation. OBJECTIVE: To evaluate cancer mortality among hyperthyroid patients, particularly after (131)I treatment. DESIGN: A retrospective cohort study. SETTING: Twenty-five clinics in the United States and 1 clinic in England. PATIENTS: A total of 35 593 hyperthyroid patients treated between 1946 and 1964 in the original Cooperative Thyrotoxicosis Therapy Follow-up Study; 91 % had Graves disease, 79% were female, and 65% were treated with (131)I. MAIN OUTCOME MEASURE: Standardized cancer mortality ratios (SMRs) after 3 treatment modalities for hyperthyroidism. RESULTS: Of the study cohort, 50.5% had died by the end of follow-up in December 1990. The total number of cancer deaths was close to that expected based on mortality rates in the general population (2950 vs 2857.6), but there was a small excess of mortality from cancers of the lung, breast, kidney, and thyroid, and a deficit of deaths from cancers of the uterus and the prostate gland. Patients with toxic nodular goiter had an SMR of 1.16 (95% confidence interval [CI], 1.03-1.30). More than 1 year after treatment, an increased risk of cancer mortality was seen among patients treated exclusively with antithyroid drugs (SMR, 1.31; 95% CI, 1.06-1.60). Radioactive iodine was not linked to total cancer deaths (SMR, 1.02; 95% CI, 0.98-1.07) or to any specific cancer with the exception of thyroid cancer (SMR, 3.94; 95% CI, 2.52-5.86). CONCLUSIONS: Neither hyperthyroidism nor (131)I treatment resulted in a significantly increased risk of total cancer mortality. While there was an elevated risk of thyroid cancer mortality following (131)I treatment, in absolute terms the excess number of deaths was small, and the underlying thyroid disease appeared to play a role. Overall, (131)I appears to be a safe therapy for hyperthyroidism.

Adult↗
PubMed1977

Digoxin in hyperthyroidism.

A patient with chronic atrial fibrillation developed hyperthyroidism. Increasing doses of digoxin were required to maintain satisfactor ventricular rate control. The systemic availability of oral digoxin was decreased in this patient. The metabolism of digoxin was studied in the hyperthyroid rats. The plasma digoxin concentrations were significantly decreased in the hyperthyroid rats. A threefold increase in digoxin excretion in the bile of the hyperthyroid rats was associated with these changes in plasma digoxin concentrations. Conversely, hypothyroid rats excreted less digoxin in the bile when compared with control and hyperthyroid rats. Thus, changes in digoxin absorption and its biliary excretion result, in part, in a decreased therapeutic effect of digoxin based on dose in hyperthyroidism.

Animals↗
PubMed1981

The influence of experimental hypo- and hyperthyroid states on acute and chronic inflammatory reactions: modified response to non-steroidal anti-inflammatory agents.

Hyperthyroid and hypothyroid states were induced in rats by administration of triiodothyronine or surgical thyroparathyroidectomy. The anti-inflammatory activity of Indomethacin, Oxametacine and Phenylbutazone was evaluated in these animals using paw oedema provoked by carrageenan granulomas induced by cotton pellets and polyarthritis induced by Freund complete adjuvant. Our results indicate that the hyperthyroid state leads to a significant inhibition of the acute inflammatory response to carrageenan, while hypothyroidism has no effect. There was a marked increase in the anti-inflammatory activity of Indomethacin and Phenylbutazone in hyperthyroid rats. By contrast, in thyroparathyroidectomised animals the anti-inflammatory effect of these drugs appeared less than in euthyroid rats. The hyperthyroid state slightly inhibited the development of the cotton pellet-induced granuloma, while hypothyroidism enhanced it. Treatment of hypothyroid animals with the anti-inflammatory drugs resulted in a significant decrease in the size of the granuloma. In the hyperthyroid state, the activity of the compounds appeared similar to that detected in euthyroid rats. Neither hyperthyroidism, nor hypothyroidism affected the inflammatory response to mycobacterial adjuvant, or the effect of anti-inflammatory drugs on the response. These results suggest that thyroid hormones may influence, to various degrees the development of acute inflammation due to carrageenan, and chronic inflammation due to implanted cotton pellets. Our results indicate also that hyper- and hypothyroid states can modify the response of the rat to some non-steroidal anti-inflammatory drugs.

Animals↗
PubMed1984

Decreased insulin receptor binding in hyperthyroidism.

The binding of 125I-insulin to insulin receptors on circulating mononuclear leukocytes was studied in ten patients with hyperthyroidism and 20 euthyroid normal volunteers. The hyperthyroid patients demonstrated significantly elevated glucose levels following an oral glucose load, despite normal insulin secretion. The infusion of insulin resulted in a delayed hypoglycaemic effect in the hyperthyroid patients; however, the inhibition of the endogenous insulin secretion as indicated by suppression of C-peptide levels was not different from euthyroid control subjects. Insulin binding to monocytes was significantly decreased in the hyperthyroid patients. Scatchard analysis of binding data indicates that a decrease of receptor number rather than receptor affinity seems to be the cause of the lowered insulin binding in hyperthyroid patients with diffuse toxic goitre. The findings of decreased insulin receptor number, mild degree of glucose intolerance despite normal insulin secretion and the delayed hypoglycaemic effect following insulin infusion suggest that peripheral insulin resistance could be involved in the highly complex pathophysiology of glucose intolerance in hyperthyroidism.

Adult↗
PubMed1998

Short-term variability of blood pressure and heart rate in hyperthyroidism.

The effect of hyperthyroidism on the short-term memory variability of blood pressure and heart rate was evaluated in 12 untreated hyperthyroid patients during thyrotoxicosis and after a 6 1/2 month treatment designed to achieve a stable euthyroid state. Beat-by-beat finger blood pressure was measured with a Finapres device. The pulse interval, from which pulse rate was derived, was obtained from the blood pressure signal. Due to the significant change in heart rhythm associated with thyrotoxicosis, both pulse interval (taken as a surrogate of heart period) and pulse rate (taken as a surrogate of heart rate) were computed. Power spectral analysis showed a reduction in the overall heart period variability in the supine position in the hyperthyroid compared to the euthyroid state. This effect was observed in the low-frequency (0.005-0.068 Hz), mid-frequency (0.068-0.127 Hz) and high-frequency (respiratory) domains as well, with a significant reduction of the modulus of these bands of 31%, 35% and 47%, respectively. The heart rate spectral modulus also exhibited a reduction of the high-frequency component (31%) in the supine position in the hyperthyroid subjects. These changes in heart rhythmicity corroborate a vagal deficit in hyperthyroidism. In addition, blood pressure spectral power exhibited a significant deficit in the orthostatism-induced mid-frequency systolic blood pressure rise in the hyperthyroid state (64%) compared with the euthyroid state. This observation may reflect a reduced vascular sympathetic activation with standing. The resulting vasodilatation could well contribute to normalize blood pressure in thyrotoxicosis in which cardiac output is increased.

Adult↗
PubMed1988

Glucoregulatory function of glucagon in hypo-, eu- and hyperthyroid miniature pigs.

The glucoregulatory function of glucagon was investigated in hypo-, eu- and hyperthyroid miniature pigs. Infusion glucagon, (3 ng x kg body weight-1.min-1) transiently increased blood glucose (p less than 0.01) and hepatic glucose production (p less than 0.01) in euthyroidism, but was without effect in hyperthyroidism. Infusing glucagon plus somatostatin (2 ng x kg body weight-1.min-1 and 0.2 microgram x kg body weight-1.min-1) transiently increased blood glucose (delta 3.0 to 4.3 mmol/l) and hepatic glucose production (delta 3.3 to 7.7 mumol x kg body weight-1.min-1) in all thyroid states, the effect was less pronounced in hyperthyroid pigs. By contrast, hypoglucagonaemia (74 to 107 pg/ml) at basal insulin (28 to 35 microU/ml) provoked hypoglycaemia (1.4 to 2.2 mmol/l) and a fall in glucose production (delta 4.7 to 8.3 mumol x kg body weight-1.min-1), which was independent of the thyroid state; the effect was most pronounced in hyperthyroidism (p less than 0.01). Hepatic glycogen content, arterial gluconeogenic precursor concentrations as well as the glycaemic response (delta 0.60 mmol/l) to alanine infusion (23 mumol x kg body weight-1.min-1) were all unaffected by hyperthyroidism. We conclude that moderate experimental hyperthyroidism reduces glucagon action due to reduced glycogen mobilisation. This may in part result from increased insulin sensitivity.

Animals↗
PubMed1982

Gastric secretion in hyperthyroidism.

The coexistence of hyperthyroidism and peptic ulcer is considered to be extremely rare. We have treated 24 patients with both hyperthyroidism and peptic ulcer during the years 1968-1978. With regard to the correlation between hyperthyroidism and peptic ulcer, we found that the mean value of gastric acid output was higher in the hyperthyroid patients than in the controls, and an extremely high gastric acid output was noted in 8 of the hyperthyroid patients. These results suggest that hyperthyroidism coexisting with peptic ulcer may not be so rare.

Adolescent↗
PubMedDate not supplied

Long-term outcomes of treatment of hyperthyroidism in Ireland.

We investigated the long-term outcome of treatment in 159 patients with hyperthyroidism first seen between 1979 and 1992. Median duration of follow-up was 10 1/2 years. We also inquired into current practice for the follow-up of hyperthyroidism by other endocrinologists in Ireland. Seven cases of unrecognised hyperthyroidism (4 per cent) and one of unrecognised hypothyroidism were identified. Among patients with Graves' disease, of those treated with an antithyroid drug, 28 per cent were in remission, 68 per cent had relapsed and 4 per cent had become hypothyroid. Of those treated by sub-total thyroidectomy, 31 per cent were in remission, 19 per cent had relapsed, 19 per cent were hypothyroid and 31 per cent were sub-clinically hypothyroid. Among patients treated with radioiodine, 19 per cent were euthyroid, 3 per cent were still hyperthyroid and three-quarters had become hypothyroid. In contrast, after radioiodine for toxic nodular goitre, 63 per cent were euthyroid and only 32 per cent had become hypothyroid (Chi Squared v. Graves' disease, P = 0.001). Of 73 patients receiving thyroxine replacement, plasma TSH was normal in only 41 per cent, although 82 per cent of patients had been seen by the family doctor within the previous 12 months. Seven of 17 other endocrinologists undertook long-term follow-up of hyperthyroid patients in their specialist clinics but none was using a computerised system to co-ordinate this. The findings confirm that careful follow-up is required for all hyperthyroid patients. The family doctor is well positioned to undertake this, but education and auditing are required.

Adolescent↗
PubMed1989

Anaesthesia for caesarean section in patients with uncontrolled hyperthyroidism.

The anaesthetic management of two patients with uncontrolled hyperthyroidism requiring Caesarean section is described. The first patient was diagnosed as hyperthyroid during pregnancy but was resistant to medical management with propylthiouracil (PTU). At 38 weeks' gestation, after optimizing her heart rate with intravenous propranolol, she received an epidural anaesthetic for the Caesarean section. The baby had manifestations of hypothyroidism immediately after birth but later became hyperthyroid. The second patient's hyperthyroidism was well controlled but she stopped her medication one week before delivery. The Caesarean section was performed under general anaesthesia for fetal distress. The baby died in the neonatal period of extreme prematurity. The anaesthetic management of the hyperthyroid parturient is discussed. Preoperative control of hyperthyroidism, bearing in mind pregnancy and time constraints, is essential. The use of PTU, propranolol, iodine, and glucocorticoids is described in the preparation of the parturient. Fetal and neonatal effects of these drugs are discussed.

Adult↗
PubMed2002

Similarities and differences in the phenotype of members of an Italian family with hereditary non-autoimmune hyperthyroidism associated with an activating TSH receptor germline mutation.

Constitutively activating germline mutations of the TSH receptor (TSH-R) are considered the cause of hereditary non-autoimmune hyperthyroidism. In this study, 10 members (8 affected and 2 unaffected) of an Italian family with hereditary non-autoimmune hyperthyroidism were investigated for the presence of mutations in the TSH-R gene. The clinical features of the disease were also analyzed. PCR-amplified fragments of the TSH-R gene were obtained from genomic DNA extracted from peripheral blood leukocytes of each family member and analyzed by direct nucleotide sequencing and restriction analysis. An identical germline TSH-R mutation was detected in all the patients with hyperthyroidism but in none of the unaffected family members. The mutation was heterozygotic and determined the substitution of valine for methionine (codon 463; ATG-->GTG) in the second transmembrane domain of the TSH-R. When expressed in chinese hamster ovary (CHO) cells, the Val463 mutant TSH-R induced constitutive activation of the TSH receptor. Analysis of the clinical features of our family and those of other families with hereditary non-autoimmune hyperthyroidism, including one with the same Val463 mutation, revealed wide variability in the phenotypical expression of the disease. Our findings indicate that an activating germline mutation in the TSH-R gene plays a key role in hereditary non-autoimmune hyperthyroidism although the onset of clinical manifestations and the evolution of the disease seem to depend heavily on other factors, thus far unidentified. The absence of a clear correlation between mutant genotypes and phenotypic expression of the disease currently limits the prognostic value of genetic testing in families with hereditary non-autoimmune hyperthyroidism.

Adult↗
PubMed2004

Role of nitric oxide in the functional response to ischemia-reperfusion of heart mitochondria from hyperthyroid rats.

We investigated the role of nitric oxide (NO) in the mitochondrial derangement associated with the functional response to ischemia-reperfusion of hyperthyroid rat hearts. Mitochondria were isolated at 3000 g from hearts subjected to ischemia-reperfusion, with or without N(omega)-nitro-L-arginine (L-NNA, an NO synthase inhibitor). During reperfusion, hyperthyroid hearts displayed tachycardia and low functional recovery. Their mitochondria exhibited O(2) consumption similar to euthyroid controls, while H(2)O(2) production, hydroperoxide, protein-bound carbonyl and nitrotyrosine levels, and susceptibility to swelling were higher. L-NNA blocked the reperfusion tachycardic response and increased inotropic recovery in hyperthyroid hearts. L-NNA decreased mitochondrial H(2)O(2) production and oxidative damage, and increased respiration and tolerance to swelling. Such effects were higher in hyperthyroid preparations. These results confirm the role of mitochondria in ischemia-reperfusion damage, and strongly suggest that NO overproduction is involved in the high mitochondrial dysfunction and the low recovery of hyperthyroid hearts from ischemia-reperfusion. L-NNA also decreased protein content and cytochrome oxidase activity of a mitochondrial fraction isolated at 8000 g. This and previous results suggest that the above fraction contains, together with light mitochondria, damaged mitochondria coming from the heaviest fraction, which has the highest cytochrome oxidase activity and capacity to produce H(2)O(2). Therefore, we propose that the high mitochondrial susceptibility to swelling, favoring mitochondrial population purification from H(2)O(2)-overproducing mitochondria, limits hyperthyroid heart oxidative stress.

Animals↗
PubMed1997

Identification of metabolic bone disease in patients with endogenous hyperthyroidism: role of biological markers of bone turnover.

Active hyperthyroidism is associated with reduced bone mass. Nevertheless, not all patients show the same risk for developing osteoporosis. Our aim was to analyze some clinical and biochemical potential predictors of low bone mass in hyperthyroid patients. We studied 127 consecutive hyperthyroid patients (110 females, 17 males; aged 42 +/- 16 years). Bone mineral density (BMD) was measured by dual X-ray absorptiometry (DXA) at lumbar spine (LS; L2-L4) and femoral neck (FN). Data were expressed as g/cm2 and T-score. Patients were placed into two groups based on recent WHO criteria: Group A, no osteoporosis (n = 98); and group B, lumbar or femoral osteoporosis (n = 29). Study protocol included evaluation of osteoporosis risk factors, anthropometrical variables, thyroid function, and bone turnover markers. Receiver-operating characteristic (ROC) plots for the precision of bone markers and multivariate analysis for the prediction of BMD and osteoporosis were performed. Group B showed greater age and proportion of menopausal females; lower weight, height, and calcium intake; longer duration of menopause; and greater levels of total and bone alkaline phosphatase and of urine hydroxyproline. No differences in thyroid function, osteocalcin, tartrate-resistant acid phosphatase, and type I collagen C-telopeptide (ICTP) were found. The best predictive model accounted for 46% and 62% of the variability of lumbar and femoral BMD respectively and correctly classified 89% of the osteoporotic hyperthyroid patients. No significant difference in ROC plots was observed. It is concluded that hyperthyroid patients with lumbar or femoral osteoporosis show a typical clinical and biochemical profile illustrating that the relationship between BMD and bone markers is better in high turnover states. Classical bone turnover markers show high performance in the evaluation of hyperthyroid bone disease.

Absorptiometry, Photon↗
PubMed2004

The effects of calcitonin on bone resorption in hyperthyroidism: a placebo-controlled clinical study.

The effects of intranasal calcitonin on bone metabolism were investigated in patients with hyperthyroidism. Urinary deoxypyridinoline (uDPD) levels were measured as a bone turnover marker and lumbar spine (L2) bone mineral density (BMD) was measured by dual-energy X-ray absorptiometry (DEXA) in 7 patients who were given only antithyroid drug (group 1), in 10 patients who were given antithyroid drug plus intranasal calcitonin (group 2), and in 10 healthy subjects who were given placebo (group 3) at the beginning and at the end of the study. The study continued until the patients with hyperthyroidism became euthyroidic according to the laboratory values. This period was approximately 3 months in groups 1 and 2. At the beginning of the study, uDPD was 21.5 +/- 2.6 nM DPD/mM creatinine in group 1, 23.3 +/- 3.6 nM DPD/mM creatinine in group 2, and 4.3 +/- 1.2 nM DPD/mM creatinine in group 3. uDPD levels measured in groups 1 and 2 were significantly higher than those in group 3 ( P << 0.001). Area BMD Z scores of the patients in groups 1 and 2 were significantly lower than the healthy controls ( P << 0.01, for both). At the end of the study, uDPD was 11.5 +/- 1.6 nM DPD/mM creatinine in group 1, 5.3 +/- 0.6 nM DPD/mM creatinine in group 2, and 4.4 +/- 1.3 nM DPD/mM creatinine in group 3. The levels of uDPD obtained in group 1 were significantly higher than those obtained in groups 2 and 3 ( P << 0.05, for both). The difference between groups 2 and 3 was not significant. Area BMD Z scores measured at the end of the study were found to be increased in groups 1 and 2 compared to early values, but the values were slightly lower than the normal values. In comparison of early and late uDPD values, the decrease in late period was statistically significant in groups 1 ( P << 0.05) and 2 ( P << 0.001). We concluded that bone turnover is high in hyperthyroidism. The treatment of hyperthyroidism decreases the rate of bone turnover, but it is not sufficient to prevent the degradation of bone in hyperthyroidism. The addition of intranasal calcitonin to the treatment of hyperthyroidism prevents the degradation of bone.

Adult↗