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[Thyroid dysfunction induced by amiodarone].

Amiodarone (2-n-butyl-3,4-diethylaminoethoxy-3',-diiodobenzoyl-benzofurone ) is a drug widely used for the treatment of cardiac arrhythmias. Due to its high iodine content and structural similarity to thyroxine it produces abnormalities in thyroid hormone metabolism and, in some cases, clinical thyroid dysfunction as well. We report 18 patients, 11 females and 7 males, whose thyroid disease developed during treatment with amiodarone (A). Age ranged from 13 to 64 years. A history of thyroid disease in a first-degree relative was present in five, and three patients had goiter prior to A therapy. Fifteen patients had atrial arrhythmias, and 3 had ventricular arrhythmias. Amiodarone was being given in doses of 200 to 800 mg daily. Thyroid function abnormalities appeared between 1 and 29 months after starting A therapy. Nine patients became clinically and chemically thyrotoxic; three patients developed diffuse thyroid enlargement and had total T4 concentration and FI4I increased with normal T3 and no signs of hyperthyroidism; and the six remaining patients became clinically hypothyroid with low values of total T4 and FTI and raised basal TSH. No relationship between dosages of A or duration of treatment and the appearance or severity of thyroid dysfunction was found. Regression of symptoms occurred in all but two patients with simple goiter between 1 and 8 months after amiodarone was discontinued and appropriate treatment was given. Our observations confirm the potential of A to induce thyroid abnormalities in patients with and without preexistent thyroid disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Amiodarone-induced thyroid dysfunction: diagnostic role of free serum thyroid hormone levels and pathogenetic significance of antithyroid antibodies.

Forty-six patients treated with amiodarone hydrochloride for a mean period of 41 +/- 3.5 months, with an average daily dose of 240 +/- 57 mg/day, have been studied. Thyroid function was assessed clinically and by laboratory tests, which included free-triiodothyronine (free-T3), free-thyroxine (free-T4) and thyrotropin. Antimicrosomal and antithyroglobulin antibodies were also looked for. Three patients (6.5%) were found to be hyperthyroid and two (4.3%) hypothyroid. Of the 41 clinically euthyroid patients, 19 (46.3%) showed one or more abnormalities in the thyroid function tests. In this group, only free-T4 was found significantly increased (p less than 0.05) as compared to both control populations. Antimicrosomal antibodies (titre greater than or equal to 1:1600) were present in 4 of 41 (9.7%) euthyroid patients, but not in hyper- or hypothyroid patients. There were no antithyroglobulin antibodies in any patients. Free hormone measurements have proved to significantly correlate with the clinical picture. Increases in free-T3 and free-T4 are the main features of hyperthyroidism, while a reduction in free-T4 serum level was specific for hypothyroidism. There are probably several mechanisms responsible for hyperthyroidism and some genetically controlled defects in synthesis and release of thyroid hormones might be among these. The presence of antithyroid antibodies could be due to deposits of amiodarone in the thyroid gland, with a consequent release of antigen from the follicle cell, but only in those patients with genetically determined defects in immunological surveillance could an autoimmune thyroiditis, with consequent hypothyroidism, develop.

Adult↗
PubMed1975

Altered plasma half-lives of antipyrine, propylthiouracil, and methimazole in thyroid dysfunction.

In normal, nonmedicated volunteers and in patients with thyroid disorders the plasma half-lives of antipyrine, propylthiouracil, and methimazole were determined after single oral doses. The plasma half-liver plus or minus S.D. of antipyrine, propylthiouracil, and methimazole were 11.9 plus or minus 1.4 hr, 6.7 plus or minus 1.0 hr, and 9.3 plus or minus 1.4 hr, respectively, in normal volunteers, but were shortened to 7.7 plus or minus 1.2 hr, 4.3 plus or minus 0.7 hr, and 6.9 plus or minus 0.6 hr, respectively, in hyperthyroid patients. In hypothyroid patients the plasma half-lives of these drugs were prolonged to 26.4 plus or minus 4.0 hr, 24.7 plus or minus 34.5 hr, and 13.6 plus or minus 4.8 hr, respectively. Return to the euthyroid state restored plasma half-lives to or toward normal. Alterations in plasma drug half-lives during thyroid dysfunction appear to result mainly from accelerated hepatic microsomal drug metabolism in hyperthyroidism and retarded drug biotransformation during hypothyroidism.

Adult↗
PubMed1988

Amiodarone pharmacokinetics. III. Influence of thyroid dysfunction on amiodarone absorption and disposition.

Hypothyroid, hyperthyroid and euthyroid rats were given 45 or 80 mg/kg i.v. or 100 mg/kg p.o. of amiodarone hydrochloride to determine the effects of thyroid dysfunction on the absorption and disposition characteristics of amiodarone. Serial blood samples were obtained for 48 hr and assayed for amiodarone and desethylamiodarone by high-performance liquid chromatography. In the hypothyroid rats, reductions in amiodarone clearance (CL) of 73% (26.9-7.3 ml/min/kg) and 61% (18.7-7.3 ml/min/kg) were observed with the 45- and 80-mg/kg i.v. bolus doses, respectively. Accompanying the decreases in CL were increases in the terminal disposition half-life (T1/2 gamma), 89% (18-34 hr) with the 45-mg/kg dose and 185% (20-57 hr) after the 80-mg/kg dose. The steady state (Vss) and apparent (Vd) volumes of distribution were smaller at the lower dose but were invariant after administration of the larger dose. Furthermore, the central compartment volume was not altered. In the hyperthyroid rats, a 67% increase in CL (12.8-21.4 ml/min/kg) and 75 to 80% increases in Vss (15.5-27.1 liters/kg) and Vd (25.0-44.8 liters/kg) were observed with the 45-mg/kg of amiodarone dose. However, no changes in CL, Vd and Vss were seen with the 80-mg/kg dose. Furthermore, gamma, T1/2 gamma and central compartment volume were not altered in the hyperthyroid rats. The effects of thyroid dysfunction on the p.o. bioavailability characteristics of amiodarone were minor. These studies demonstrated that the disposition kinetics of amiodarone are altered in hypo- and hyperthyroidism.

Amiodarone↗
PubMed1986

Masked thyroid dysfunction among elderly patients with atrial fibrillation.

Seventy-five elderly patients with atrial fibrillation (41 males and 34 females with a mean age of 75.6 years) were studied to evaluate the incidence of masked thyroid dysfunction. A thyrotropin (TSH)-releasing-hormone (TRH) test (intravenous injection of 250 micrograms of synthetic TRH) was performed in the patients and 30 age matched controls without atrial fibrillation. In the controls, no abnormal TRH stimulated TSH response was observed. In the patients with atrial fibrillation, no response of TSH to TRH (hyperthyroidism) was found in 5 cases (6.6%), while hyperresponse of TSH to TRH (hypothyroidism) was found in 6 cases (8.0%). Thyroid dysfunction (hyper or hypothyroidism) was more frequently observed in the patients than in the controls (p less than 0.05). Two of 5 hyperthyroid patients had normal thyroid hormone levels. All patients with hyperthyroidism were treated with antithyroid drugs or 131I. Unfortunately, atrial fibrillation persisted in all but 1 case. It is concluded that the TRH test is a useful screening test for detecting those patients with abnormal thyroid function among elderly patients with atrial fibrillation, and that hypothyroidism should be considered as a cause of atrial fibrillation in the elderly.

Aged↗
PubMed1977

Plasma and urinary digoxin in thyroid dysfunction.

The response to a single oral dose of 0.5 mg digoxin has been studied in eight patients, of whom four were hyperthyroid and four were hypothyroid, both before and after treatment for their thyroid dysfunction. The post-dose plasma digoxin levels were significantly lower in the hyperthyroid patients when they were thyrotoxic than when they became euthyroid. In only one hypothyroid patient was the post-dose plasma digoxin level significantly higher before treatment than it was after and in the others the digoxin values reached were either the same as, or lower than, before treatment. There was a significant correlation between the creatinine clearance and the urinary concentrations of digoxin and these both altered with change in thyroid status. Total urinary digoxin excretion did not change. Pharmacokinetic analysis suggested that digoxin was distributed in a way compatible with a two-compartment model and that the volume of the central compartment was high in thyrotoxic patients and low in hypothyroid patients. In both cases it reverted to a median value after treatment. It is recommended that plasma digoxin levels should be monitored in all patients with thyroid dysfunction who require therapeutic digoxin.

Aged↗
PubMed1987

Thyroid dysfunction during chronic amiodarone therapy.

Clinical and laboratory features of 99 patients receiving long-term amiodarone therapy were analyzed to determine which individuals may be at a high risk for developing amiodarone-induced thyroid dysfunction. The group of 68 men and 31 women was followed up for an average of 27 months (range 3 to 60). There were no differences in age, sex, dose of amiodarone, type or severity of underlying heart disease or baseline serum thyroxine levels in patients who developed hypothyroidism (n = 32) or hyperthyroidism (n = 5) or remained euthyroid (n = 62). Baseline serum thyrotropin levels were statistically higher in patients who became hypothyroid, but there was considerable overlap with the other patient groups. Serum reverse triiodothyronine (reverse T3), which has been suggested to be a marker of amiodarone efficacy, correlated directly with serum thyroxine levels, and was not an independent variable. There was no pattern to the time course for development of thyroid dysfunction, which occurred in 49% of those followed up and developed as early as 1 month or, in one individual, as late as after 3 years of amiodarone therapy. There are few guidelines for replacement therapy in patients with amiodarone-induced hypothyroidism. L-thyroxine dosage was adjusted cautiously in these high risk individuals to achieve serum thyroxine levels within the reference range of euthyroid individuals taking amiodarone: the mean dosage required was 136 micrograms/day. Normalization of serum thyrotropin (TSH) would have required doses of L-thyroxine that were judged to be excessively high.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Thyroid dysfunction in multi-transfused iron loaded thalassemia patients.

Seventy-two transfusion-dependent iron loaded thalassemia patients were investigated for thyroid dysfunction by estimating circulating thyroid hormones (T4 and T3) and basal thyroid stimulating hormone (TSH). They were also evaluated for their liver function (biochemically) and iron overload by estimating serum ferritin. Thyroid failure (hypothyroidism) was documented in 14 patients (19.4%). In all, 3 groups were seen, i.e. Group 1: Normal T4, T3, TSH (58 patients: 80.6%); Group 2: Compensated hypothyroidism characterized by normal T4, T3 and raised TSH (9 patients: 12.5%); Group 3: Decompensated hypothyroidism characterized by decreased T4 and increased TSH (5 patients: 6.9%). Interestingly, impaired thyroid function could not be correlated with age, amount of blood transfused, liver dysfunction or degree of iron overload. It is postulated that an inter-play between chronic hypoxia, liver dysfunction and iron overload may be responsible for the thyroid damage.

Body Height↗
PubMed1987

Superoxide dismutase level in human erythrocytes and its clinical application to the patients with cancers and thyroidal dysfunctions.

The activity, content and true specific activity of superoxide dismutase (SOD) were determined for human erythrocytes of 105 normal healthy subjects. At the same time the activities of erythrocyte SOD are also determined in patients with lung cancer, lymphoma, leukemia and thyroidal dysfunctions. The mean SOD activity of healthy subjects assayed by the method of inhibition of xanthine autoxidation was 11.0 X 10(3) units/g of hemoglobin (Hb). The mean SOD content of healthy subjects assayed by an immunodiffusion method was 456 micrograms/g of Hb. Both the activity and the content of SOD showed normal distributions, while no significant variations in regard to sex and age were detected. A high positive correlation between the activity and the content of SOD was observed in normal healthy subjects (r = 0.77, p less than 0.001). True specific activity was calculated from the levels of activity and content of SOD. The mean true specific activity of SOD in human erythrocytes was 23.7 units/micrograms of SOD. There was no significant difference in true specific activity among age groups. The activity of erythrocyte SOD was determined in 38 patients with lung cancer (n = 15), malignant lymphoma (n = 11) and acute myeloid leukemia (n = 12). Patients with malignant lymphoma and acute myeloid leukemia showed a significant decrease in enzyme activity (p less than 0.01) while the patients with lung cancer (9 squamous cell carcinomas and 6 small cell carcinomas) showed a normal value of SOD activity. Furthermore, patients with malignant lymphoma and acute myeloid leukemia who were in remission and were not being treated with anticancer drugs also showed a significant decrease in SOD activity. These observations therefore indicate that a low level of erythrocyte SOD activity is related to cancer and that degree of the activities varies with the type of cancer. A total of 18 determinations of erythrocyte SOD activity were made on 16 patients with thyroidal dysfunction. Patients with hyperthyroidism showed a significant increase in SOD activity (p less than 0.01), while patients with hypothyroidism showed the same SOD activity as those of healthy subjects. A significantly high positive correlation was found between erythrocyte SOD activity and the level of thyroxine in serum (r = 0.60, p less than 0.01). The author suggests therefore that erythrocyte SOD activity has a close relationship to the state of the thyroid hormones.

Erythrocytes↗
PubMed1990

Comparison of basal serum TSH concentration by immunoradiometric assay and TRH stimulation test in the diagnosis of thyroid dysfunction.

The mean basal serum TSH (IRMA) concentrations and their increments after exogenous TRH stimulation in euthyroid subjects and patients with borderline and definite hypo or hyperthyroidism were reported. In euthyroid subjects, the increment of serum TSH (IRMA) after TRH stimulation was higher in females than in males. The measurement of basal serum TSH (IRMA) alone could discriminate euthyroid subjects from patients with thyroid dysfunction. Significant correlation between basal serum TSH (IRMA) concentrations and their corresponding increment of serum TSH (IRMA) at 30 minute after TRH stimulation in the whole group of patients was observed. Therefore, the measurement of basal serum TSH (IRMA) concentration had sufficient discriminatory value in differentiating patients with or without thyroid dysfunction and obviating the need to perform TRH stimulation test.

Adult↗
PubMed1988

The value of serum antimicrosomal antibody testing in screening for symptomatic postpartum thyroid dysfunction.

We investigated the value of a screening program for postpartum thyroiditis in a heterogeneous American population and used serum antithyroid antibodies to identify postpartum women at risk. Blood was drawn from 1034 consecutive women on their second postpartum day and tested for antimicrosomal and antithyroglobulin antibodies by hemagglutination. Seventy-two women (7.0%) were seropositive for antimicrosomal antibodies, but only seven (0.7%) had antithyroglobulin antibodies. There was a significant difference in the racial prevalence of antimicrosomal antibodies, with seropositivity in 52 of 588 white women (8.8%) versus nine of 367 black women (2.5%; p less than 0.001). Thirty-four of 51 (67%) antimicrosomal seropositive women followed at least 6 months post partum developed biochemical thyroid dysfunction and 20 of these patients required treatment for hypothyroidism. The mean (+/- SEM) serum thyroxine and thyrotropin levels in these patients before treatment were 3.0 +/- 0.3 micrograms/dl (normal 6.1 to 12.3 micrograms/dl) and 77 +/- 17 mU/L (normal 0.3 to 4.0 mU/L), respectively. Psychologic interviews revealed a significant increase in impaired concentration, carelessness, depression, and total complaints when patients with postpartum hypothyroidism were compared with postpartum euthyroid women. Medical evidence now suggests that postpartum thyroiditis is a common event and causes significant symptoms in women who develop hypothyroidism. Therefore, we propose that serum antimicrosomal antibody testing of postpartum women provides a feasible cost-effective screening method of identifying women likely to suffer from this disease.

Autoantibodies↗
PubMed1977

Thyroid dysfunction following external irradiation to the neck for Hodgkin's disease in childhood.

Thyroid function was studied in 32 patients who had received neck irradiation during childhood for Hodgkin's disease. All except one patient received a dose of 2500-3000 rad over a period of 19-25 days. In 12 patients lymphangiography was performed. Clinically all patients were considered euthyroid. One had a thyroid swelling which was cystic in nature. Five (16%) patients were biochemically hypothyroid, 17 (53%) were euthyroid with an elevated basal serum TSH concentration and a further seven (22%) were euthyroid with a normal basal serum TSH level but an augmented thyroid-stimulating hormone (TSH) response to thyrotrophin-releasing hormone (TRH). Only three (9%) patients had completely normal thyroid function tests. The basal serum TSH concentration and the peak serum TSH response to TRH were significantly greater in the patients who received neck irradiation and lymphangiography than in those who received neck irradiation alone. In addition the free thyroxine index decreased significantly as the time interval between treatment and study increased in the lymphangiography group. These data demonstrate that the normal thyroid gland is vulnerable to the damaging effects of external irradiation, and that the combination of neck irradiation and lymphangiography is more likely to result in thyroid dysfunction than is neck irradiation alone. Furthermore, in view of the deterioration in thyroid function with time, periodic clinical and biochemical assessment of thyroid function is clearly indicated.

Adolescent↗
PubMed1991

Reversible thyroid dysfunction during treatment with GM-CSF.

To investigate whether autoimmunity against thyroid antigens is induced or exacerbated by granulocyte-macrophage colony-stimulating factor, thyroid function and thyroid autoantibodies were studied in 14 patients with advanced breast cancer and 11 with soft-tissue sarcoma who received several cycles of doxorubicin and cyclophosphamide plus GM-CSF 250 micrograms/m2 intravenously daily for 10 days in every 21 day cycle. All patients had normal thyroid function before treatment. In 2 patients with pre-existing thyroid antibodies, thyroid dysfunction developed but disappeared after cessation of GM-CSF. No other autoimmune abnormalities appeared. Stimulation of antigen-presenting cells by GM-CSF may bring about this phenomenon.

Adult↗
PubMed1989

A newer avenue for evaluation of thyroid dysfunction.

Attempt has been made to rationalise the biochemical assessment of patients suspected to have thyroid dysfunction by introduction of a new rapid and supersensitive immunoradiometric assay (IRMA) for TSH. 294 patients were subjected to thyroid investigation viz; tT3, tT4 and TSH (IRMA). Of these, 51 (17.34%) were hypothyroid, 22 (7.48%) were hyperthyroid and 221 (75.1%) were euthyroid. The ratio of thyroid disorder in male to female was 1:3.38. In all patients with hyperthyroidism TSH (IRMA) was 0.05 to undetectable and it was more than 4.5 ulu/ml in hypothyroid patients. TSH (IRMA) was low in one euthyroid patient a 0.34% incidence of false negativity. In 2 patients with subclinical hyperthyroidism TSH (IRMA) was low while tT3 and tT4 were normal. TSH (IRMA) therefore may obviate the need for more time consuming and expensive TRH test and simplify the approach to thyroid function tests in patients suspected to have masked or overt hyperthyroidism.

Adolescent↗
PubMed1987

Effects of amiodarone and thyroid dysfunction on myocardial calcium, serum calcium and thyroid hormones in the rat.

1 Myocardial calcium content was found to be elevated and serum calcium reduced in hypothyroid rats. 2 Treatment of rats with amiodarone at either 30 mg kg-1 or 150 mg kg-1 daily did not result in any significant changes in myocardial or serum calcium. 3 The administration of amiodarone to hypothyroid rats attenuated the changes in serum but not myocardial calcium, suggesting that amiodarone may exert a thyroid hormone-like effect in the hypothyroid state. 4 The administration of amiodarone to thyroid hormone-treated rats resulted in attenuation of the effects on serum calcium and calculated intracellular calcium; this was consistent with an antagonistic interaction between amiodarone and thyroid hormones. 5 Administration of amiodarone resulted in significant changes in circulating thyroid hormone levels in the rat; triiodothyronine was reduced and basal thyrotrophin elevated compared to euthyroid controls. Serum thyroxine was not changed; this is in contrast to the effects in man. 6 Amiodarone does not exert its anti-arrhythmic action via changes in total myocardial calcium content in the euthyroid rat; nonetheless the described interactions between the drug and thyroid hormones may be involved in its mechanism of action.

Amiodarone↗
PubMed1989

Thioredoxin and glutaredoxin systems of rat liver cytosol are not influenced by thyroid dysfunction.

The relation of thyroid hormone status to the function of hepatic cytosolic components activating microsomal reverse triiodothyronine (rT3) 5'-monodeiodination was studied in rats. Hyperthyroidism was induced by administration of thyroxine and hypothyroidism, by thyroidectomy. The DTT-stimulated microsomal rT3 5'-monodeiodination rate was increased by 125% in hyperthyroid rats and reduced to about 30% in hypothyroid rats (when compared with euthyroid animals). Thyroid status was unrelated to NADPH-dependent activation of microsomal 5'-deiodinase by cytosol components or to cytosolic concentrations of thioredoxin and glutaredoxin, which stimulate in vitro microsomal deiodination of thyroid hormone.

Animals↗
PubMed1989

Thyroid dysfunction in Hodgkin's disease.

Radiotherapy to the neck and/or polychemotherapy late effects on the thyroid were investigated in 51 patients (34 males and 17 females) with Hodgkin's disease. Except for two untreated, recently diagnosed patients, all were studied after 1 to 105 months (median, 27.5 months) of completion of polychemotherapy. Age ranged from 6.2 to 36.6 years (median, 13.6 years). Patients were divided according to treatment into four groups: (A) patients treated with CVPP (cyclophosphamide, vinblastine, procarbazine, and prednisone); (B) 22 patients treated with CVPP plus radiotherapy (median radiation dose to the thyroid, 3000 cGy); (C) seven patients with ACOP/BVP (adriamycin, cyclophosphamide, vincristine, prednisone, bleomycin, vinblastine, procarbazine); and (D) seven patients treated with different polychemotherapy protocols, four of whom also received radiotherapy. Elevated basal and/or post-TRH, -TSH levels were found in the following: Group A: two of 12 patients (17%); Group B: 11 of 22 (50%); Group C: four of seven (57%); and Group D: two of seven (28%). Positive antimicrosomal thyroid antibody titers (AM Ab) were found in the following: Group A: three of 12 patients (25%); Group B: six of 21 (28%), Group C: two of seven (28%); and Group D: one of six (17%). Of 46 patients studied, 12 (26%) had positive AM Ab; 37 of 46 patients were younger than 20 years of age, 11 (30%) of whom had positive AM Ab versus 4% in the normal population (P less than 0.001). Two recently diagnosed, untreated patients had either high TSH response to TRH or positive AM Ab. In conclusion, higher frequency of thyroid dysfunction was observed in patients receiving radiotherapy (50% versus 27%). Prevalence of positive AM Ab, apparently unrelated to therapy, was higher in young patients than in the normal population. A predisposition to autoimmune thyroid disease seems to be present in these patients, but it is not possible to discern how lymphoma and thyroiditis are interrelated.

Adolescent↗
PubMed1989

Induction of experimental thyroid dysfunction in rats with implantable pellets of thyroxine or propylthiouracil.

Subcutaneously implanted pellets containing the thyroid hormone thyroxine or the thyrotoxic agent propylthiouracil were used to induce hyper- or hypothyroidism in rats. The results obtained were compared to those produced by daily subcutaneous injection of these substances. The thyroxine pellets caused substantial elevation of serum thyroxine concentrations for at least 25 days, whereas the propylthiouracil pellets caused a pronounced decrease of serum thyroxine concentrations. Changes in heart weight and rectal temperature were consistent with the observed alterations of serum thyroxine concentrations. Treatment with propylthiouracil was associated with small elevations of serum total protein, urea nitrogen, and creatine concentrations regardless of the method of administration of this agent. It is concluded that implantable pellets are an effective and convenient means of administering drugs for producing thyroid dysfunction in rats.

Animals↗