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[Influence of hyperthyroidism defined as TSH serum level on QT corrected interval dispersion (QTcd)].

BACKGROUND: Electrocardiographic dispersion reflects the heterogenity of ventricular repolarisation. It has been suggested that changes QT dispersion in thyroid dysfunction can be prognostic factor of different arrhytmias aspecially ventricular arrhytmias. Calculation can be done from easy availabe tests such as: TSH serum level and resting electrocardiogram. AIM: The aim of the present study was to evaluate the prognostic value between TSH serum level, QT corrected interval value and corrected interval dispersion value.Are there any relationship between QTcd and TSH serum level. METHODS: From 314 person with hyperthyroidism included to the study group 46 patients with isolate hyperthyroidism whom have made TSH serum leve land resting electrocardiogram. In this group was 36 (78.3%) women and 10 (21.7%) men aged 38 to 78. The medium age was 52.3 +/- 9.9 years. To the observation include the patient with TSH level below 0,4 uU/ml in sreening. The results has been analysed in two subgroups: first A (1A)--high level hyperthyroidism (25 person; 18 women (72.0%), 7 men (28%); second B(2B)--low level hyperthyroidism (21 person; 18 85.7%)women, 7 men (14.3%). RESULTS: In hyperthyroidism group (1A+1B) with TSH serum level below 0.4 uU/ml QTc dispersion increase. Relation seems to be inversely proportional. The lower TSH serum level the higher percent increasing distance of QTcd, especially in high level hyperthyroidism subgroup(1A) with TSH seru level below 0.1 uU/ml. For QTcd > or = 65 ms sensivity is 88.0%; specisicity is 42.9%. We didn't observe serious ventricular arrhytmias in the both subgroups. CONCLUSIONS: Indeed there is evidence that invesigating QT c interval dispersion (QTcd) in thyroid dysfunction may be a useful parameter in hyperthyroidism especially in high level hyperthyroidism subgroup (1A). The long QTcd suggest proarythmic susceptibility in this subjects subhyperthyroidism group with another risk stratification predicts increasing QTcd such as dyselectrolytaemia, previous myocardial infarct, coronary artery disease, diabetes, stroke or antyarrhytmic drugs.

Adult↗

Diagnosis of occult hyperthyroidism in cats.

As expertise among small animal practitioners grows, feline hyperthyroidism is being diagnosed earlier in the course of the disease. There are, in fact, a growing number of cats with clinical signs of hyperthyroidism and palpably large thyroid glands whose serum total thyroxine (T4) and triiodothyronine (T3) concentrations are within the normal or borderline range. This condition can be referred to as "occult" hyperthyroidism. Early detection and treatment of feline hyperthyroidism presents an obvious advantage in avoiding some of the deleterious effects of chronic thyroid hormone excess (eg, cardiomyopathy). Recent advances have been made in the diagnosis of occult hyperthyroidism in cats. It has been found, for instance, that serum thyroid hormone concentrations can fluctuate in and out of the normal range in some cats with hyperthyroidism. Recent work also has laid the groundwork for use of a T3 suppression test as an aid in the diagnosis of early, mild, or occult hyperthyroidism in cats. The purpose of this chapter is to discuss these and other developments, as well as to discuss some of the problems confronted in diagnosing occult hyperthyroidism in cats.

Animals↗

Adrenergic binding sites and enzyme activities in the heart of hyperthyroid rats.

In present study interactions of some adrenergic drugs with the binding of 3H-norepinephrine (NE) and response of some enzymatic systems in the heart of rats with pharmacological hyperthyroidism have been investigated. Binding of NE to cardiac particles was inhibited by isoproterenol, propranolol and in lower concentrations by another beta-blocking drug trimepranol both in control and hyperthyroid hearts in the same degree. However, after addition of nonradioactive norepinephrine (10(-3) M) the degree of displacement was lower in hyperthyroid than in euthyroid group. Activity of adenylate cyclase was lower in hyperthyroid cardiac particles. This difference remained preserved after stimulation by norepinephrine or NaF. The activities of hormone-sensitive lipase and lipoprotein lipase were increased in preparation of hyperthyroid hearts. The phosphorylase "a" activity was also increased in hyperthyroid cardiac particles. There was no change in cardiac adrenergic binding sites properties in hyperthyroidism with the exception of less displacement of NE by nonlabelled hormone. The results indicate that the increased lipolytic and phosphorylase "a" activities in hyperthyroid hearts are not necessarily linked to elevated activity of adenylate cyclase.

Adenylyl Cyclases↗

[Clinical aspects, diagnosis and drug therapy of hyperthyroidism].

Graves' disease and toxic uni- or multinodular goiter are the most frequent causes of hyperthyroidism. Graves' disease is caused by thyroid stimulating immunoglobulins which are directed against the TSH receptor of thyroid follicular cells. Graves' disease affects more females than males and is associated with diffuse goiter and a rapid appearance of symptoms and signs of hyperthyroidism. Patients with Graves' disease are on average younger than patients with toxic nodular goiter. The diagnosis of Graves' disease is usually easy, particularly if signs of endocrine opthalmopathy are present. Toxic nodular goiter is seen more often in older patients with pre-existing goiters. Symptoms and signs of hyperthyroidism often appear only slowly. Hyperthyroidism in these older patients can be oligosymptomatic. Older patients should therefore be investigated for the presence of hyperthyroidism, even if they present only a few symptoms or signs which could suggest this diagnosis. The development of ultrasensitive TSH assays has simplified the diagnosis of hyperthyroidism and made the TRH-test, often used in the past, almost superfluous. At the present time, it is practically always possible to differentiate between Graves' disease and toxic nodular goiter as the cause of hyperthyroidism on the basis of clinical and laboratory findings alone, and in many cases thyroid scintiscans are therefore no longer necessary. A patient with newly diagnosed Graves' disease is treated with antithyroid drugs (carbimazole or PTU) for one year. If hyperthyroidism persists after this one year of antithyroid drug treatment, or if it recurs, another year of therapy with carbimazole or PTU is indicated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Serum thyroxine and triiodothyronine responses of hyperthyroid cats to thyrotropin.

OBJECTIVE: To document circulating total thyroxine (T4) and triiodothyronine (T3) responses after administration of thyrotropin (thyroid-stimulating hormone [TSH]) to hyperthyroid and healthy cats and assess the value of these responses as an additional diagnostic test for hyperthyroidism. DESIGN: Prospective case series. ANIMALS: 21 healthy and 40 hyperthyroid cats. PROCEDURES: Serum total T4 and T3 concentrations were measured by radioimmunoassay before and 6 hours after administration of 0.5 IU of bovine TSH/kg of body weight. RESULTS: In healthy cats, serum total T4 concentration increased after administration of TSH (mean +/- SD, 114.0 +/- 36.4 nmol/L) representing a mean increment 3 times baseline concentration (mean +/- SD, 33.7 +/- 7.6 nmol/L). In hyperthyroid cats, the relative increase in serum total T4 concentration was significantly (P < 0.001) different; baseline values (mean +/- SD, 236.2 +/- 146.0 nmol/L) increased minimally after TSH administration (mean +/- SD, 308.1 +/- 178.9 nmol/L) There was a significant negative correlation (rs = -0.366) between relative increase in serum total T4 concentration after TSH administration and baseline concentration in hyperthyroid cats. In 3 cats with equivocal baseline serum total T4 concentration, the T4 response to TSH administration was indistinguishable from that in healthy cats. Serum total T3 response to TSH administration was significantly (P < 0.001) lower in hyperthyroid, compared with healthy, cats but the T3 response in healthy cats was more variable than that for T4 CONCLUSIONS: Thyrotoxic cats with high baseline serum total T4 concentration have a limited T4 response to TSH stimulation. Hyperthyroid cats with equivocal baseline serum total T4 concentrations have T4 response after TSH stimulation similar to those of healthy cats. Measurement of serum total T3 concentration provides no additional information. CLINICAL RELEVANCE: The TSH response test is of limited value in diagnosing hyperthyroidism in cats.

Animals↗

Congenital nonautoimmune hyperthyroidism in a nonidentical twin caused by a sporadic germline mutation in the thyrotropin receptor gene.

Congenital hyperthyroidism is usually caused by maternal-to-fetal transfer of thyroid-stimulating antibodies from a mother with autoimmune thyroid disease. Very recently, activating thyrotropin (TSH) receptor germline mutations were detected in a few patients with sporadic nonautoimmune congenital hyperthyroidism, as well as in familial forms of nonautoimmune hyperthyroidism defining a new pathophysiological entity of hyperthyroidism. In this report, we describe a nonidentical twin girl with severe congenital hyperthyroidism. The twin brother and the mother were euthyroid. Skull radiographs revealed premature synostosis of the sagittal sutures. Hyperthyroidism was inadequately controlled with antithyroid drugs and radioiodine therapy. After a near-total thyroidectomy performed at age 3, the patient became hypothyroid and required thyroid hormone replacement. At age 14, hyperthyroidism recurred. A hyperplastic remnant of the right upper lobe was removed surgically, resulting in euthyroidism. Over the following years, thyroid hormone levels increased gradually and at age 19 she was again hyperthyroid. There was no clinical or biochemical evidence of an autoimmune process. The patient's neurologic development was impaired and her intelligence is subnormal. Direct sequencing of the TSH receptor gene revealed a heterozygous mutation resulting in a substitution of threonine632 by isoleucine in the sixth transmembrane segment, an amino acid change known to result in constitutive activation of the cyclic adenosine monophosphate (cAMP) pathway. The mutation was absent in the parents and the twin brother, indicating a de novo germline mutation. Early recognition of this disorder is important because of the resistance to standard treatment, special therapeutic implications, and the possibility of familial transmission.

Child↗

TSH receptor-adenovirus-induced Graves' hyperthyroidism is attenuated in both interferon-gamma and interleukin-4 knockout mice; implications for the Th1/Th2 paradigm.

The role of the Th1/Th2 balance in the pathogenesis of murine Graves' hyperthyroidism is controversial. In BALB/c mice injected with adenovirus expressing TSH receptor (TSHR-adeno model), we found that suppression of TSHR-specific Th1 immune responses by exogenous interleukin-4 (IL-4), alpha-galactosylceramide or helminth (Schistosoma mansoni) infection was associated with inhibition of hyperthyroidism, indicating the critical role for Th1 cytokines. In contrast, BALB/c IL-4 knockout (KO), but not interferon-gamma (IFN-gamma) KO mice failed to develop Graves' hyperthyroidism when injected with TSHR-expressing M12 B lymphoma cells (TSHR-M12 model), suggesting the importance of Th2 cytokine IL-4. To reconcile differences in these two models, we used IL-4 KO and IFN-gamma KO BALB/c mice in the TSHR-adeno model. Unlike wild-type (wt) BALB/c mice in which 60% developed hyperthyroidism, only 13 and 7% of IL-4 KO and IFN-gamma KO mice, respectively, became hyperthyroid. Thyroid stimulating antibodies were positive in most hyperthyroid mice. TSHR antibody titres determined by TSH binding inhibition and ELISA were comparable in all three groups. IgG1 and IgG2a TSHR antibody titres were similar in IFN-gamma KO and wt mice, whereas IgG1 TSHR antibody titres and TSHR-specific splenocyte IFN-gamma secretion were lower in IL-4 KO than in IFN-gamma KO and wt mice, respectively. Our results clearly implicate both IFN-gamma and IL-4 in development of hyperthyroidism in the TSHR-adeno model. These data, together with the previous report, also indicate different cytokine requirements in these two Graves' models, with IFN-gamma being more important in the TSHR-adeno than the TSHR-M12 model. Moreover, our previous and present observations indicate a difference in the role of exogenous versus endogenous IL-4 in TSHR-adenovirus induced Graves' hyperthyroidism.

Adenoviridae↗

Comprehensive study of urinary cortisol metabolites in hyperthyroid and hypothyroid patients.

OBJECTIVE: To further analyse the significance and mutual relationship of thyroid function-linked alterations in cortisol metabolism that have been separately and variously reported. PATIENTS AND MEASUREMENTS: Twenty-four-hour urine samples from 21 patients with hyperthyroidism (Graves' disease), 16 patients with hypothyroidism (Hashimoto's thyroiditis), 21 healthy age- and sex-matched controls for hyperthyroidism, and 16 healthy age- and sex-matched controls for hypothyroidism were evaluated for 6beta-hydroxycortisol (6beta-OHF), tetrahydrocortisol (THF), tetrahydrocortisone (THE), allo-tetrahydrocortisol (allo-THF), urinary free cortisol (UFF), urinary free cortisone (UFE) and 17-hydroxycorticosteroid (17-OHCS). RESULTS: Urinary 17-OHCS, THE and allo-THF levels increased considerably in hyperthyroid patients compared to the controls, while UFF and THF showed no difference between the two groups. Urinary 6beta-OHF was significantly lower in the hyperthyroid patients than in the controls. Both the urinary allo-THF + THF/THE and the UFF/UFE ratios were significantly lower in the hyperthyroid patients than in the controls, whereas only the former was significantly higher in the hypothyroid patients than in the controls. The urinary allo-THF/THF ratio was significantly higher in the hyperthyroid patients and significantly lower in the hypothyroid patients than in the controls. In an analysis of pooled subjects including all groups (n = 64), free T4 levels correlated negatively (P < 0.0001) with the urinary allo-THF + THF/THE ratio but not with the UFF/UFE ratio. The serum levels of free T4 correlated positively (P < 0.0001) with the urinary allo-THF/THF ratio. CONCLUSION: The thyroid hormones seem to affect the total 11beta-HSD activity (allo-THF + THF/THE) more strongly than the renal 11beta-HSD2 activity (UFF/UFE). 5alpha-reductase activity (allo-THF/THF) is also enhanced in hyperthyroidism, while the reduction of urinary 6beta-OHF in hyperthyroidism might be a secondary effect of the altered activity of the total 11beta-HSD and 5alpha-reductase.

17-Hydroxycorticosteroids↗

Susceptibility rather than resistance to hyperthyroidism is dominant in a thyrotropin receptor adenovirus-induced animal model of Graves' disease as revealed by BALB/c-C57BL/6 hybrid mice.

We investigated why TSH receptor (TSHR) adenovirus immunization induces hyperthyroidism more commonly in BALB/c than in C57BL/6 mice. Recent modifications of the adenovirus model suggested that using adenovirus expressing the TSHR A subunit (A-subunit-Ad), rather than the full-length TSHR, and injecting fewer viral particles would increase the frequency of hyperthyroidism in C57BL/6 mice. This hypothesis was not fulfilled; 65% of BALB/c but only 5% of C57BL/6 mice developed hyperthyroidism. TSH binding inhibitory antibody titers were similar in each strain. Functional TSHR antibody measurements provided a better indication for this strain difference. Whereas thyroid-stimulating antibody activity was higher in C57BL/6 than BALB/c mice, TSH blocking antibody activity was more potent in hyperthyroid-resistant C57BL/6 mice. F(1) hybrids (BALB/c x C57BL/6) responded to A-subunit-Ad immunization with hyperthyroidism and TSHR antibody profiles similar to those of the hyperthyroid-susceptible parental BALB/c strain. In contrast, ELISA of TSHR antibodies revealed that the IgG subclass distribution in the F(1) mice resembled the disease-resistant C57BL/6 parental strain. Because the IgG subclass distribution is dependent on the T helper 1/T helper 2 cytokine balance, this paradigm can likely be excluded as an explanation for susceptibility to hyperthyroidism. In summary, our data for BALB/c, C57BL/6, and F(1) strains suggest that BALB/c mice carry a dominant gene(s) for susceptibility to induction of a thyroid-stimulating antibody/TSH blocking antibody balance that results in hyperthyroidism. Study of this genetic influence will provide useful information on potential candidate genes in human Graves' disease.

Adenoviridae↗

Serum antibodies against the flavoprotein subunit of succinate dehydrogenase are sensitive markers of eye muscle autoimmunity in patients with Graves' hyperthyroidism.

Thyroid-associated ophthalmopathy is an autoimmune disorder of the extraocular muscles and orbital connective tissue, which is usually associated with Graves' hyperthyroidism. Well-studied markers of ophthalmopathy are eye muscle membrane antigens, reportedly of approximately 64-kDa molecular mass. One, originally identified only as the 64-kDa protein, has recently been shown to be the flavoprotein (Fp) subunit of mitochondrial succinate dehydrogenase, which has a correct molecular mass of 67 kDa. We have used purified beef heart Fp as antigen in an enzyme-linked immunosorbent assay for cross-reactive human autoantibodies. Sera have been screened from patients with thyroid-associated ophthalmopathy classified according to activity and presence or not of eye muscle disease, and from those with Graves' hyperthyroidism without eye involvement. Also examined were serum samples taken periodically from 20 patients with Graves' hyperthyroidism during 24 months of treatment of their hyperthyroidism with antithyroid drugs. Four of these patients had ophthalmopathy at the onset, 12 developed ophthalmopathy, and 4 did not develop any eye signs during treatment. Anti-Fp subunit antibodies were detected in 73% of patients with active ophthalmopathy and evidence of eye muscle involvement but only in 25% if there was only congestive ophthalmopathy. These values were 0% and 11% for patients with chronic ophthalmopathy, with or without eye muscle dysfunction, respectively. The antibodies were also detected in 14% of patients with Graves' hyperthyroidism without evident ophthalmopathy, 11% of patients with nonimmunologic thyroid disorders, 12% of type I diabetics, and 12% of age- and sex-matched normal subjects. Significantly, appearance of anti-Fp antibodies predicted the development of ophthalmopathy in 5 of the 6 patients with Graves' hyperthyroidism, who developed eye muscle dysfunction after treatment of the hyperthyroidism, and coincided with the onset of eye muscle signs in the other patient. Antibodies were not detected in any of 6 patients who developed congestive ophthalmopathy without evidence of eye muscle damage or in 4 patients who did not develop any eye signs. In conclusion, we have shown a close relationship between eye muscle disease and serum antibodies against the Fp subunit of succinate dehydrogenase in patients with Graves' hyperthyroidism.

Adult↗

A novel murine model of Graves' hyperthyroidism with intramuscular injection of adenovirus expressing the thyrotropin receptor.

In this work we report a novel method to efficiently induce a murine model of Graves' hyperthyroidism. Inbred mice of different strains were immunized by i.m. injection with adenovirus expressing thyrotropin receptor (TSHR) or beta-galactosidase (1 x 10(11) particles/mouse, three times at 3-wk intervals) and followed up to 8 wk after the third immunization. Fifty-five percent of female and 33% of male BALB/c (H-2(d)) and 25% of female C57BL/6 (H-2(b)) mice developed Graves'-like hyperthyroidism with elevated serum thyroxine (T(4)) levels and positive anti-TSHR autoantibodies with thyroid-stimulating Ig (TSI) and TSH-binding inhibiting Ig (TBII) activities. In contrast, none of female CBA/J (H-2(k)), DBA/1J (H-2(q)), or SJL/J (H-2(s)) mice developed Graves' hyperthyroidism or anti-TSHR autoantibodies except SJL/J, which showed strong TBII activities. There was a significant positive correlation between TSI values and T(4) levels, but the correlations between T(4) and TBII and between TSI and TBII were very weak. TSI activities in sera from hyperthyroid mice measured with some chimeric TSH/lutropin receptors suggested that their epitope(s) on TSHR appeared similar to those in patients with Graves' disease. The thyroid glands from hyperthyroid mice displayed diffuse enlargement with hypertrophy and hypercellularity of follicular epithelia with occasional protrusion into the follicular lumen, characteristics of Graves' hyperthyroidism. Decreased amounts of colloid were also observed. However, there was no inflammatory cell infiltration. Furthermore, extraocular muscles from hyperthyroid mice were normal. Thus, the highly efficient means that we now report to induce Graves' hyperthyroidism in mice will be very useful for studying the pathogenesis of autoimmunity in Graves' disease.

Adenoviridae↗

The incidence of hyperthyroidism in patients with thyroid cancer in an area of iodine deficiency.

BACKGROUND: The incidence of hyperthyroidism among thyroid malignancy varies greatly depending on the geographical area and iodine intake. The aim of the study was to evaluate the association of hyperthyroidism and thyroid cancer (TC) in an iodine deficient area. PATIENTS AND METHODS: Medical records of 422 patients who underwent operation for TC between 1992 and 2000 in Ankara Oncology Hospital were reviewed. The characteristics of TC patients with hyperthyroidism were analyzed in respect to gender, age, histopathological type, thyroid function status, tumor size, extrathyroidal invasion, local recurrences, distant metastasis, AMES and MACIS scoring. RESULTS: In the present patient series, among 422 patients with TC, hyperthyroidism was found in 12 patients (2.8%). None of the patients had Graves' disease. Of 12 patients with hyperthyroidism, 9 patients had papillary carcinoma, 1 patient had follicular carcinoma and 2 patients had follicular variant of papillary carcinoma. The tumor was in the active nodule in 5 patients. CONCLUSION: The existence of hyperthyroidism among patients with differentiated TC is a clinical entity. Patients with hyperthyroidism and nodules require a careful approach in order to establish or exclude the possibility of TC especially in formerly iodine deficient areas.

Adenocarcinoma, Follicular↗

Pharmacokinetics of propranolol and sotalol in hyperthyroidism.

The elimination and bioavailability of two beta-blocking agents, propranolol and sotalol, were studied in 10 thyrotoxic patients, both before and after treatment with iodine-131. Each subject received in random order propranolol 160 mg and sotalol 160 mg as single oral doses both while hyperthyroid and after euthyroidism had been achieved. The pharmacokinetics of sotalol was not affected by hyperthyroidism, whereas serum propranolol concentrations were significantly lower during hyperthyroidism than in the euthyroid state. During hyperthyroidism, the bioavailability of propranolol was significantly reduced (p less than 0.05) and its clearance was increased (p less than 0.005), whereas there was no difference in its serum t 1/2. This indicates that the bioavailability of propranolol in hyperthyroidism is reduced by a mechanism which may depend on increased first-pass metabolism in the liver, or on an increased distribution volume of the drug. Both propranolol and sotalol caused a slight decrease in serum tri-iodothyronine concentration. As the effects of beta-blocking agents on the symptoms of hyperthyroidism are correlated with the serum concentration of the drugs, sotalol, with its long half-life and unaltered elimination in hyperthyroidism, has certain advantages over propranolol in the treatment of thyrotoxicosis.

Adult↗

The effect of hyperthyroidism on gastric emptying rates and pancreatic exocrine and biliary secretion in man.

Malabsorption and diarrhea in hyperthyroidism has been attributed in part to an increased rate of gastrointestinal transit as measured with barium sulfate suspension. Data are unavailable on the effect of hyperthyroidism on gastric emptying rates of normal food and pancreatic enzyme secretion. These functions have been studied in 4 hyperthyroid patients and compared to results obtained when treatment achieved euthyroidism. Pancreatic trypsin secretion was half the euthyroid level in the hyperthyroid state. No significant change in bile salts occurred, although there was a tendency for a greater proportion of dihydroxy bile salts while hyperthyroid. Gastric emptying rates of a mixed fat, protein, and carbohydrate liquid meal were normal. Similarly the gastric emptying rate of a beef stew plus chicken liver meal was normal. We conclude that in hyperthyroidism gastric emptying rates of "physiologically active" food is normal. Pancreatic enzyme secretion is depressed in hyperthyroidism and may contribute to maldigestion.

Adolescent↗

[Correlation of "latent hyperthyroidism" with psychological and somatic changes].

The study reported here was undertaken to establish the degree to which a person in a preclinical state of hyperthyroidism, with (by definition) euthyroid T3 and T4 levels but suppressed TRH on testing, already exhibits psychological changes and clinical symptoms. Two groups of 20 patients each, with clear clinical and preclinical hyperthyroidism (as defined by laboratory parameters), were studied, as well as a group of 20 controls. The subjects' psychological state of mind was investigated using self-rating scales, including the state-trait-anxiety inventory (STAI), "Befindlichkeits"-Skala (Bf-S'), depression scale (D-S'), and a list of adjectives (EWL-K) with 14 different aspects of affective moods. Cognitive achievements were evaluated using the d2 test. Subjects were examined for somatic symptoms in accordance with Crooks' index of hyperthyroidism. The results clearly showed that typical psychological and somatic changes are already present in preclinical hyperthyroidism, these changes being partly identical with those of definite hyperthyroidism. In both patient groups, a significant increase in anxiety, a sense of not feeling well, and emotional irritability were found, as well as a tendency towards depressiveness, and an increased lack of vitality and activity. Attentiveness and concentration in both patient groups were lower than in the control group. Both patient groups showed the same prevalence of symptoms, such as palpitations, preference of cold over heat, excessive sweating, nervousness, fine digital tremor, and increased heart rate. With regard to the results, the diagnosis "preclinical hyperthyroidism" thus gains importance. Further prospective studies are required to answer the question whether antithyroidal treatment will influence the described psychological and somatic state of patients with preclinical hyperthyroidism.

Adult↗

Management of recurrent hyperthyroidism in patients with Graves' disease treated by subtotal thyroidectomy.

If the aim of surgical treatment for Graves' disease is not permanent hypothyroidism, it is difficult to avoid recurrent hyperthyroidism completely. The management of recurrent hyperthyroidism, however, is neither easy nor obvious. Improvement in the sensitivity of TSH assay has allowed the diagnosis of latent hyperthyroidism. Little is known about the clinical course of latent hyperthyroidism. We studied the management and outcome of recurrent hyperthyroidism in patients with Graves' disease treated by subtotal thyroidectomy. Between January 1988 and August 1991, 1115 patients with Graves' disease were treated by surgery. Postoperative thyroid function was evaluated by free T3, free T4 and TSH measurements. One hundred seventy-five patients with suppressed TSH secretion for at least 6 months were categorized as having recurrent hyperthyroidism. Eighty patients (45.1%) also had elevated thyroid hormone levels, (group 1). The remaining 95 patients (54.9%) had normal thyroid hormone levels with suppressed TSH values (group 2). In group 1, 58 patients were treated with antithyroid drug (ATD), 12 with iodine and 10 with radioiodine (RI). Remission of Graves' disease was obtained in 22 patients (11 by ATD, 1 by iodine and 10 by Ri). On the other hand, patients in group 2 were followed up without medication, and spontaneous remission was observed in 21 of theln (22.1%). It was difficult to induce remission of overt recurrent Graves' disease by ATD or iodine. In contrast spontaneous remission could be obtained in some patients with postoperative latent hyperthyroidism.

Adolescent↗

Sympathovagal response to orthostatism in overt and in subclinical hyperthyroidism.

Heart rate variability (HRV) is a measure of the physiological variation of R-R intervals, reflecting the sympathovagal balance. In both overt and subclinical hyperthyroidism, a relative increase in sympathetic activity has been demonstrated, mainly due to a decrease in vagal activity. The modifications of HRV during orthostatism in normal subjects resemble those seen in hyperthyroidism. We have studied the response of 19 patients with overt hyperthyroidism and 12 with subclinical hyperthyroidism during orthostatism using HRV and compared the results to those of 32 healthy controls. In the three groups, the R-R intervals decreased in the same proportion after orthostatism. The low frequency power (LF)/[LF + high frequency power (HF)] ratio, which reflects the sympathetic tone, also increased in the same proportion in the three groups. However, the mechanisms of the modulation of the sympathovagal balance during orthostatism were different among the three groups. In controls, the relative increase of sympathetic tone after orthostatism was due principally to a decrease in vagal tone (reflected by decreased power in the HF band), while in overt hyperthyroidism, where the power in the HF band was already minimal in the lying position, there was a clear increase in the LF band power during orthostatism. The results were intermediate in the subclinical hyperthyroidism group, reflecting a continuum of effects of the thyroid hormone excess on the autonomic nervous system. Our study shows that despite an apparent normal cardiovascular adaptation to orthostatism in hyperthyroidism, the modulation of the autonomic nervous system is profoundly modified.

Adult↗

Hyperthyroidism after surgery for primary hyperparathyroidism.

BACKGROUND: The coexistence of hyperthyroidism and primary hyperparathyroidism (pHPT) has been reported. We have questioned whether hypercalcemia or surgical trauma contribute to transient hyperthyroidism following parathyroid surgery. METHODS: Twenty-six pHPT and eleven breast cancer patients were compared regarding pre-, peri- and postoperative thyrotropin (TSH), free thyroxine (T4) and free triiodothyronine (T3) concentrations. Thyroglobulin concentration, occurrence of autonomous thyroid nodules, and variables reflecting surgical trauma were compared in pHPT patients with and without postoperative hyperthyroidism. RESULTS: Postoperatively, eleven pHPT patients demonstrated T4 and T3 concentrations above normal, and nine developed symptoms of mild thyrotoxicosis. A parallel rise in TSH and T4 concentrations was seen during both parathyroid and breast cancer surgery. Compared with patients with no postoperative hyperthyroidism, patients with postoperative hyperthyroidism showed a parallel rise in mean thyroglobulin and T4/T3 concentrations as well as higher thyroglobulin concentrations. However, there was no difference in variables assessing surgical trauma nor in occurrence of autonomous thyroid nodules. The peri-operative rise in TSH was preceded by a decrease in calcium. CONCLUSION: Transient hyperthyroidism after parathyroid surgery is not infrequent. The condition seems to be self-limiting, since symptoms invariably subsided without treatment. Manipulation of the thyroid gland is most likely the major contributing factor to postoperative hyperthyroidism. However, it may not be the sole explanation, since our data suggest a more multifactorial scenario.

Aged↗