bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECTS ON GROWTH HORMONE SECRETION FOLLOWING INTRAVENOUS AND SUBCUTANEOUS INJECTIONS OF GROWTH HORMONE‐RELEASING FACTOR (hGRF‐44 NH2): COMPARISON OF IMMUNOREACTIVE PLASMA GRF LEVELS
Authors: SASSOLAS GENEVIÈVE , BIOT‐LAPORTE SYLVIANE , COHEN R. , CHARFI A. ELM , FERRY S. , BORSON FRANÇOISE 
Published: March 2008

SUMMARYThe effects of subcutaneous administration of three doses of human growth hormone‐releasing factor (hGRF‐44 NH2 or hGRF) at doses of 100, 300 and 600 μg were studied in six normal young men. GH responses obtained with 100 and 300 μg were negligible. In contrast, the 600 μg dose gave a profile of response comparable in timing and magnitude to that obtained with i.v. hGRF at maximal effect doses (20, 80, 100 μg). Plasma immunoreactive hGRF levels (IR‐hGRF) were compared after s.c. and i.v. hGRF. Mean maximal plasma concentrations were comparable with s.c. 600 μg and i.v. 20 μg. Peaks occurred earlier with i.v. hGRF (5 min as opposed to 15 min): however, return to undetectable values was obtained between 90 and 120 min after s.c. or i.v. injections. These data suggest a great loss of the peptide between the subcutaneous space and blood, without delayed absorption. High variability in plasma IR‐hGRF concentrations between the subjects after the same s.c. doses was observed.
EFFECT OF CALCITONIN ON GASTROINTESTINAL REGULATORY PEPTIDES IN MAN
Authors: STEVENSON J. C. , ADRIAN T. E. , CHRISTOFIDES N. D. , BLOOM S. R. 
Published: March 2008

SUMMARYA major physiological role of calcitonin in humans appears to be regulation of skeletal turnover. It has been suggested that another function of calcitonin is to prevent post‐prandial rises in calcium, particularly in animals, but the importance of such a function in man remains to be determined. Although it is known that calcitonin has an inhibitory effect on the secretion of gastrin and insulin, its actions on other gut and pancreatic hormones have not previously been studied. To investigate interrelations between calcitonin and gastrointestinal regulatory peptides, 0·5 mg synthetic human calcitonin was administered to 10 fasting patients. No changes in the plasma concentrations of glucose, somatostatin, neurotensin, enteroglucagon, vasoactive intestinal polypeptide or bombesin were observed. In contrast, profound falls in the circulating levels of gastrin, insulin and pancreatic glucagon were seen, reaching a maximum shortly after the peak of plasma calcitonin concentration. Marked changes were also observed in the levels of motilin, pancreatic polypeptide and, to a lesser extent, gastric inhibitory polypeptide, but the maximal falls occurred about 40 min later, coinciding with a significant fall in serum calcium. It is possible that the effect of calcitonin on these hormones was direct, perhaps receptor‐mediated. The falls in levels of motilin and pancreatic polypeptide could have been further enhanced by changes in extracellular calcium ion concentrations. Whether any of these effects of calcitonin occur physiologically remains to be determined. However, these findings suggest new therapeutic possibilities for calcitonin.
PROLACTIN SECRETION AND BIOLOGICAL ACTIVITY IN FEMALES WITH GALACTORRHOEA AND NORMAL CIRCULATING PROLACTIN CONCENTRATIONS AT REST
Authors: JOHNSTON D. G. , HAIGH J. , PRESCOTT R. W. G. , HEATON A. , KENDALL‐TAYLOR P. , BAYLIS P. , ALBERTI K. G. M. M. , ROWE R. , FRIESEN H. , COOK D. , WATSON M. 
Published: March 2008

SUMMARYProlactin secretion and biological activity have been investigated in 20 females with persistent idiopathic galactorrhoea who had normal resting serum prolactin levels at presentation. Results were compared with those in 34 normal controls. Hyperprolactinaemia, which was persistent in one and intermittent in the other, developed in two patients over an observation period of 1·5 to 8·5 years. Resting prolactin levels stayed normal in the remaining eighteen who were further investigated. Menstruation was disordered in only six of the 18, while ovulation occurred (serum progesterone > 20 nmol/1) in all seven patients who were studied over a 5 week period. Serum prolactin concentrations over 24 h were similar in patients and controls (24 h mean ± SEM prolactin, 288 ± 36 mU/1, patients, n= 7; 291±21 mU/1, controls, n= 9) as were prolactin levels estimated twice weekly for 5 weeks. Prolactin responses to thyrotrophin‐releasing hormone, 200 μg (at 20 min, 2417 ± 658 mU/1, patients, n= 7; 2113 ± 424 mU/1, controls, n= 8), the dopamine antagonist, domperidone, 10 mg (at 30 min, 5949 ± 536 mU/1, patients, n= 7; 5858 ± 460 mU/1, controls, n= 8) and insulin‐induced hypoglycaemia (at 60 min, 1441 ± 551 mU/1, patients, n= 7; 1298 ± 183 mU/1, controls, n= 7) were similar in patients and controls. Two different radioimmunoassays using two different antisera gave similar estimates of serum prolactin levels and prolactin bioactivity in serum was normal in an in‐vitro bioassay based on the ability of prolactin to stimulate proliferation of Nb2 node rat lymphoma cells (basal bioassayable prolactin, patients 355 ± 43 mU/1, n= 10; controls 348 ± 64 mU/1, n= 7). Metabolic abnormalities similar to those previously noted in hyperprolactinaemia were observed in the patients' 24 h profiles. These included mild hyperglycaemia (24 h mean ± SEM glucose, 5·47 ± 008 mmol/l, patients; 5·05±0·14 mmol/1, controls; P < 0·05) and elevations in circulating lactate, pyruvate and alanine. Blood glycerol was decreased (24 h mean ± SEM, 0·044±;0·004 versus 0·058±0·004 mmol/1, P <0·05). In the majority of patients with idiopathic galactorrhoea, prolactin concentrations, regulation of secretion and bioactivity in vitro are normal. The galactorrhoea and metabolic abnormalities suggest increased tissue sensitivity to the lactogenic and metabolic actions of prolactin, while ovarian cyclical function is relatively spared.
COMPARISON BETWEEN BIOACTIVITY AND IMMUNOREACTIVITY OF SERUM PROLACTIN IN URAEMIA
Authors: MOORADIAN A. D. , MORLEY J. E. , KORCHIK W. P. , MA K. W. , HARTFEL M. A. , PARSONS J. A. 
Published: March 2008

SUMMARYThe lactogenic potency of sera from 24 male uraemic patients on regular haemodialysis and 14 control subjects was measured by Nb2 node rat lymphoma cell bioassay, and was compared to serum prolactin levels measured by radioimmunoassay. Sera with immunoreactive growth hormone levels exceeding 5 ng/ml were excluded from comparisons. The uraemic patients had a higher serum immunoreactive prolactin (48.2 ± 10.5 ng/ml) than controls (13.3 ± 1.3 ng/ml (P < 0.01). Similarly the lactogenic potency of uraemic serum was higher than that of the control sera (25.5 ± 3.9 vs 12.6 ± 1.4 ng/ml, P <0.02). The ratio of immunoreactive serum prolactin to the lactogenic potency of the serum was significantly higher in the uraemic group (1.80 ± 0.14 vs 1.10 ± 0.10, P < 0.01) suggesting decreased bioactivity of prolactin in uraemic serum. To examine whether low molecular weight inhibitory molecules were responsible for this discrepancy, the lactogenic potency of 8 uraemic sera was studied before and after 4 h of dialysis against 1 litre of haemodialysis medium. Two of the eleven sera studied showed a significant increment in lactogenic potency after dialysis (47% and 57%). We conclude that there is a disparity between the bioactive and the immunoreactive serum prolactin concentrations in patients with chronic renal failure and that a dialysable factor may be partly responsible for this discrepancy in some cases.
DOES GROWTH HORMONE RELEASING FACTOR DESENSITIZE THE SOMATOTROPH? INTERPRETATION OF RESPONSES OF GROWTH HORMONE DURING AND AFTER 10‐HOUR INFUSION OF GRF 1–29 AMIDE IN MAN
Authors: DAVIS J. R. E. , SHEPPARD M. C. , SHAKESPEAR R. A. , LYNCH S. S. , CLAYTON R. N. 
Published: March 2008

It is unclear whether growth hormone releasing factor (GRF) administration in vivo may desensitize the somatotroph. To investigate this possibility we have examined the effects of 10‐h infusion of the equipotent 1–29 amide analogue of hpGRF on serum GH levels and on the subsequent GH response to a bolus dose of GRF (1–29). Four normal adult males received an intravenous infusion of 1–29 GRF (1 μg/kg/h) from 0800 to 1800 h, with blood samples taken at 10 min intervals. A 100 μg intravenous bolus dose of GRF was given at 1800 h, and sampling continued for a further 90 min. GH levels were near or below the limit of detection (0·5 mU/1) throughout the control 10 h period. During GRF infusion there was increased GH release with pulses of irregular frequency and amplitude (up to 80 mU/1) continuing throughout the entire infusion period. There was no apparent reduction in total GH released towards the latter part of the infusion. On the control day, 100 μg GRF bolus increased mean (± SEM) GH from 0·82 ± 0·21 mU/1 to a peak of 59·0 ± 44·8 mU/1 (P < 0·002). Following 10‐GRF infusion, responses to bolus injection of GRF were reduced, but variable. In two subjects a small rise in GH levels occurred (basal 6·4 and 7·2 rising to peak values of 11·2 and 23·0 mU/1 respectively). In the other two subjects, GH levels fell but in these the GRF bolus had coincided with a GH peak.The loss of GRF responsiveness after GRF infusion may be due to ‘desensitization’. However the response of GH to GRF bolus injection appears to be partly related to the timing of the bolus with the pulses of GH induced by the previous infusion. Caution is needed in the interpretation of acute GRF tests following a period of GRF exposure.
LATE INCREASE IN SERUM 1,25‐DIHYDROXYVITAMIN D ONE MONTH AFTER SURGERY FOR ADENOMATOUS HYPERPARATHYROIDISM
Authors: D'AMOUR P. , GILBERT F. , GASCON‐BARRE M. , BOUTIN J. M. , HAVRANKOVA J. , BELANGER R. , MATTE R. 
Published: March 2008

SUMMARYThis study was designed to follow the evolution of serum 1,25(OH)2D after surgery for primary hyperparathyroidism. Ten patients were studied before and for up to 85 d after removal of a single parathyroid adenoma. Blood and 24 h urine were obtained at various time points, for the measurement of serum or urinary phosphate and calcium indices. Before surgery, serum calcium (2·91 ± 0·06 mmol/l; mean ± SEM), parathyroid hormone (354 ± 47 pg/ml) and 1,25(OH)2D (61·2 ± 7·8 pg/ml) were elevated while serum phosphate (1·01 ± 0·07 mmol/l) tended to be low. Relative hypoparathyroidism was evident for up to 5 d after surgery with the lowest value for serum parathyroid hormone (41 ± 16 pg/ml) on day 1, serum calcium (2·12 & 0·06 mmol/l) on day 3 and highest value for serum phosphate (1·41 ± 0·13 mmol/l) on day 5. As expected, serum 1,25(OH)2D levels decreased to 35·9 ± 4·2 pg/ml 24 h after surgery. Stabilization of serum and urinary parameters to normal values was seen between day 5 and day 27; the only exception was serum 1,25(OH)2D, which increased again at day 27 to 57·6 ± 5·0 pg/ml, a value as high as that before surgery. It was still elevated at day 50 (58·3 ± 4·3 pg/ml), but returned towards normal values in three out of four patients (44 ± 3·9 pg/ml) by day 80. No variation in 25(OH)D or 24,25(0H)2D was seen throughout the study. 1,25(OH)2D values could be related to serum parathyroid hormone values before surgery (r= 0·659, P > 0·05) but not after. The secondary increase in serum 1,25(OH)2D could not be related to variations in serum calcium, phosphate, parathyroid hormone or diet. Further studies will be required to explain this phenomenon.
ABNORMAL CIRCADIAN RHYTHM OF MELATONIN IN DIABETIC AUTONOMIC NEUROPATHY
Authors: O'BRIEN I. A. D. , LEWIN I. G. , O'HARE J. P. , ARENDT JOSEPHINE , CORRALL R. J. M. 
Published: March 2008

SUMMARYThe circadian rhythm of melatonin secretion from the pineal body is entrained to the light‐dark cycle and is controlled via sympathetic fibres originating from the superior cervical ganglia. We have therefore examined plasma melatonin profiles in diabetics with and without evidence of autonomic neuropathy and in normal matched controls. The physiological increase in nocturnal plasma melatonin concentration was not observed in diabetics neuropaths. There was no consistent pattern in the diabetics without neuropathy; only three out of the eight subjects in this group had a sustained nocturnal increase in melatonin. Normal diurnal variation of plasma cortisol was present in all groups of subjects. The present study shows that diabetic patients with evidence of autonomic neuropathy lack the normal circadian changes of plasma melatonin concentration. This provides confirmation for the control of pineal function via the sympathetic nervous system in man. The impaired melatonin profiles observed in diabetic patients without apparent autonomic neuropathy suggest that a subclinical state of sympathetic denervation may exist in this group of diabetics.
THE EFFECTS OF EXOGENOUS MELATONIN ON ENDOCRINE FUNCTION IN MAN
Authors: WRIGHT J. , ALDHOUS M. , FRANEY C. , ENGLISH J. , ARENDT J. 
Published: March 2008

SUMMARYAt two different times of year (spring and autumn) an oral preparation of the pineal neurohormone melatonin, or placebo, was administered to 12 healthy volunteers (10 men and two women in spring: the same group minus one man in autumn) daily at 1700 h for 1 month (spring), or 3 weeks (autumn) using a double‐blind cross‐over protocol. The daily dose was 2 mg melatonin in 5 ml corn‐oil, and placebo consisted of the vehicle only. In spring the anterior pituitary hormones LH, PRL, GH together with T4, cortisol, testosterone and melatonin were measured at 1– to 6–h intervals for 24 h in plasma on the day following the last dose. In autumn PRL, cortisol and melatonin levels were measured on the last day of treatment. Subjective fatigue, mood and sleep records were kept throughout the studies. Melatonin increased early evening fatigue and actual sleep, but had no effect on mood: these results are reported in full elsewhere. Melatonin administration had no effect on the levels or 24‐h rhythm of LH, GH, T4, testosterone or cortisol. An earlier fall in the nocturnal PRL was observed on both occasions. Overall PRL levels were higher in spring than in autumn. In five of the subjects, the secretion of endogenous melatonin was advanced by 1–3 h in the presence of exogenous melatonin. These observations suggest that the potential therapeutic use of melatonin as a hypnotic or in the treatment of jet lag is unlikely to be complicated by undesirable endocrine effects.
HIGH ACTIVITY OF CYCLIC 3′,5′‐NUCLEOTIDE PHOSPHODIESTERASE IN SERA OF PATIENT WITH PHAEOCHROMOCYTOMA
Authors: NAKAI AKIRA , NAGASAKA AKIO , OHYAMA TAKAKO , AONO TOSHIHIRO , IWASE KATSUMI , HASEGAWA HARUHIKO , HAYAMI SHIRO , HIDAKA HIROYOSHI , TANAKA TOSHIO , NIINOMI MITSURO , NIHEI NORIYUKI , NAKAGAWA HIFUMI , OHTANI SUSUMU , MIYAKAWA SHUICHI , KAWASE KYOHEI 
Published: March 2008

SUMMARYOur previous observations that serum cyclic 3′,5′‐nucleotide phosphodiesterase activity varied in thyroid disorders and was positively correlated with thyroid function stimulated us to investigate the phosphodiesterase levels in sera of patients with pituitary and adrenal disorders, and the response to glucagon in normal subjects. Both serum cyclic AMP phosphodiesterase (cyclic AMP‐PDE) and cyclic GMP phosphodiesterase (cyclic GMP‐PDE) activities were measured at a low substrate concentration. Serum cyclic AMP‐PDE activity was elevated in five patients with phaeochromocytoma and was not elevated in patients with Cushing's syndrome or acromegaly, compared to the level in normal subjects. Increased enzyme activities returned to normal after resection of the tumours. Intramuscular injection of glucagon to five healthy subjects elevated cyclic AMP levels and cyclic AMP‐PDE activity in plasma. These results imply that the increased cyclic AMP level by the activation of cyclase may have induced cyclic AMP‐PDE in the target organ and the soluble cyclic AMP‐PDE may leak into blood vessels from target organs.
LACK OF EFFECT OF MUSCARINIC CHOLINERGIC BLOCKADE ON THE GH RESPONSES TO GRF 1–29 AND TRH IN ACROMEGALIC SUBJECTS
Authors: JORDAN V. , DIEGUEZ C. , VALCAVI R. , ARTIOLI C. , PORTIOLI I. , RODRIGUEZ‐ARNAO M.D. , GOMEZ‐PAN A. , HALL R. , SCANLON M. F. 
Published: March 2008

SUMMARYIt is well known that muscarinic cholinergic blockade either reduces or abolishes stimulated GH release in normal subjects. In this study we have investigated whether cholinergic muscarinic blockade could reduce the GH responses to GRF 1–29 and TRH in acromegalic subjects. Eight acromegalic subjects underwent two GRF tests (GRF 1–29, 1 μg/kg i.v.) with and without pirenzepine (0.6 mg/kg, i.v.). A further four of these patients received TRH (200 μg/kg, i.v.) on separate occasions with and without pirenzepine (0.6 mg/kg, i.v.). Cholinergic muscarinic blockade did not alter the GH responses to GRF and TRH in patients with acromegaly. These findings are in contrast with previous data reported on the effects of cholinergic blockade on stimulated GH levels in normal subjects and in patients with type I diabetes mellitus and are compatible with the view that somatotroph adenomas are functionally disconnected from hypothalamic control mechanisms.
DISCORDANT RESPONSES OF PROLACTINOMA TO TWO DIFFERENT DOPAMINE AGONISTS
Authors: AHMED S. R. , SHALET S. M. 
Published: March 2008

SUMMARYA 19‐year‐old woman presented with headaches, temporal lobe epilepsy and primary amenorrhoea. There was a family history of multiple endocrine adenomatosis. Investigation revealed normal visual fields and acuity, hyperpro‐lactinaemia (48 000 mU/l) and a very large pituitary tumour with extrasellar spread. Treatment with bromocriptine reduced the tumour size and the prolactin level to 2440 mU/1. Six months after the start of therapy, resistance to bromocriptine developed and the prolactin concentration progressively rose to pretreatment levels, despite increasing the dose of bromocriptine to 40 mg/d. At this stage treatment with a second dopamine agonist, pergolide, was effective in reducing the prolactin concentration to normal within four months. Serial CT scans at 1, 6 and 12 months on dopamine agonist therapy showed a progressive decrease in tumour size, which seemed to be maintained even during the period of rising prolactin concentrations due to bromocriptine resistance. This case illustrates that during dopamine agonist therapy a discrepancy may exist in the clinical response as judged by reduction in tumour size and decrease in the circulating prolactin level. Furthermore, in patients with prolactinomas, pergolide may induce a response when resistance to bromocriptine develops.
THE PREOPERATIVE AND POSTOPERATIVE INVESTIGATION OF TSH AND PROLACTIN RELEASE IN THE MANAGEMENT OF PATIENTS WITH HYPERPROLACTINAEMIA DUE TO PROLACTINOMAS AND NONFUNCTIONAL PITUITARY TUMOURS: RELATIONSHIP TO ADENOMA SIZE AT SURGERY
Authors: SCANLON M. F. , PETERS J. R. , SALVADOR J. , RICHARDS S. H. , JOHN R. , HOWELL S. , WILLIAMS E. D. , THOMAS J. P. , HALL R. 
Published: March 2008

SUMMARYWe report here our results of the pre‐ and post‐operative assessment of prolactin and TSH status in 41 hyperprolactinaemic patients who underwent pituitary surgery over a 5 year period. Preoperatively in patients with prolactinomas (n= 33) the TSH response to domperidone decreased with increasing adenoma size. When the data are expressed on a group mean basis the exaggerated TSH response to domperidone in preoperative prolactinoma patients was reduced significantly in patients rendered normoprolactinaemic by surgery but persisted in those who remained hyperprolactinaemic. Similarly the reduced preoperative PRL responses to domperidone and TRH were significantly increased by successful surgery. In contrast patients with stalk‐compression hyperprolactinaemia (n= 6) due to larger lesions which were not prolactinomas all showed reduced or absent TSH responses to domperidone. The PRL responses to domperidone and TRH were reduced or absent both in patients with prolactinomas and in those with stalk‐compression hyperprolactinaemia. All patients with stalk‐compression hyperprolactinaemia showed a delayed pattern of TSH response to TRH with 60 min values being greater than 20 min ones. In contrast a normal pattern of TSH response to TRH was observed in all patients with hyperprolactinaemia due to prolactinomas. Postoperatively TSH and PRL responses were largely unchanged in patients with stalk‐compression hyperprolactinaemia regardless of whether normoprolactinaemia was restored by surgery. In conclusion a reduced or absent PRL response to TRH or domperidone is not diagnostic of the presence of a prolactinoma since it occurs in hyperprolactinaemic patients with prolactinomas or stalk‐compression. In contrast, the TSH response to acute dopamine antagonism is exaggerated in most patients with small prolactinomas but not in those with stalk‐compression hyperprolactinaemia and we have found this to be helpful diagnostically since the presence of an exaggerated TSH response to dopamine antagonism is evidence against the presence of stalk‐compression hyperprolactinaemia. The observation of a delayed TSH response to TRH in a hyperprolactinaemic patient should alert the clinician to the possibility of stalk‐compression hyperprolactinaemia due to a large lesion which may not be a prolactinoma.
SOMATOSTATIN AND OXYTOCIN INFUSION INHIBITS THE RISE OF PLASMA β‐ENDORPHIN, β‐LIPOTROPHIN AND CORTISOL INDUCED BY INSULIN HYPOGLYCAEMIA
Authors: PETRAGLIA FELICE , FACCHINETTI F. , D'AMBROGIO G. , VOLPE ANNIBALE , GENAZZANI ANDREA R. 
Published: March 2008

SUMMARYThe present study investigated the possible effect of somatostatin and oxytocin on the basal and stress‐induced rise of beta‐endorphin (β‐END), beta‐lipotrophin (β‐LPH) and cortisol in the human. For this purpose somatostatin (4.1 μg/min for 120 min or oxytocin (0·4 μg/min for 120 min) was infused into two different groups of seven healthy subjects; 30 min after the start of the infusion, placebo or insulin (0·1 IU/kg body weight, B.W.) was injected on two different days. In a third experimental step, an insulin tolerance test was performed during saline infusion to evaluate stress‐related effects on the different hormonal secretions under basal conditions. Plasma levels of β‐END, β‐LPH and cortisol were measured by radioimmunoassay. Extraction and chromatographic procedures preceded the assay for β‐END and β‐LPH. Neither somatostatin nor oxytocin significantly modified basal plasma levels of β‐END, β‐LPH and cortisol. However these treatments blunted the rise of the three hormones seen at 45 and 60 min during insulin‐induced hypoglycaemia (P> 0·01). These results indicate that somatostatin and oxytocin may influence the β‐END, β‐LPH and cortisol increase induced by stress in humans, without affecting their basal secretion.
IS HUMORAL THYROID AUTOIMMUNITY RELEVANT IN AMIODARONE IODINE‐INDUCED THYROTOXICOSTS (AIIT)?
Authors: MARTINO E. , MACCHIA E. , AGHINI‐LOMBARDI F. , ANTONELLI A. , LENZIARDI M. , CONCETTI R. , FENZI G. F. , BASCHIERI L. , PINCHERA A. 
Published: March 2008

SUMMARYAmiodarone, an iodine containing drug, may induce thyrotoxicosis by an uncertain mechanism. In this study the role of thyroid autoimmunity was evaluated in 28 consecutive patients referred to us because they had become hyperthyroid during long‐term amiodarone administration. Titres of thyroglobulin and thyroid microsomal antibodies, TSH binding‐inhibitory and thyroid stimulating antibodies were evaluated. Underlying thyroid disorders were demonstrated in 20 patients (9 of them had toxic diffuse goitre, seven toxic multinodular goitre and four toxic adenoma), while eight patients did not show any apparent thyroid gland abnormality. Circulating thyroid autoantibodies could be found in all amiodarone iodine‐induced hyperthyroid patients with toxic diffuse goitre and in one with toxic multinodular goitre, whilst they were absent in the other patients. These studies suggest that thyroid autoimmunity has little if any role in the development of thyrotoxicosis in amiodarone treated patients without underlying thyroid disorders. Furthermore, in amiodarone‐iodine‐induced thyrotoxicosis associated with various thyroid diseases, the humoral markers of thyroid autoimmunity show an incidence similar to that observed in spontaneous hyperthyroidism.