Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hyperthyroidism”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,063 records · Page 59Linked to original sources
PubMed1993

Comparison of direct versus indirect determination of zinc concentration in erythrocytes in euthyroid and hyperthyroid subjects.

Zinc concentration in erythrocytes is a suitable marker of peripheral tissue response to thyroid hormones. Therefore, the determination of erythrocyte zinc concentration has become an important marker for duration of preexisting hyperthyroidism in the clinical laboratory. We compared a new indirect erythrocyte zinc determination method with a commonly used direct method in 42 euthyroid and 14 hyperthyroid subjects. Zinc concentrations (median and range) obtained by direct and indirect methods were 172.8 (134.4-241.1) and 176.8 (143-243.9) mumol/l erythrocytes in the euthyroid group and 117.1 (71-141.9) and 118.5 (73-137) mumol/l erythrocytes in the hyperthyroid group. Values measured by the indirect method were slightly higher in both groups. Regression analysis showed a good correlation (r = 0.967, p = 0.0001). The influence of the anticoagulants, potassium EDTA and heparin, on erythrocyte and plasma zinc values was studied, and zinc concentrations in serum and plasma were compared. No statistically significant differences were found. Thus, the indirect determination of erythrocyte zinc concentration is a simple and rapid technique well suited for use in clinical laboratory work, yielding accurate and reliable results. For the indirect method reference concentrations were established in a collective of 102 thyroid healthy subjects. An erythrocyte zinc concentration of 176.3 +/- 23.9 mumol/l (mean +/- SD) was found with a cut-off limit of 138 mumol/l to hyperthyroidism.

Biomarkers↗
PubMed1998

Biochemical evaluation of oxidative stress in propylthiouracil treated hyperthyroid patients. Effects of vitamin C supplementation.

In this study the impact of vitamin C supplementation on oxidative damage as assessed by thiobarbituric acid reactive substances and markers of antioxidant status: namely Cu/Zn superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione were investigated in 24 hyperthyroid patients under propylthiouracil therapy (3x100 mg/day) for five days and in 15 healthy controls. Ascorbic acid (1000 mg/day) was given as a supplement for 1 month to both the patients and controls during the study period. Heparinised blood samples were taken at the beginning and the end of one month ascorbic acid supplementation. Comparison of the hyperthyroid patients with the controls revealed higher lipid peroxidation (p<0.001), higher Cu/Zn superoxide dismutase activity (p<0.001), higher glutathione level (p<0.001) and lower glutathione reductase activity (p<0.001). Vitamin C supplementation to hyperthyroid patients caused significant increases in glutathione concentration (p<0.001) and glutathione peroxidase activity (p<0.001), whereas there were significant decreases in glutathione reductase (p<0.001) and Cu/Zn superoxide dismutase activities (p<0.01). Thiobarbituric acid reactive substances and thiobarbituric acid reactive substances/glutathione ratio were significantly decreased (p<0.01). Vitamin C supplementation to euthyroid controls caused significant increases in glutathione concentration (p<0.001) and glutathione peroxidase and Cu/Zn superoxide dismutase activities (p<0.001), whereas there was a significant decrease in glutathione reductase (p<0.001). The thiobarbituric acid reactive substances/glutathione ratio was significantly decreased (p<0.05). Our findings reveal the potentiation of antioxidant status and a relief in oxidative stress in both propylthiouracil treated hyperthyroid patients and controls in response to vitamin C supplementation.

Adult↗
PubMed1977

Decreased parathyroid function in hyperthyroidism: interrelationships between serum parathyroid hormone, calcium-phosphorus metabolism and thyroid function.

Serum immunoreactive parathyroid hormone (S-iPTH) was measured together with serum and urinary calcium and phosphorus in 45 hyperthyroid patients in order to assess parathyroid fe of hyperthyroidism. The prevalence of hypercalcaemia was 51.1% using serum calcium values corrected for individual variations in serum albumin concentration compared to 15.6% using the uncorrected calcium values. S-iPTH was decreased and inversely correlated to serum calcium values. S-iPTH was decreased and inversely correlated to serum calcium (corrected). Subnormal levels of S-iPTH were found in 28.9% of the patients. The urinary excretion of calcium and phosphorus was increased and positively correlated to the degree of hyperthyroidism. The tubular reabsorption of calcium (TRCa%) was decreased, positively correlated to S-iPTH and inversely correlated to serum calcium. Increased mobilisation of bone mineral in hyperthyroidism is suggested mainly to be responsible for the elevated serarathyroid function.

Adolescent↗
PubMed1977

Bone changes in hyperthyroidism: interrelationships between bone morphometry, thyroid function and calcium-phosphorus metabolism.

Iliac-crest biopsies were obtained from 40 untreated hyperthyroid patients after double-labelling with tetracycline. Histomorphometric analyses were performed on undecalcified and decalcified bone sections. The morphometric and chemical data were compared with those in normal control groups and the results of the morphometric analyses were related to thyroid function and to chemical quantities of calcium-phosphorus metabolism. The bone turn-over was increased in the hyperthyroid patients with an increase both in bone resorption and bone formation. Serum alkaline phosphphatase was increased and positively correlated to the amount of osteoid and to the extent of tetracycline-labelled surfaces. The osteoclastic resorption was positively and the bone formation inversely correlated to thyroid activity. This might explain the reduced amount of trabecular bone found in hyperthyroidism. The most striking feature was, however, a pronounced increase in osteoclastic activity in cortical bone followed by increased porosity. The osteoclastic resorption in cortical bone was positively correlated to serum concentrations and urinary excretions of calcium and phosphorus. This indicates that increased cortical osteoclastic resorption is mainly responsible for bone mineral mobilisation in hyperthyroidism.

Adolescent↗
PubMed1981

The disappearance of L-thyroxine and triiodothyronine from plasma and red and white skeletal muscle after administration of one sc dose of L-thyroxine to hyperthyroid and euthyroid rats.

Rats were made hyperthyroid by repeated sc injections of L-thyroxine (T4) in a two-week period. At several time-points after the last injection, the triiodothyronine (T3) and T4 concentrations in plasma and red and white skeletal muscle were determined by a radioimmunoassay. This was done to investigate the relationship between the change in thyroid-hormone concentration in plasma and muscle and to see whether this change was similar in both muscle types. The results show that: 1. Information about the T3 and T4 concentrations in the muscles of the hyperthyroid rats can only be obtained by direct measurement in the muscles and cannot be gathered from the plasma-T3 concentration at any time-point or from below-normal plasma-T4 concentrations. 2. In hyperthyroid rats T4 and T3 are cleared more rapidly from the plasma than from the skeletal muscle. 3. A proportionally higher T3 concentrations is present in the red compared with the white skeletal muscle of hyperthyroid rats.

Animals↗
PubMed1985

Elevated metabolic clearance rate of 1 alpha,25-dihydroxyvitamin D3 in hyperthyroidism.

Metabolic clearance rate (MCR) and daily production rate (DPR) of 1 alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3) were measured in 7 hyperthyroid patients and 8 control subjects after a single injection of tritiated 1,25(OH)2D3. Using a bicompartmental analysis, MCR of 1,25(OH)2D3 was found to be significantly higher in hyperthyroid than in control subjects (11.5 +/- 4.4 vs 5.9 +/- 2.4 ml/min (SD), P less than 0.01). No significant difference in plasma 1,25(OH)2D and DPR of 1,25(OH)2D3 was demonstrated. MCR was again measured 1 month after initiation of treatment in 4 hyperthyroid patients and remained elevated. In 2 of these patients, MCR was once more determined 6 months later and had declined towards normal. No correlation was found between MCR and DPR and either plasma calcium, phosphate, immunoreactive PTH, 1,25(OH)D and T3 values. In conclusion, MCR of 1,25(OH)2D3 is elevated in hyperthyroidism, but this finding is probably unrelated to the effect of thyroid hormones on bone metabolism.

Adult↗
PubMed1985

Altered plasma catecholamines and numbers of alpha- and beta-adrenergic receptors in platelets and leucocytes in hyperthyroid patients normalized under antithyroid treatment.

We measured plasma catecholamines, alpha- and beta-adrenoreceptor numbers and the accumulation of cyclic adenosine monophosphate (cAMP) in the unstimulated state and in response to 10 mumol/l (-) isoproterenol in blood cells from 29 euthyroid controls and from 18 patients with spontaneous hyperthyroidism. In the thyrotoxic patients plasma norepinephrine (1.14 +/- 0.5 nmol/l) and epinephrine (0.3 +/- 0.14 nmol/l) were significantly decreased compared with plasma norepinephrine (1.87 +/- 0.7 nmol) and epinephrine (0.41 +/- 0.19 nmol/l) in the controls (P less than 0.01 and P less than 0.05, respectively) and the values obtained in subjects rendered euthyroid by antithyroid treatment (P less than 0.001, respectively). alpha-adrenoceptor density in platelet membranes obtained from patients in the hyperthyroid state (114 +/- 38 sites per cell) was significantly decreased when compared with controls (159 +/- 48 sites per cell, P less than 0.01) and the values from patients under effective antithyroid treatment (136 +/- 35 sites per cell, P less than 0.01). On the contrary, a significant increase in beta-adrenoceptor density in mononuclear leucocyte (MNL) membranes was found in hyperthyroid patients (1751 +/- 237 sites/cell) when compared with controls (1510 +/- 351 sites/cell, P less than 0.05) and the same patients following antithyroid treatment (1455 +/- 260 sites/cell, P less than 0.001). The equilibrium dissociation constants (KD) did not change in hyperthyroidism. Basal cAMP concentrations in MNL were higher in untreated thyrotoxicosis (45 +/- 18 pmol/10(6) cells/10 min) than in patients in the euthyroid state (35 +/- 9 pmol/10(6) cells/10 min, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1986

Plasma somatostatin is elevated in primary hypothyroidism compared with hyperthyroidism.

Increased pancreatic somatostatin (somatotrophin release inhibiting factor (SRIF) has been found in hypothyroid rats. Therefore, we wanted to investigate plasma SRIF in patients with hypo- and hyperthyroidism. Two groups of patients, 7 cases with autoimmune hypothyroidism, 31-75 years old, and 7 cases with Graves' disease, 19-43 years old, were compared with regard to plasma SRIF before, during and after an arginine infusion (0.5 g/kg/20 min). None of the patients suffered from diabetes mellitus or obesity. Plasma SRIF was higher in the hypothyroid patients (mean basal value 21.5 +/- 3.9, peak value 28.7 +/- 5.1 pmol/l) compared with the hyperthyroid group (mean basal value 11.6 +/- 3.3, peak value 16.2 +/- 4.0 pmol/l). The hypothyroid group also had significantly higher serum insulin values during arginine stimulation. No difference was found in plasma glucagon, serum growth hormone (GH) or blood glucose. In conclusion, plasma SRIF is elevated in primary hypothyroidism compared with hyperthyroidism. The reason for this finding is uncertain, but a reduced SRIF clearance is a possible explanation. The association of our findings with the reduced glucose tolerance in hyperthyroidism is discussed.

Adult↗
PubMed1988

The circadian rhythm of melatonin in hypothyroidism and hyperthyroidism.

UNLABELLED: In order to determine the influence of thyroid function on the pineal gland in humans, the circadian rhythm of the serum melatonin concentration was estimated in 16 women with thyroid disorders: 8 with hypothyroidism and 8 with hyperthyroidism, as well as in 5 healthy controls. A significant melatonin circadian rhythm was observed in all the three groups studied. The melatonin rhythm parameters derived from cosinor analysis: mesor (controls: 0.163 +/- 0.03 nmol/l (+/- SEM), hypothyroid patients: 0.176 +/- 0.22 nmol/l, and hyperthyroid patients: 0.167 +/- 0.04 nmol), amplitude (0.155, 0.145 and 0.138 nmol/l, respectively), acrophase (1:38, 2:22 and 1:51 h, respectively) did not differ significantly in the three groups studied. Integrated 24-h melatonin secretion was also similar in patients and controls. The melatonin concentrations were positively correlated with TSH levels in hypothyroidism, and negatively correlated with T3 in hyperthyroidism. IN CONCLUSION: in patients with hypo- and hyperthyroidism the circadian rhythm of melatonin secretion is not altered.

Adult↗
PubMed2002

Nitric oxide synthase activity in hyperthyroid and hypothyroid rats.

OBJECTIVE: Thyroid disorders are accompanied by important changes in haemodynamic and cardiac functions and renal sodium handling. Since nitric oxide (NO) plays a crucial role in regulating vascular tone and renal sodium excretion, the present paper was designed to determine whether changes in the activity of NO synthase (NOS) participate in the cardiovascular and renal manifestations of thyroid disorders. METHODS: We measured NOS activity in the heart (left and right ventricles), vessels (aorta and cava) and kidney (cortex and medulla) of euthyroid, hyperthyroid and hypothyroid rats after 6 weeks of treatment. NOS activity was determined by measuring the conversion of L-[(3)H]-arginine to L-[(3)H]-citruline. RESULTS: NOS activity was higher in all tissues from hyperthyroid rats when compared with controls, except in the right ventricle. In the hypothyroid group, NOS activity showed a more heterogeneous pattern, with significant increases in both ventricles but significant reduction in the aorta, while in the vena cava, renal cortex and medulla the enzyme activity also tended to be higher, but significance was not reached. CONCLUSIONS: These data indicated that NOS activity was upregulated in tissues primarily related to blood pressure control in hyperthyroid rats, suggesting that an increased NO production may contribute to the hyperdynamic circulation in hyperthyroidism and may have a protective homeostatic effect in the target organs of the hypertension that accompanies this endocrine disease. The aortic and renal findings in hypothyroid rats suggested a possible role for NOS in the increased peripheral resistance and the normal pressure-diuresis-natriuresis response of these hypotensive animals, although hypothyroidism produced a heterogeneous tissue response in NOS activity.

Animals↗
PubMed2004

Thyrotoxic adenoma followed by atypical hyperthyroidism due to struma ovarii: clinical and genetic studies.

OBJECTIVE: Atypical forms of hyperthyroidism represent a diagnostic challenge for clinicians. Struma ovarii is an ovarian teratoma and constitutes a rare cause of ectopic thyroidal hormonal production. We describe a case of struma ovarii that combined two different sources of hyperthyroidism in the same patient and report genetic studies in order to contribute a better understanding of the autonomy and tumorigenesis of the struma ovarii. CASE REPORT: A 73-year-old nulliparous woman presented a thyroid toxic adenoma that was successfully treated with 10 mCi radioiodine. Unexpectedly, a new onset of hyperthyroidism prompted us to look for a second etiology. A whole-body scan with (123)I detected a pelvic hyperfixation suggesting struma ovarii, and a thyroid differentiated left ovarian teratoma 3 cm in size was surgically removed. We screened for mutations of thyroid-stimulating hormone receptor and Gs-alpha protein genes, as these mutations are common in thyroid adenomas. We did not identify any mutations. Androgen receptor study demonstrated a monoclonal status. Comparative genomic hybridization did not reveal any chromosomal abnormality. However, loss of heterozygosity analysis showed several structural abnormalities, compared with the majority of benign ovarian teratomas, which show a normal karyotype. CONCLUSIONS: This is the first well-documented report of thyrotoxic struma ovarii revealed after treatment of a single thyroid toxic adenoma. We have shown in this case that struma ovarii originates from a single germ cell, and, albeit benign, this tumor presents several chromosomal abnormalities. Struma ovarii-induced hyperthyroidism is likely to be mediated by mechanisms different from those of the classical thyroid toxic adenoma.

Adenoma↗
PubMed1997

Atrial flutter: an uncommon pediatric manifestation of hyperthyroidism.

OBJECTIVE: Atrial flutter is an uncommon arrhythmia in the pediatric population except for the immediate newborn period or following atrial repair of congenital heart disease. In children the diagnosis of atrial flutter may be difficult, attributable to rapid atrioventricular conduction and superimposition of flutter waves on QRS and T waves. Atrial flutter secondary to hyperthyroidism has been rarely reported in older adults, but there are no reports of children presenting with atrial flutter as the initial manifestation of hyperthyroidism. CASE REPORT: We report an interesting case of hyperthyroidism in a 3-year-old presenting with congestive heart failure and atrial flutter with 1:1 atrioventricular conduction. The responses to adenosine administration and to cardioversion were unusual and ultimately helpful in suggesting the diagnosis of hyperthyroidism. CONCLUSION: When atrial flutter is encountered in a pediatric patient in whom there is 1:1 atrioventricular conduction, a lack of a response to adenosine, and persistent sinus tachycardia after cardioversion, the clinician should be alert to the possibility of thyrotoxicosis.

Adenosine↗
PubMed1989

The circadian variation of blood pressure and heart rate in patients with hyperthyroidism.

The circadian variation of blood pressure (BP) and heart rate (HR) was examined in 18 normal subjects, 15 patients with essential hypertension treated with beta-blockers and 21 patients with hyperthyroidism. Most of the patients with hyperthyroidism were also treated with beta-blockers. The 24 hr BP was measured with an ambulatory blood pressure monitoring device (UBP-100) every 5 min. A nocturnal fall in BP and HR was observed in the patients with essential hypertension treated with beta-blockers and the patients with mild to moderate hyperthyroidism as well as normal subjects. On the other hand, in patients with severe hyperthyroidism the nocturnal fall was observed in HR alone, and the fall was small in its amplitude. There was a significant negative correlation between triiodothyronine (T3) level and percentage amplitude of the nocturnal fall in systolic BP (n = 21, r = -0.5, p less than 0.01). However, this relation was not significant in diastolic BP and HR. These results indicate that excess thyroid hormone may modulate the circadian variation of BP and HR.

Adrenergic beta-Antagonists↗
PubMed2006

Experimental hyperthyroidism and central mediators of stress axis and thyroid axis activity in common carp (Cyprinus carpio L.).

The effect of experimental hyperthyroidism, realized by T(4) injection, on central mediators of the hypothalamo-pituitary-interrenal axis (HPI-axis) in common carp (Cyprinus carpio L.) was studied. Our results show that hyperthyroidism evokes a marked 3.2-fold reduction in basal plasma cortisol levels. Corticotropin-releasing hormone-binding protein (CRH-BP) mRNA levels in the hypothalamus, measured by real-time quantitative PCR, were significantly elevated by 40%, but CRH, urotensin-I, prepro-TRH, prohormone convertase-1 (PC1), and POMC mRNA levels were unchanged. In the pituitary pars distalis, PC1, CRH receptor-1, and POMC mRNA levels were unaffected, as was ACTH content. Plasma alpha-MSH concentrations were significantly elevated by 30% in hyperthyroid fish, and this was reflected in PC1 and POMC mRNA levels in pituitary pars intermedia that were increased 1.5- and 2.4-fold respectively. The alpha-MSH content of the pars intermedia was unchanged. Hyperthyroidism has profound effects on the basal levels of a central mediator, i.e., CRH-BP, of HPI-axis function in unstressed carp in vivo, and we conclude that HPI- and hypothalamo-pituitary-thyroid-axis functions are strongly interrelated. We suggest that the changes in plasma cortisol, thyroid hormone, and alpha-MSH levels reflect their concerted actions on energy metabolism.

Animals↗
PubMed1986

Growth hormone responses to growth hormone-releasing factor (1-29) in euthyroid, hypothyroid and hyperthyroid rats.

In order to investigate whether the impaired GH secretion associated with hypothyroidism and hyperthyroidism is due to a hypothalamic or a pituitary disorder, we have studied plasma GH responses to GH-releasing factor (1-29) (GRF) in euthyroid, hypothyroid and hyperthyroid rats. Hypothyroid rats showed a significant (P less than 0.001) reduction in GH responses to GRF (5 micrograms/kg) at 5 min (350 +/- 35 vs 1950 +/- 260 micrograms/l), 10 min (366 +/- 66 vs 2320 +/- 270 micrograms/l) and 15 min after GRF injection (395 +/- 72 vs 1420 +/- 183 micrograms/l; mean +/- S.E.M.) compared with euthyroid rats. Hyperthyroid rats showed a significant (P less than 0.05) decrease in GH responses to 5 micrograms GRF/kg after 30 min (200 +/- 14 vs 325 +/- 35 micrograms/l) but not at other time-points, or after the administration of 1 microgram GRF/kg. These data indicate that in hypothyroidism and perhaps hyperthyroidism there is an alteration in the responsiveness of the somatotroph to GRF administration.

Animals↗
PubMed1999

Local renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy.

We have reported previously that thyroid hormone activates the circulating and tissue renin-angiotensin systems without involving the sympathetic nervous system, which contributes to cardiac hypertrophy in hyperthyroidism. This study examined whether the circulating or tissue renin-angiotensin system plays the principal role in hyperthyroidism-induced cardiac hypertrophy. The circulating renin-angiotensin system in Sprague-Dawley rats was fixed by chronic angiotensin II infusion (40 ng/min, 28 days) via mini-osmotic pumps. Daily i.p. injection of thyroxine (0.1 mg/kg per day, 28 days) was used to mimic hyperthyroidism. Serum free tri-iodothyronine, plasma renin activity, plasma angiotensin II, cardiac renin and cardiac angiotensin II were measured with RIAs. The cardiac expression of renin mRNA was evaluated by semiquantitative reverse transcriptase-polymerase chain reaction. Plasma renin activity and plasma angiotensin II were kept constant in the angiotensin II and angiotensin II+thyroxine groups (0.12+/-0.03 and 0.15+/-0.03 microgram/h per liter, 126+/-5 and 130+/-5 ng/l respectively) (means+/-s.e.m.). Despite stabilization of the circulating renin-angiotensin system, thyroid hormone induced cardiac hypertrophy (5.0+/-0.5 vs 3.5+/-0.1 mg/g) in conjunction with the increases in cardiac expression of renin mRNA, cardiac renin and cardiac angiotensin II (74+/-2 vs 48+/-2%, 6.5+/-0.8 vs 3.8+/-0.4 ng/h per g, 231+/-30 vs 149+/-2 pg/g respectively). These results indicate that the local renin-angiotensin system plays the primary role in the development of hyperthyroidism-induced cardiac hypertrophy.

Analysis of Variance↗
PubMed2006

Effect of neonatal hyperthyroidism on GH gene expression reprogramming and physiological repercussions in rat adulthood.

UNLABELLED: The neonatal period (NP) is a critical phase of the development in which the expression pattern of most genes is established. Thyroid hormones (TH) play a key role in this process and, alterations in its availability in the NP may lead to different patterns of gene expression, which might reflect in the permanent expression of several genes in the adulthood. GH gene expression in the pituitary is greatly dependent on TH in the early postnatal life; thus, modifications of thyroid state in NP might lead to alterations in GH gene expression as well as to physiological repercussions in the adult life. This study aimed to investigate this possibility by means of the induction of a neonatal hyperthyroidism in rats (4 mug of 3,5,3'-triiodo-l-thyronine (T3)/100 g body weight, s.c.) for 5, 15 or 30 days, and further evaluation of GH gene expression, as well as its physiological consequences in adult rats subjected to a transient hyperthyroidism in the first 30 days of life. GH mRNA level was shown to be increased in T3-treated rats for 5 days; when the treatment was extended to 15 or 30 days, the GH mRNA levels were similar to the control group. Moreover, rats treated with T3 for 30 days and killed when 90 days old, i.e., 60 days at the end of the T3 treatment, showed decreased GH mRNA content, body weight, bone mineral density, and lean body mass. IN CONCLUSION: (1) T3 effects on GH gene expression depend on the period of life in which the hyperthyroidism is set and on the length of T3 treatment in the NP and (2) transient neonatal hyperthyroidism leads to a lower GH mRNA expression in adult life accompanied by physiological repercussions indicative of GH deficiency.

Aging↗
PubMed2000

Difference in symptom profile between generalized anxiety disorder and anxiety secondary to hyperthyroidism.

OBJECTIVE: The differential diagnosis between subclinical hyperthyroidism and Generalized Anxiety Disorder (GAD) is often a difficult problem to solve without laboratory examination. The aim of this pilot study was to assess whether there are differences in the symptom profile between these two disorders. METHODS: Fifty patients took part in the study: Twenty-five were hyperthyroid patients, and twenty-five were GAD patients. The diagnosis was based on the TSH values and the DSM-IV criteria, respectively. The Hamilton Anxiety Scale (HAS) and the list of fifty-one symptoms produced by the detailed expansion of HAS items were used to quantify the anxiety symptomatology. The differences in the frequencies between the two diagnostic groups were calculated at each categorical response for every item of both scales. Forward Stepwise Discriminant Function Analysis was performed twice using HAS items and the fifty-one-list items. RESULTS: The symptoms of anxiety in subclinical hyperthyroidism were not identical to those of GAD. Four Hyperthyroid/Anxiety Indices (HAI I-IV) were developed. These indices reach optimum classification of patients (3 of them reach 100% sensitivity and specificity). CONCLUSION: The results of the current study suggest that it is possible to differentiate between GAD and subclinical cases of hyperthyroidism by the careful study of clinical symptomatology. This may be of particular help in isolated areas without laboratory support, but replication of the indices in other samples is indicated.

Adult↗