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PubMed2005

Effect of iopanoic acid on radioiodine therapy of hyperthyroidism: long-term outcome of a randomized controlled trial.

CONTEXT: Telepaque [iopanoic acid (IA)] is believed to rapidly ameliorate hyperthyroidism; however, it may preclude subsequent 131I therapy, possibly delaying it for several months. OBJECTIVE: Our objective was to see how early patients, made euthyroid with Telepaque, can be treated with 131I and to compare their short- and long-term outcome with patients treated with 131I, after making them euthyroid with carbimazole and beta-blockers. DESIGN: We conducted a randomized controlled trial. SETTING AND PATIENTS: We studied 200 hyperthyroid patients at a tertiary care teaching institute. INTERVENTIONS: The IA group received Telepaque, 500 mg/d orally, for 7 d and then no medication for 1 wk followed by 131I therapy if radioiodine neck uptake had recovered. The control group received 30-40 mg oral carbimazole daily until patients became euthyroid followed by 131I. MAIN OUTCOME: After 1 wk of Telepaque therapy and 6 wk of carbimazole, almost all patients became clinically and biochemically euthyroid, and 86 and 94% of patients were ready for 131I therapy after 1 and 2 wk off Telepaque, respectively. The cure rate, defined as euthyroid plus hypothyroid, after the first dose of 131I in controls and the IA group was 80 and 76.2%, respectively (P = 0.54). Thirty-two percent among controls and 25% in the IA group became hypothyroid within 1 yr (P = 0.33); thereafter, the annual rate of hypothyroidism was about 2% in both groups. After a mean follow-up duration of 11 yr, 58% of patients in the control group and 51% in the IA group were hypothyroid. CONCLUSIONS: Telepaque rapidly ameliorates hyperthyroidism without jeopardizing the subsequent radioiodine therapy, and the outcome of radioiodine therapy in this subset of patients is in no way different compared with those prepared by carbimazole.

Adult↗
PubMed2005

Glucose and lipid fluxes in the adipose tissue after meal ingestion in hyperthyroidism.

BACKGROUND: Although insulin resistance is well established in hyperthyroidism, information on the effects of insulin on adipose tissue (AD) is limited. METHODS: To investigate this, a meal was given to 12 hyperthyroid (HR) and 10 euthyroid (EU) subjects. Blood was withdrawn for 360 min from veins draining the anterior abdominal sc AD and from the radial artery. Blood flow was measured with 133Xe. Lipoprotein lipase (LPL) was calculated as triglyceride flux across AD, and AD-lipolysis was calculated as glycerol flux minus LPL. RESULTS: Both groups displayed comparable postprandial glucose levels, with the HR having higher insulin levels than the EU. In AD of HR vs. EU: 1) blood flow was increased [area under curve 0-360 min (milliliters per 100 milliliters of tissue); 1746 +/- 208 vs. 1344 +/- 102, P = 0.001], but glucose uptake was normal [area under curve 0-360 min (micromoles per 100 milliliters of tissue); 501 +/- 114 vs. 368 +/- 48]; 2) fasting rates of lipolysis (nanomoles per minute per 100 milliliters of tissue; 329 +/- 75 vs. 89 +/- 22, P = 0.02) and nonesterified fatty acid (NEFA) release (nanomoles per minute per 100 milliliters of tissue; 841 +/- 146 vs. 316 +/- 97, P = 0.01), and plasma NEFA levels (micromoles per liter; 623 +/- 50 vs. 454 +/- 57, P = 0.03) were increased, but were all rapidly suppressed to levels similar to those in EU after the increase in plasma insulin levels after the meal; and 3) LPL was not stimulated by insulin. CONCLUSIONS: In hyperthyroidism, AD lipolysis and glucose uptake are resistant to insulin. The defect in lipolysis is manifested in the fasting state, whereas postprandially this rate is rapidly suppressed to normal. This may relieve tissues from the burden of NEFAs after the meal, thus facilitating muscle glucose disposal by insulin.

Adipose Tissue↗
PubMed1975

Erythropoiesis and erythropoietin in hypo- and hyperthyroidism.

Qualitative and quantitative studies of erythropoiesis in 23 patients with hypothyroidism and 21 patients with hyperthryoidism included routine hematologic evaluation, bone marrow morphology, status of serum iron, B12 and folate red blood cell mass and plasma volume by radioisotope methods, erythrokinetics and radiobioassay of plasma erythropoietin. A majority of patients with the hypothyroid state had significant reduction in red blood cell mas per kg of body weight. The presence of anemia in many of these patients was not evident from hemoglobin and hematocrit values due to concomitant reduction of plasma volume. The erythrokinetic data in hypothyroid patients provided evidence of significant decline of the erythropoietic activity of the bone marrow. Erythroid cells in the marrow were depleted and also showed reduced proliferative activity as indicated by lower 3H-thymidine labeling index. Plasma erythropoietin levels were reduced, often being immeasurable by the polycythemic mouse bioassay technique. These changes in erythropoiesis in the hypothyroid state appear to be a part of physiological adjustment to the reduced oxygen requirement of the tissues due to diminished basal metabolic rate. Similar investigations revealed mild erythrocytosis in a significant proportion of patients with hyperthyroidism. Failure of erythrocytosis to occur in other patients of this group was associated with impaired erythropoiesis due to a deficiency of hemopoietic nutrients such as iron, vitamin B12 and folate. The mean plasma erythropoietin level of these patients was significantly elevated; in 4 patients the levels were in the upper normal range whereas in the rest, the values were above the normal range. The bone marrow showed erythyroid hyperplasia in all patients with hyperthyroidism. The mean 3H-thymidine labeling index of the erythroblasts was also significantly higher than normal in hyperthyroidism; in 8 patients the index was within the normal range whereas in the remaining 13 it was above the normal range. Erythrokinetic studies also provided evidences of increased erythropoietic activity in the bone marrow. It is postulated that thyroid hormones stimulate erythropoiesis, sometimes leading to erythrocytosis provided there is no deficiency of hemopoietic nutrients. Stimulation of erythropoiesis by thryoid hormones appears to be mediated through erythropoietin.

Biological Assay↗
PubMed1975

Pharmacodynamics of propylthiouracil in normal and hyperthyroid subjects after a single oral dose.

Serum levels of propylthiouracil were measured in 8 normal persons and in 7 patients with hyperthyroidism after a single, 300 mg, oral dose of 6-n-propyl-2-thiouracil (PTU). The patients with hyperthyroidism were restudied after 3, 6, and 9 weeks of individualized treatment with PTU. The serum half-life of the drug in normal subjects was 1.65 h. In patients with hyperthyroidism the serum half-life was similar, and it did not change significantly as the euthyroid state was achieved.

Half-Life↗
PubMed1976

Prolactin response to arginine in normal subjects and in patients with hyperthyroidism.

The effect of arginine on serum prolactin concentrations was studied in 18 normal subjects and in 7 patients with hyperthyroidism in normal subjects, arginine infusion produced an increase of serum prolactin at least 6 ng/ml from the baseline, and the mean peak level (25.2 +/- 3.3 ng/ml, mean +/- SE) was significantly higher than the basal level (8.6 +/- 5.2 ng/ml, P less than 0.001). There was no significant difference in the peak levels between sexes. Unlike prolactin, concomitant serum thyrotropin levels did not change after the arginine infusion. In hyperthyroid patients, the increment of serum prolactin after arginine infusion at 30 min (3.9 +/- 1.5 ng/ml) was significantly lower than that of the normal controls which were matched by age and sex (17.1 +/- 4.4 ng/ml, P less than 0.05). After treatment when these patients were euthyroid, the increment of prolactin after arginine infusion at 30 min was significantly increased (16.3 +/- 4.3 ng/ml, P less than 0.05) and had reached the level of control subjects. These data indicate that the prolactin response to arginine in hyperthyroidism is diminished.

Adult↗
PubMed1976

Androsterone sulfate concentrations in plasma in hypo- and hyperthyroidism.

Androsterone sulfate concentrations have been measured in the plasma of 16 hypothyroid women and 14 hyperthyroid women by a gas-liquid chromatographic technique and in 23 hypothyroid and 18 hyperthyroid women by radioimmunoassay. In obth studies androsterone sulfate concentrations were significantly higher in the hyperthyroid groups. In one hypothyroid subject, blood was obtained at 20-minute intervals over 24 hours before and after the administration of triiodothyronine; plasma androsterone sulfate, initially 25 mug per dl, increased three-fold as a consequence of treatment.

Adult↗
PubMed1976

Alteration in intracellular sodium concentration and ouabain-sensitive ATPase in erythrocytes from hyperthyroid patients.

The activity of the ouabain-sensitive sodium-potassium-activated component of the ATP-hydrolyzing enzyme system (ouabain sensitive ATPase) was studied in the erythrocyte membranes of 10 patients with hyperthyroidism, and found to be decreased in all 10 patients. The mean ouabain-sensitive ATPase activity was 43 +/- 4 nmol Pi/mg tissue/h in the patients, compared with 69 +/- 5 nmol Pi/mg tissue/h in the erythrocyte membranes of 10 paired control subjects. The mean concentration of sodium within the erythrocytes was 10.8 +/- 0.9 nmol/liter of red blood cells in the patients and 7.2 +/- 0.3 nmol/liter of red blood cells in the controls. The decrease in ouabain-sensitive ATPase activity did not appear to be associated with a change in the ligand sensitivity of ATPase, nor was there a difference in the activity of the ouabain-insensitive component of ATPase. Serial studies to follow the effects of treatment of hyperthyroidism on red cell membrane ATPase were performed repeatedly in one of these patients. There was a significant inverse correlation between L-thyroxine (T4) and ouabain-sensitive ATPase, as both variables returned to normal. Normal erythrocyte membranes were assayed for ATPase activity in the presence of varying concentrations of L-triiodothyronine (T3) and T4, and following pre-incubation with T4. No significant effect on erythrocyte membrane ATPase was demonstrated in either series of experiments. It can be concluded from these studies that the decreased sodium efflux in the erythrocytes of patients with hyperthyroidism is associated with a decrease in the activity of the ouabain-sensitive component of ATPase in the erythrocyte membrane. The failure to reproduce this effect in vitro suggests that it does not represent a direct effect of the thyroid hormones on the mature erythrocyte membrane.

Adenosine Triphosphatases↗
PubMed1976

Dissociation of responsiveness to thyrotropin-releasing hormone and thyroid suppressibility following antithyroid drug therapy of hyperthyroidism.

Responsiveness to synthetic thyrotropin-releasing hormone (TRH), thyroid suppressibility by triiodothyronine (T3) and the outcome of hyperthyroidism following prolonged therapy with thionamides were studied in a group of 35 patients with toxic diffuse goiter. TRH and T3 suppression tests were performed 10 days to 24 months (mean 4 months) after withdrawal of antithyroid drugs. Nineteen patients were euthyroid and had a normal thyrotropin (TSH) response to TRH, while 4 were recovering from mild hypothyroidism due to overtreatment and had an exaggerated response. No response was observed in 12 patients with recurrent hyperthyroidism. Positive T3 suppression tests were found only in 10 of the 30 cases examined. Peak and net 2 h secretion responses of TSH to TRH exhibited a significant inverse correlation with the levels of serum thyroxine and serum triiodothyronine, but were unrelated to the degree of thyroid suppressibility. Relapse or recurrence of thyrotoxicosis occurred in at least 9 of the 23 patients having no evidence of hyperthyroidism at the time of TRH test. Each of them was found to be responsive to TRH, while the T3 suppression test was negative in 8 and had to be discontinued in one because of thyrotoxic symptoms. The present data indicate that during the early period after completion of a prolonged course of antithyroid drug therapy responsiveness to TRH in toxic diffuse goiter is: a) correlated with circulating thyroid hormones, b) unrelated to the degree of thyroid suppressibility by T3 and c) of little value in predicting the long-term results of treatment.

Adult↗
PubMed1977

Juvenile hyperthyroidism with elevated thyrotropin (TSH) and normal 24 hour FSH, LH, GH and prolactin secretory patterns.

An 11 year old boy was found to have hyperthyroidism and elevated serum TSH concentrations. Hyperthyroidism was first diagnosed at 4 years of age. After antithyroid drug therapy, a subtotal thyroidectomy was done when he was 7 years old. Goiter and hyperthyroidism gradually recurred, and an elevated serum TSH concentration (90 microU/ml) was found when first measured at age 12 years. There was no evidence of a pituitary tumor. Thyrotropin-releasing hormone (TRH) administration resulted in a marked increase in serum TSH concentrations. Triiodothyronine, thyroxine and dexamethasone administration lowered the serum TSH concentration. There was diurnal variation in TSH secretion. Growth hormone (GH) and prolactin responses to provocative stimuli and 24 h secretion patterns were normal. FSH and LH secretion was normal for age and stage of sexual development. The 24 h cortisol pattern demonstrated normal episodic secretion, although the mean 24 h concentration was high (10.5 microgram/dl). These data suggest that this patient's TSH hypersecretion is due to partial resistance of the thyrotrophs to the inhibitory action of thyroid hormone.

Adolescent↗
PubMed1983

Plasma inactive renin in patients with hyperthyroidism.

Active and inactive PRA were measured after 1 h at rest in 16 normal controls and 20 patients with hyperthyroidism. In some of the patients these measurements were repeated after they had become euthyroid or received 90 mg propranolol for 1 week. Inactive PRA was determined as the difference between total PRA after trypsin activation and active PRA. Active PRA was significantly higher (P less than 0.01) in untreated patients than in normal subjects; however, the inactive PRA of patients was not different compared with that of normal subjects. Active PRA was normalized, and inactive PRA did not change after achievement of euthyroidism. The proportion of active of total PRA was significantly correlated with the levels of serum thyroid hormones (T3 and T4) in hyperthyroid patients (r = 0.46; P less than 0.05 and r = 0.55; P less than 0.01, respectively). The administration of propranolol reduced active PRA (P less than 0.05) and increased inactive PRA slightly but not significantly. These results indicate that in hyperthyroidism, the in vivo conversion of inactive renin to active renin is probably facilitated by increased sympathetic activity.

Adult↗
PubMed1983

beta-Adrenoceptor-adenosine 3',5-monophosphate system in human leucocytes before and after treatment for hyperthyroidism.

Modifications in characteristics of the beta-adrenoceptor-cAMP system were observed in leucocytes from 10 patients in the hyperthyroid state after antithyroid treatment. These include 1) an increased number of beta-adrenoceptors without a change in their affinity, 2) an increased magnitude of stimulation of adenylate cyclase by isoprenaline, without a change in the NaF-stimulated enzyme activity, 3) an increased cAMP-dependent protein kinase activity ratio, and 4) an increased activity of cAMP-phosphodiesterase. Moreover, the plasma cAMP levels were markedly elevated during the hyperthyroid state. It is suggested that the above changes may in part constitute the molecular basis for the reputed catecholamine supersensitivity in the hyperthyroid state.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1984

Bromocriptine therapy for hyperthyroidism due to increased thyrotropin secretion.

We describe a patient with TSH-induced hyperthyroidism successfully treated with bromocriptine. A 25-yr-old woman was found to have hyperthyroidism due to excessive TSH secretion; no pituitary tumor was found. Her serum T4 level ranged between 21.9 and 25.9 micrograms/dl and that of T3 between 283 and 314 ng/dl. Serum TSH was between 5 and 9 microU/ml with an exaggerated response to TRH. Basal metabolic rate was +26 to +38%. Serum PRL was also elevated (79 ng/ml). Administration of bromocriptine for 4 months decreased serum TSH and PRL levels to normal with a concomitant fall in levels of serum T3 and T4. Regression of the clinical manifestations of hyperthyroidism occurred during bromocriptine drug therapy. These results suggest that reduction in hypothalamic dopaminergic tone may have contributed to the inappropriately increased TSH secretion in the patient.

Adult↗
PubMed1985

Management of hyperthyroidism in children and adolescents.

Between 1961 and 1984, 262 patients with hyperthyroidism due to Graves' disease between the ages of 3 and 18 yr were treated in the author's clinic. This paper compares the results of different treatment methods. Initial treatment was surgery for 7 patients, radioiodine for 73, and an antithyroid drug for 182. Seven drug-treated patients subsequently had surgery. Of 14 surgically treated patients, 5 relapsed and received radioiodine, 5 became hypothyroid, 3 were lost to follow-up, and 1 remained euthyroid. Sixteen drug-treated patients were lost to follow-up; 7 are still taking drugs. Of the remaining 99 drug-treated patients not achieving remission, 92 received radioiodine, and 7 had surgery (1 later relapsed and received radioiodine). The principal reasons for abandoning drugs were toxicity, noncompliance, poor control, and failure to achieve sustained remissions. Of 61 drug-treated patients who achieved remission, 22 relapsed (21 were treated with radioiodine and 1 with drug). Remissions after antithyroid drug therapy persist in 39 patients, 2 of whom are now hypothyroid and 10 of whom have been in remission less than 2 yr. Of the 239 subjects whose treatment is complete, 191 (80%) ultimately had radioiodine. One radioiodine treatment eliminated hyperthyroidism in 163 patients, 2 treatments were effective in 17, and 3 treatments were effective in 1. The remaining 5 patients were lost to follow-up after radioiodine before the outcome of therapy could be determined. No increase in congenital abnormalities was found in 63 children of these patients, regardless of treatment. Radioiodine is a safe, simple, and economical therapy for patients with hyperthyroidism and is now considered the initial treatment of choice for such patients.

Adolescent↗
PubMed1986

Pharmacology of propylthiouracil (PTU) in pregnant hyperthyroid women: correlation of maternal PTU concentrations with cord serum thyroid function tests.

Previous studies have characterized the pharmacology of propylthiouracil (PTU) in normal and hyperthyroid subjects, but there is little information available regarding PTU pharmacokinetics in pregnant hyperthyroid women. We investigated the serum PTU response to an oral dose of PTU in six hyperthyroid pregnant women both ante- and postpartum. The serum PTU profile during the third trimester of pregnancy was qualitatively similar to that in nonpregnant subjects, but serum PTU concentrations were consistently lower in the late third trimester compared with postpartum values. Cord serum PTU concentrations were consistently higher than simultaneously obtained maternal serum PTU concentrations, suggesting slower PTU clearance in the fetus. There was a significant inverse correlation (r = -0.92; P = 0.026) between the maternal serum PTU area under the curve in the third trimester and the cord serum free T4 index.

Adult↗
PubMed1988

Protein synthesis and quantitative morphology in thyroid tissue from hyperthyroid patients after preoperative treatment with antithyroid or beta-adrenergic antagonist drugs.

The rate of protein synthesis was measured in thyroid tissue obtained from three groups of patients undergoing thyroid surgery: group I (n = 18), hyperthyroid patients preoperatively treated with an antithyroid drug and T4; group II (n = 11), hyperthyroid patients preoperatively treated with a beta-adrenergic antagonist drug; and group III (n = 9), euthyroid patients operated on for multinodular goiter or adenoma. Quantitative morphology was studied in the resected thyroid tissue from the patients in groups I (n = 15) and II (n = 6) who had Graves' disease. While serum thyroid hormone levels became normal during preoperative treatment in group I, they remained elevated in the group II patients. The rate of protein synthesis was 2-fold higher in thyroid tissue from patients in group II than in those in groups I and III. A tendency toward an increased amount of epithelium and a reduced amount of colloid was found in thyroid tissue from patients in group II. There was a positive correlation between the rate of protein synthesis, and distribution of epithelium, and the epithelium to colloid ratio, respectively, in thyroid tissue. These results suggest that the thyroid gland of hyperthyroid patients remains hyperactive during treatment with beta-adrenergic antagonist drugs.

Adrenergic beta-Antagonists↗
PubMed1988

Hyperthyroidism due to selective pituitary resistance to thyroid hormones in a 15-month-old boy: efficacy of D-thyroxine therapy.

A 15-month-old boy had clinical features of hyperthyroidism. In spite of elevated serum thyroid hormone levels (mean serum T4, 230 nmol/L; T3, 4.2 nmol/L), serum TSH levels ranged between 3.3-5.6 mU/L and rose to 35.4 mU/L after TRH stimulation. There was no abnormal serum thyroid hormone binding or any evidence of a pituitary tumor. The boy was treated with carbimazole for 6 months and became euthyroid. However, his thyroid size enlarged, and serum TSH rose to 45 mU/L. In an attempt to suppress TSH secretion, 3,5,3'-triiodothyroacetic acid was added to carbimazole in daily doses from 0.7-1.4 mg. This combined therapy failed to suppress TSH secretion (serum TSH, 10.2 mU/L) and led to recurrence of symptoms of hyperthyroidism. A trial using highly purified dextrothyroxine (contamination by L-T4, 0.05%) as sole therapy then was carried out. Serum TSH levels promptly declined to normal, both basally and after TRH stimulation (basal, 2.4 mU/L; peak, 13.8 mU/L). During a 24-month follow-up period, the boy remained euthyroid. Serum TSH levels remained in the normal range, as did his serum L-T4 levels (93 nmol/L). Complete remission was achieved using a 5-mg daily dose of D-T4. Temporary discontinuation of D-T4 led to prompt relapse of hyperthyroidism. Our patient's TSH hypersecretion appears to be due to selective pituitary resistance to thyroid hormones. Purified D-T4 effectively inhibited TSH secretion in this patient, without inducing significant side-effects, even when the daily dose was high. The cause of partial pituitary unresponsiveness to thyroid hormones is not known. We suggest that transport of thyroid hormones into the thyrotroph cells could be deficient in our patient.

Dextrothyroxine↗
PubMed1990

Negative correlation between the change in bone mineral density and serum osteocalcin in patients with hyperthyroidism.

To assess the changes in bone mineral density and osteoblastic activity in patients with hyperthyroidism and to investigate the relationship between those changes, we measured bone mineral density and serum osteocalcin in 109 patients with Graves' disease, comprising 75 untreated patients and 34 patients under treatment, and 200 normal controls. The degree of change in bone mineral density was quantified with Z transformation, in which we used means and SDs of bone mineral densities obtained in the process of age- and sex-matched 1:1 pairing developed by ourselves. Bone mineral density was low in female patients with hyperthyroidism in the spine, femur neck, trochanter, and Ward's triangle, but was not low in male patients. Serum osteocalcin was elevated in patients with untreated Graves' disease and correlated negatively with the Z values of bone mineral densities of the spine, femur neck, and trochanter. In conclusion, indices of osteoblastic activity were elevated in patients with hyperthyroidism, probably secondary to a thyroid hormone-induced increase in bone resorption which resulted in reduced bone mineral density. Quantification of the change in bone mineral density by using the parameters derived in the process of age- and sex-matched pairing seems to be an efficient method for statistical analyses.

Adolescent↗
PubMed1991

Hyperthyroidism due to a pituitary adenoma composed of two different cell types, one secreting alpha-subunit alone and another cosecreting alpha-subunit and thyrotropin.

A 37-yr-old female presented with clinical signs and symptoms of mild hyperthyroidism, high serum levels of free T4 (24.2 pmol/L), free T3 (11.7 pmol/L), and sex hormone-binding globulin (157 nmol/L) as well as measurable (by immunofluorometric assay) serum TSH concentrations (1.9 mU/L) in the absence of any known methodological interference. The above finding indicated the presence of hyperthyroidism due to inappropriate secretion of TSH, whose neoplastic origin was documented by computed tomographic scan showing a 1-cm pituitary adenoma. The diagnosis was confirmed by elevated alpha-subunit levels (9.2 micrograms/L) and alpha-subunit/TSH molar ratio (25.2) as well as absent TSH suppression after T3 administration. TRH injection (200 microgram, iv) caused impaired TSH (from 3.0 to 4.8 mU/L) and unexpectedly exaggerated alpha-subunit (from 8.8 to 18.2 micrograms/L) responses. Such a discrepancy was also observed after other dynamic tests. Double gold particle immunostaining of the adenomatous tissue removed at surgery showed that all of the cells contained secretory granules positive for alpha-subunit, while very few cells were positive for TSH beta and alpha-subunit. In conclusion, the present study demonstrates the existence of TSH-induced hyperthyroidism due to a pituitary adenoma composed of two different cell types: one secreting alpha-subunit alone and another cosecreting alpha-subunit and TSH.

Adenoma↗