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PubMed1976

[Thyroid cancers masked by hyperthyroidism. 12 cases].

The main object of this report was to attract again attention to the fact that obvious hyperthyroidism does not exclude the possibility of associated thyroid carcinoma, although this is an exceptional association. The 12 cases presented here may be added to about 30 cases found in the world literature. They were observed over a period of 13 years by the same surgical team and correspond to 0,3 p. 100 of all thyroid operations, 1 p. 100 of operated cases of hyperthyroidism and 3,6 p. 100 of cases of thyroid carcinoma. Contrary to most published cases, 11 or these cases out of 12, presented, clinically, mainly as hyperthyroidism the carcinotous lesion was either palpabale clinically in the form of a very small nodule (6 cases) or totally latent and discovered operation or even on histology as in 5 cases. Hyperthyroidism produced in 3 cases the classical picture of Graves' disease, in 6 cases that of toxic nodular goiter and, in 2 cases, that of a solitary toxic adenoma. The hyperplasia and the carcinoma were always in anatomically different areas. There is no apparent physiopahtological link and the classical notion of para-neoplastic hyperthyroidism seems debatable in most cases presented here, even in the cases of diffuse hyperfunctional hyperplasia. In any case, whatever the pathogenesis of this association, its possibility should be brought to mind in a case of hyperthyroidism. Surgery should always be advised in cases of toxic adenoma and in Graves' disease when the goiter is irregular and, especially, when a nodule is found. The course and prognosis seem to be mainly dictated by the histological type and the local spread or distant spread of the carcinoma, hyperthyroidism does not aggravate seriously the prognosis.

Adult↗
PubMed1993

[Iodine-induced hyperthyroidism in urology caused by using roentgen contrast media. Risks and prevention].

The presence of functionally autonomous portions of the thyroid is a precondition for the occurrence of iodine-induced hyperthyroidism after the administration of i.v. contrast media, in the form either of latent immunogenic hyperthyroidism (Basedow's disease) or of localized or diffuse autonomy. The normal thyroid can compensate an iodine excess in multiple ways. In the malfunctioning thyroid, however, autoregulation mechanisms may fail, resulting in complicated forms of hyperthyroidism. In Germany autonomy-correlated hyperthyroidism occurs much more often than in other countries in which sufficient alimentary iodine is present. Especially in elderly patients with long-standing nodular goitres, there is an elevated risk of iodine-induced hyperthyroidism arising from thyroidal autonomy. These cases may differ from those seen in younger patients. An existing hyperthyroidism may worsen dramatically after administration of contrast media. To prevent an iodine-induced thyrotoxic crisis, contrast media should only be given to patients with latent of manifest hyperthyroidism when vital indications are present, and then only after thyrostatics have been administered. To evaluate the morphology of the renal collecting system and ureter in these cases a retrograde rather than an intravenous pyelography should be performed. When this is combined with determination of serum creatinine and creatinine clearance, functional and morphological evaluation, respectively, of the upper urinary tract are possible.

Aged↗
PubMed1996

Effect of treatment of hyperthyroidism on renal function in cats.

OBJECTIVE: To determine whether increases in BUN and serum creatinine (SCr) concentrations, which have been reported to develop after surgical bilateral thyroidectomy in hyperthyroid cats, also develop after treatment of hyperthyroidism with radioactive iodine and methimazole. DESIGN: Prospective, clinical trial. ANIMALS: 58 hyperthyroid cats. PROCEDURE: Urine specific gravity, SCr, BUN, and serum thyroxine (T4) concentrations were determined before and 30 and 90 days after treatment of hyperthyroidism with radioactive iodine, methimazole, or surgical bilateral thyroidectomy. RESULTS: Mean SCr and BUN concentrations determined 30 and 90 days after treatment were significantly higher than those measured before treatment. Mean SCr, BUN, and T4 concentrations were not different among groups before treatment or 30 and 90 days after treatment. CLINICAL IMPLICATIONS: Reduction of serum T4 concentrations after treatment of hyperthyroidism may result in azotemia in older cats with chronic renal disease. Treating azotemic hyperthyroid cats with methimazole until it can be determined whether correction of the hyperthyroid state will exacerbate the azotemia may be prudent.

Animals↗
PubMed1995

Psychiatric disturbances associated with hyperthyroidism: an analysis report of 30 cases.

BACKGROUND: Hyperthyroidism has numerous physical and mental concomitants. This study attempted to explore the clinical features, treatment and outcome of a psychiatric disturbance which developed during hyperthyroid disease. METHODS: A retrospective study was made of 30 patients, hospitalized with psychiatric disturbances and concurrent diagnoses of hyperthyroidism between January 1990 and May 1994. Data included age, sex, date of admission or consultation, age of onset of thyroid and psychiatric disorders, duration of thyroid and psychiatric disorders, psychiatric discharge diagnoses, psychiatric symptoms/signs, treatment and outcome. Follow-up investigations were done after one year. RESULTS: Among the 30 patients, 27 (90.0%) were female and 3 (10.0%) were male. The psychiatric disturbances had persisted from a few days to a decade following the presenting hyperthyroidism, with an average of seventeen months. There were 6 (20.0%) patients who were diagnosed with neurotic disorders, 11 (36.7%) with mood disorders, 8 (26.7%) with schizophrenia-like syndromes and 5 (16.7%) with delirium. The psychiatric features were variable; insomnia, irritability and anxiety most commonly occurred. Most (96.7%) of these patients accepted both antithyroid and psychotropic medication therapy. Follow-up investigations were made after one year. Twenty-six patients were analyzed, including 13 (50%) who had recovered completely, 9 (34.6%) who recovered partially, and 4 (15.4%) who showed no change in mental status. CONCLUSIONS: A variety of psychiatric features were found in the hyperthyroid patients, concomitantly with their psychiatric disturbances. Half of the patients showed a chronic or unremitting psychiatric condition after normalization of thyroid function tests. It is possible that the present psychiatric disturbances could be caused or precipitated by hyperthyroidism, or simply occur independently by chance. It is suggested a foremost benefit would be incorporation of internist and psychiatrist into the care of hyperthyroid patients with psychiatric disturbances which may improve the clinical condition.

Adolescent↗
PubMed1997

Serum angiotensin-converting enzyme and plasma atrial natriuretic peptide levels in hyperthyroid and hypothyroid rabbits.

BACKGROUND: It is known that serum angiotensin-converting enzyme (ACE), and plasma atrial natriuretic peptide (p-ANP) levels increase in hyperthyroidism. However, the precise mechanism of the effects of thyroid hormone on ANP release remains to be clarified. No study investigating serum ACE together with p-ANP levels has been performed in experimental hyperthyroid and hypothyroid rabbits. The present study was designed in order to provide additional evidence of increased ANP production and secretion in hyperthyroidism and to investigate the relationships between ANP, ACE and thyroid hormones. METHODS: Male New Zealand white rabbits (2.3-3.4 kg) were used throughout the study. Hyperthyroidism was induced by daily intraperitoneal administration of L-thyroxin (50 micrograms/100 g). Hypothyroidism was induced by daily intraperitoneal injection of propylthiouracil (2 mg/100 g body weight). Twelve days after the end of treatment, animals were sacrificed under anesthesia and blood samples were obtained from the aorta for serum ACE and thyroid hormone and p-ANP determinations. RESULTS: Serum ACE, plasma renin activity (PRA) and p-ANP were higher in hyperthyroid rabbits and lower in hypothyroid rabbits than in euthyroid rabbits. ANP concentration in atria was lower in hyperthyroid rabbits and higher in hypothyroid rabbits than in euthyroid rabbits. p-ANP, PRA and serum ACE levels were positively correlated with serum thyroxin levels. Inverse correlation was found between serum thyroxin and ANP concentration in atria (a-ANP), and between p-ANP and a-ANP. CONCLUSIONS: Our results indicate that not only p-ANP but also serum ACE activity was markedly increased in experimental hyperthyroid rabbits. It was thought that there were both direct and indirect effects of thyroxin on the release of ANP.

Animals↗
PubMed1999

[Cardiopulmonary parameters in hyperthyroidism].

BACKGROUND: Hyperthyroid patients often suffer from impaired exercise capacity with dyspnoea. Two well established, non-invasive methods were used to evaluate the influence of hyperthyroidism on cardiopulmonary function. PATIENTS AND METHODS: In 42 patients with hyperthyroidism we performed spirometry and cardiopulmonary exercise testing before and after 7 days of propranolol therapy as well as in euthyroidism. RESULTS: In hyperthyroidism reduced vital capacity and 1-second capacity were observed (95.5 +/- 2.4% vs 102.6 +/- 1.5%; p = 0.0087; 89.4 +/- 2.3% vs 95.2 +/- 2.2%; p = 0.0179). No changes showed during beta-blockade. At the anaerobic threshold reduced tidal volume and enhanced respiratory frequency were noted (1119.8 +/- 48.9 ml vs 1289.3 +/- 62.7 ml; p = 0.0227; 28.3 +/- 0.8 vs 25.4 +/- 0.9; p = 0.0012). A significant tachycardia could be shown. Impaired response to exercise in pulse and respiratory frequency were observed. Work at the anaerobic threshold was impaired in hyperthyroidism (70 +/- 5 watts vs 86.9 +/- 5.7 watts; p = 0.016) and did not change during propranolol therapy. Oxygen pulse at the anaeorbic threshold was reduced in hyperthyroidism (7.7 +/- 0.4 ml O2/beat vs 9.1 +/- 0.4 ml O2/beat; p = 0.0012) and increased with propranolol (8.9 +/- 0.4 ml O2/beat; p = 0.0001). CONCLUSION: In hyperthyroidism significant changes in cardiopulmonary function were noted at rest and exercise. High resting function and impaired response to exercise suggest a cardiopulmonary work with low efficiency. Propranolol leads to economization and lowers patients complaints.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Evidence for an active immune response in acute hyperthyroidism (Graves' disease).

Activated lymphocytes, identified by an autoradiographic labeling method, were found to be present in the peripheral blood of the majority of 20 patients with acute hyperthyroidism (Graves' disease). The number of such cells in the blood was significantly greater than that found in 30 healthy controls (p less than 0.00001), and in 13 patients who had previously suffered from acute hyperthyroidism, and who were judged to be euthyroid following therapy (p less than 0.025). This latter group included two patients in whom such activated lymphocytes had been found in the blood during the acute phase of their illness. Furthermore, there were significant differences between the number of such activated circulating lymphocytes in the group of patients with acute hyperthyroidism and five patients suffering from hyperthyroidism due to a toxic thyroid nodule (p less than 0.001), five patients suffering from primary myxedema (p less than 0.001), or in 14 patients with a nontoxic multinodular goiter (p less than 0.05). Identification and counting of circulating T and B lymphocytes by fluorescent immunolabeling and rosette-forming techniques in a small number of the patients with acute hyperthyroidism failed to reveal significant differences from the normal. The results suggest that in acute hyperthyroidism there is active stimulation of the cellular immune system, and that this effect is specific to the early, untreated phase of the disease. This response is different to other thyroid diseases, including hyperthyroidism due to a toxic thyroid nodule.

Adolescent↗
PubMed2005

Prospective screening for coeliac disease in patients with Graves' hyperthyroidism using anti-gliadin and tissue transglutaminase antibodies.

INTRODUCTION: Coeliac disease (CD) is associated with autoimmune thyroid disease (AITD) although its prevalence among those with Graves' hyperthyroidism in the UK is unknown. We determined the prevalence and evaluated the role of screening for CD prospectively in a consecutive cohort of patients with Graves' hyperthyroidism using IgA class antibodies to gliadin (AGA) and tissue transglutaminase (anti-tTG). METHODS: All patients with Graves' hyperthyroidism attending the thyroid clinic over a 9-month period were offered screening for CD using AGA (normal < 3 mg/l) and anti-tTG (normal < 15 micro/ml). Comparison was made with an age- and sex-matched healthy control group from the local population whose sera were tested for anti-tTG. In patients with borderline or raised anti-tTG (> 7 micro/ml) endomysial antibody (EmA) was measured. Serum IgA was also measured to exclude IgA deficiency. Patients with raised AGA, raised or borderline anti-tTG, positive EmA, IgA deficiency or haematinic deficiencies were offered endoscopic duodenal biopsy. RESULTS: A total of 115 patients (97 female and 18 male) with Graves' hyperthyroidism were offered screening tests and 111 accepted. AGA was raised in 15 patients, anti-tTG was raised in two (both positive for EmA) and equivocal in six (one positive for EmA). IgA deficiency was present in three. Four patients were known to have haematinic deficiencies. Twenty-five patients were invited and 19 agreed to have endoscopic duodenal biopsy. Three new patients were found to have CD while two patients were already known to have CD, thus five of 111 patients with Graves' hyperthyroidism had CD. One of 115 healthy controls had a strong positive anti-tTG (> 200 micro/ml) and EmA indicating probable CD. CONCLUSIONS: Screening 111 consecutive patients with Graves' hyperthyroidism revealed AGA in 14%, anti-tTG in 2% and IgA deficiency in 3%. Two patients were known to have CD. Screening detected three new cases. The prevalence of CD in patients with Graves' hyperthyroidism was 4.5% as compared with 0.9% in matched healthy controls. Routine screening for CD should be considered.

Adult↗
PubMed1986

Discordant hypothyroxinemia and hypertriiodothyroninemia in treated patients with hyperthyroid Graves' disease.

Hypothyroxinemia and hypertriiodothyroninemia may occur in the course of antithyroid drug or 131I treatment for hyperthyroid Graves' disease. To determine the frequency of combined high serum T3 and low serum T4 concentrations during such treatment and to assess the clinical significance of its recognition, we reviewed 60 patients treated for hyperthyroid Graves' disease with antithyroid drugs (n = 43) or radioactive iodine (n = 17). Six of these patients (10%) were found to have high serum T3 and low serum T4 concentrations during therapy. Four were receiving antithyroid drugs, and 2 had received radioactive iodine. At the time this abnormality occurred, 4 patients were euthyroid, 1 was hypothyroid, and 1 was hyperthyroid. The serum TSH concentration was increased in 2, at the upper limit of normal in 1, and undetectable in 3 patients. In 2 clinically euthyroid patients, these biochemical findings resolved spontaneously. After discontinuation or reduction in the dose of antithyroid drug, clinical and chemical euthyroidism was restored in 2 additional patients with previously elevated TSH levels. In 2 patients, both of whom previously had undetectable serum TSH levels, clinical hyperthyroidism persisted or recurred, and additional therapy was required. No patient developed permanent hypothyroidism during the period of follow-up (1-22 months). An additional 19 of the 60 patients (32%) had an elevated serum T3 level with a normal serum T4 concentration during the course of follow-up. Among these 19 patients, the magnitude of serum T3 elevation was not different between clinically euthyroid (n = 13) and hyperthyroid (n = 6) patients. We conclude that discordance of serum T4 and T3 concentrations is frequently encountered in patients with hyperthyroid Graves' disease during or after therapy. In such patients, the low serum T4 level does not predict hypothyroidism, nor does a high serum T3 level predict hyperthyroidism. Furthermore, the serum T3 concentration in these patients correlates poorly with their clinical thyroid status.

Adolescent↗
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↗