bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECT OF NALOXONE ON NEUROHYPOPHYSEAL PEPTIDE RESPONSES TO BREAST FEEDING AND BREAST STIMULATION IN MAN
Authors: JOHNSON M. R. , ANDREWS M. A. , SECKL J. R. , LIGHTMAN S. L. 
Published: March 2008

SUMMARYWe have investigated the role of endogenous opioid peptides in the release of oxytocin (OT) in response to breast feeding and breast stimulation in humans. Five breast feeding women were studied on two separate occasions within 4 weeks of delivery. Saline or naloxone, 4 mg bolus and 6 mg/h, was administered intravenously, in random order. Blood samples were taken at regular intervals. In the saline‐infused group OT rose from a baseline of 1.1 |Mp 0.1 pmol/l (mean |Mp SEM) to a peak of 7.0 |Mp 0.9 after 6 min, and in the naloxone‐infused group from 1.0 |Mp 0.1 pmo1/1 to 5.8 |Mp 1–3 (P < 0.05). There were no significant differences between the two groups at any time point. Plasma vasopressin (AVP) did not change. In the second study six women in the luteal phase of the menstrual cycle were investigated on two occasions at least 48 h apart. They were similarly infused with either naloxone or saline in random sequence. A mechanical breast pump provided breast stimulation. In saline‐infused women OT levels rose from a baseline of 1.0 |Mp 0.1 pmol/1 (mean |Mp SEM) to a peak of 10 |Mp 1.1 (P < 0.05) after 6 min, and in naloxone infused women from 1.1 |Mp 0.1 pmol/l to 3.0 |Mp 1.4 (NS). There were no differences in OT between the groups. AVP did not change. We conclude that endogenous opioid peptides do not modulate OT release during breast feeding or breast stimulation in women.
INAPPROPRIATELY ELEVATED PLASMA INSULIN‐LIKE GROWTH FACTOR II IN RELATION TO SUPPRESSED INSULIN‐LIKE GROWTH FACTOR I IN THE DIAGNOSIS OF NON‐ISLET CELL TUMOUR HYPOGLYCAEMIA
Authors: TEALE J. D. , MARKS V. 
Published: March 2008

SUMMARYThe diagnosis of non‐islet cell tumour (hypoinsulinaemic) hypoglycaemia has been complicated by contradictory biochemical evidence. Although insulin‐like growth factor II (IGF‐II) has been identified as the hypoglycaemic agent, plasma levels are often not elevated. In this study specific radioimmunoassay procedures for the measurement of IGF‐I and IGF‐II are described. Reference data on plasma IGF‐II concentrations in relation to a wide range of IGF‐I levels have been accumulated using plasma samples from acromegalic, hypopituitary and insulinoma (i.e. hyperinsulinaemic hypoglycaemia) patients as well as normal subjects from all age groups. The reference data indicate that a low plasma IGF‐I value is normally associated with a relatively low plasma IGF‐II level. Within a group of hypoinsulinaemic hypoglycaemia patients, a small number, invariably with evidence of a neoplasm, had low plasma IGF‐I concentrations but apparently normal IGF‐II levels. We propose that, in such cases, an apparently normal plasma IGF‐II value is inappropriately high for the low plasma IGF‐I level and, in association with non‐ketotic hypoinsulinaemia and suppressed plasma growth hormone (GH), is diagnostic of a non‐islet cell tumour as the cause of hypoglycaemia.
ROLE OF CHOLINERGIC MUSCARINIC PATHWAYS ON THE FREE FATTY ACID INHIBITION OF GH RESPONSES TO GHRH IN NORMAL MEN
Authors: PEÑALVA ANGELA , GAZTAMBIDE SONIA , VAZQUEZ JOSE ANTONIO , DIEGUEZ CARLOS , CASANUEVA FELIPE F. 
Published: March 2008

SUMMARYIn order to explore the mechanisms by which free fatty acids (FFA) inhibit GH secretion, we studied the effect of the acetylcholinesterase inhibitor pyridostigmine (120 mg p. o.) on the FFA blockade of GH responses to the administration of GHRH (100 μg i. v.) in seven normal subjects. GHRH‐induced GH secretion was significantly reduced following elevation of circulating FFA levels by lipid‐heparin infusion and significantly potentiated by previous pyridostigmine treatment. Peak GH levels following combined administration of pyridostigmine plus lipid—heparin plus GHRH were significantly higher (P < 0.01) than after GHRH alone and significantly lower than after pyridostigmine plus GHRH (P < 0.01). In conclusion, central cholinergic activation by pyridostigmine, with the presumed reduction in somatostatin discharge, reversed the blocking effect of FFA on GHRH‐stimulated GH release. Conversely, FFA were able to reduce even a maximal GH stimulation by pyridostigmine plus GHRH.
BAROREFLEX‐GOVERNED SYMPATHETIC OUTFLOW TO MUSCLE VASCULATURE IS INCREASED IN HYPOTHYROIDISM
Authors: FAGIUS JAN , WESTERMARK KERSTIN , KARLSSON ANDERS 
Published: March 2008

SUMMARYMicroelectrode recording of muscle nerve sympathetic activity (MSA), which is baroreflex‐governed and involved in cardiovascular homeostasis, was made in five patients with hypothyroidism and in seven patients with hyperthyroidism prior to treatment and after recovery to euthyroidism. Patients with hypothyroidism had a higher level of MSA when hypothyroid than after recovery (mean |Mp SEM 39.3 |Mp 7.1 and 26.8 |Mp 7.9 bursts/min, respectively, P < 0.05), whereas hyperthyroidism was not accompanied by a change in the number of sympathetic bursts/min. The response of MSA to manouvres known to influence the neural outflow via baroreceptors and other receptor inputs was not changed with altered thyroid function. The findings provide direct evidence of an increased sympathetic activity in hypothyroidism, but suggest that other physiological properties of MSA are intact in thyroid disease.
THE EFFECT OF GALANIN ON BASELINE AND GHRH‐INDUCED GROWTH HORMONE SECRETION IN OBESE CHILDREN
Authors: LOCHE S. , PINTUS S. , CELLA S. G. , BOGHEN M. , VANNELLI S. , BENSO L. , MÜLLER E. E. , CORDA R. , PINTOR C. 
Published: March 2008

SUMMARYWe have evaluated the effect of the administration of galanin (Gal), a newly identified hypothalamic peptide, on baseline and GHRH‐induced GH rise in five obese children and in seven controls. The GH response to GHRH (hpGRF(1–29), 1 μg/kg i. v.), and to Gal (15 μg/kg/h for 1 h), evaluated both as the maximum GH peak and as integrated area under the curve (AUC), was significantly lower in the obese children than in the controls. Simultaneous administration of Gal plus GHRH significantly increased the GH response to GHRH in all the obese subjects, so that their mean peak GH levels and AUC after Gal plus GHRH were similar to those of the control children after GHRH. Also, in control children Gal caused a significant augmentation of the GH response to GHRH. Mean peak GH levels and mean AUC after Gal plus GHRH were significantly higher in the controls than in the obese children given the same treatment. Our data indicate that obese children have a blunted GH response to Gal, which, however, is able to enhance the GH response to GHRH. This observation strengthens the view that the mechanism of action of Gal involves modulation of endogenous somatostatin (SRIH) release. In addition, similarity between the effects of Gal and pyridostigmine on baseline and GHRH‐stimulated GH release in obese children may indicate the existence of a cholinergic link in the action of Gal.
THYROID FUNCTION IN CHORIOCARCINOMA: DEMONSTRATION OF A THYROID STIMULATING ACTIVITY IN SERUM USING FRTL‐5 and HUMAN THYROID CELLS
Authors: KENNEDY R. L. , SHERIDAN E. , DARNE J. , GRIFFITHS H. , DAVIES R. , PRICE A. , COHN M. 
Published: March 2008

SUMMARYHyperthyroidism is a well recognized complication of gestational trophoblastic tumours (GTT) and may be due to high circulating concentrations of human chorionic gonadotrophin (hCG) or its variants. We have studied 24 clinically euthyroid women with GTT. Eight were biochemically hyperthyroid with low or undetectable serum thyrotrophin (TSH) and had a mean serum hCG of 3612 |MX 103 IU/1 compared to 76.2 |MX 103 IU/1 in the other patients (P < 0.01). Purified hCG stimulated iodide uptake into FRTL‐5 cells with 25 |MX 103 IU/1 being equivalent in potency to 1 mU/1 of thyrotrophin (TSH). Sixteen out of the 24 sera (67%) stimulated iodide uptake when applied to the cells at a 1:10 dilution. Sera from all eight hyperthyroid patients contained thyroid stimulating activity. The mean hCG concentration in the 16 stimulatory sera was 238.2 |MX 103 IU/1 compared to 37.1 |MX 103 IU/1 in the other eight sera (P < 0.01). Six men with hCG‐secreting testicular tumours were biochemically euthyroid although three of their sera stimulated iodide uptake into FRTL‐5 cells. In human thyroid cells the mean cAMP production over 4 h with sera from five healthy controls was 54.2 |Mp 1.81 pmol/mg cell protein compared to 67.0 |Mp 3.8 pmol/mg protein with sera from five choriocarcinoma patients (P < 0.02). Serum from patients with gestational trophoblastic tumours contains a thyroid stimulating activity which may be hCG and whose presence correlates with hyperthyroidism.
THE EPIDEMIOLOGY OF THYROTOXICOSIS IN NEW ZEALAND: INCIDENCE AND GEOGRAPHICAL DISTRIBUTION IN NORTH CANTERBURY, 1983–1985
Authors: BROWNLIE B. E. W. , WELLS J. E. 
Published: March 2008

SUMMARYIn a 3‐year (1983‐1985) epidemiological study of thyrotoxicosis in North Canterbury, New Zealand, the annual incidence was 25.8 per 100 000 (female 40.7, male 10.5). Thyroid scintiscanning showed that 64% had diffuse hyperplasia (DH), 27% toxic multinodular goitre (TMG), 7% toxic uninodular goitre (TUG), and 2% zero uptake. The calculated annual incidence of toxic diffuse goitre (DH) was 15 per 100 000, and for toxic nodular goitre (TMG and TUG combined) was 8 per 100 000. The age‐related incidence for toxic diffuse goitre peaked in middle life whereas toxic nodular goitre showed an increasing incidence with age. There was no significant seasonal variation or rural/urban difference in incidence. Analysis of geocoded addresses did not identify areas of high incidence. The variable duration of symptoms prior to diagnosis limits the search for possible environmental trigger factors. North Canterbury was an endemic goitre area prior to the introduction of iodized salt 50 years ago, and the incidence of toxic nodular goitre is likely to fall in future.
LONG‐TERM TREATMENT OF METASTATIC MEDULLARY THYROID CARCINOMA WITH THE SOMATOSTATIN ANALOGUE OCTREOTIDE
Authors: MAHLER C. , VERHELST J. , DE LONGUEVILLE M. , HARRIS A. 
Published: March 2008

SUMMARYThree patients with symptomatic metastatic medullary thyroid carcinoma (MTC), one with sporadic form and two with MEN IIa, were treated with the long‐acting somatostatin analogue octreotide (SMS 201–995, Sandoz) for 3 to 17 months. Octreotide was administered subcutaneously in a starting dose of 0.6 to 1.0 mg/day by automatic pump (Travax ASH6, Travenol). Symptoms of diarrhoea, weight loss and malaise improved in all patients. Maximal percentage decrease in mean serum calcitonin was 47, 52 and 81% of the basal values, and was observed 1–3 months from the beginning of treatment. Likewise, carcinoembryonic antigen (CEA) levels initially dropped to 45, 60 and 63% of the levels before therapy. A continuing effect was seen in the two patients with MEN Ha after 15 and 17 months of treatment. However, after the initial decrease, calcitonin (CT) levels went up again to 67 and 68% of the basal values and the dose of octreotide had to be increased to 1.5 mg and 2.0 mg/day. CEA also returned to 84 and 105% of the pretreatment titres. Response to 1.5 mg/day octreotide was lost in the patient with the sporadic form of disease after 3 months. Side‐effects were minimal. Effects on tumour size could not be evaluated. These suggest that octreotide might be a valuable adjuvant in the long‐term management of metastatic MTC. Tachyphylaxis may occur.
HORMONAL PROFILES FOLLOWING CLOMIPHENE CITRATE THERAPY IN CONCEPTION AND NONCONCEPTION CYCLES
Authors: (SCHWARTZ) ZEEV SHOHAM , BORENSTEIN RICHARD , LUNENFELD BRUNO , PARIENTE CLARA 
Published: March 2008

SUMMARYThe hormonal profiles following clomiphene citrate (CC) administration during a single cycle were compared in infertile women who conceived and in those who did not. Of 41 treated patients, ovulation was assumed to have occurred in 28 and was confirmed by clinical pregnancy in five. In the 28 women who presumably ovulated, two distinct patterns of hormonal secretion were observed. A normal response was exhibited by 17 patients (including the five who became pregnant). The other 11 patients exhibited an abnormal response, characterized by significantly higher luteinizing hormone (LH)/follicle‐stimulating hormone (FSH) ratios than in the normal response group from day 9 until the occurrence of the LH peak (days 9 and 10, P > 0.05; days 11 and 12, P > 0.001), and significantly higher oestradiol (E2) levels throughout the cycle (P > 0.01). In addition, in comparison with the normal response group their LH levels during the follicular phase were significantly higher (P > 0‐05) but their LH peaks at ovulation were significantly lower (P > 0.02). Moreover, their progesterone levels, in contrast to those in the normal response group, began to increase prior to the LH peak and remained high during the early and mid‐luteal phases. None of the women who exhibited this abnormal gonadotrophin response to CC therapy achieved a clinical pregnancy. Exposure to high LH levels in the follicular phase following CC therapy seems to reduce the rate of fertilization and/or to contribute to early embryonic loss.
CV205–502, A NEW NON‐ERGOT DOPAMINE AGONIST, REDUCES PROLACTINOMA SIZE IN MAN
Authors: BARNETT P. S. , DAWSON J. M. , BUTLER J. , COSKERAN P. B. , MACCABE J. J. , McGREGOR A. M. 
Published: March 2008

SUMMARYSeven patients with large prolactin‐secreting pituitary adenomas were treated for 8 weeks with once‐daily doses of the new, potent, non‐ergot, long‐acting dopamine agonist CV205–502. In five patients previous treatment with bromocriptine had failed to control their disease or been poorly tolerated and had therefore ceased. In all seven patients serum prolactin levels fell over the 8‐week period of CV205–502 treatment with the decrease ranging from 33 to 99%. Associated with this decline in prolactin all patients showed symptomatic improvement with two of the five women beginning to menstruate and the two patients with visual field impairment showing marked improvement. Tolerance of the drug, with doses at 8 weeks ranging from 0.075 to 0.3 mg, was excellent with only minimal and transient side‐effects being noted in three patients in none of whom was discontinuation of therapy necessary. In one patient non‐compliance after 6 weeks of therapy was associated with a rapid return of her serum prolactin towards pretreatment levels. In all seven patients the clinical and biochemical improvement was accompanied by a marked reduction in tumour size. Since the introduction of bromocriptine, an ergot alkaloid‐derived dopamine agonist (Thorner et al., 1980), into clinical practice in the early 1970s its role in the treatment of hyperprolactinaemic states has become well established (Besser et al., 1972). In patients with proved prolactin‐secreting pituitary adenomas (prolactinomas) the use of bromo‐criptine has been shown to be associated not only with suppression of prolactin secretion and restoration of gonadal function but also with reduction in adenoma size (McGregor et al., 1979). Bromocriptine is currently the treatment of choice for large prolactinomas (macroadenomas) (Vance and Thorner, 1987). Whilst the majority of patients with macroadenomas treated with bromocriptine show a decline in prolactin levels, in the
LUTEINIZING HORMONE AND FOLLICLE STIMULATING HORMONE SECRETION PATTERNS IN FEMALE ATHLETES WITH AND WITHOUT MENSTRUAL DISTURBANCES
Authors: PIRKE K. M. , SCHWEIGER U. , BROOCKS A. , TUSCHL R. J. , LAESSLE R. G. 
Published: March 2008

SUMMARYThirty‐one young female athletes and 13 age‐matched sedentary controls were studied throughout one menstrual cycle or over a 6 week period. Blood was sampled on 5 days per week. Episodic gonadotrophin secretion was measured in the early follicular phase and in the late luteal phase by blood sampling over a 12‐h period at 15‐min intervals. Eight athletes had anovulatory cycles, nine had impaired progesterone (P4) secretion during the luteal phase and 14 had normal cycles as judged from oestradiol (E2) and P4 plasma levels. Athletes with normal cycles had shorter cycles, lower E2 maxima at midcycle, and lower E2 and P4 concentrations during the luteal phase than had sedentary controls. Episodic luteinizing hormone (LH) secretion in the early follicular phase was significantly impaired in the anovulatory athletes: the average LH values over 12 h and the number of secretion episodes were significantly reduced. No significant changes were seen in follicle stimulating hormone secretion.
EFFECTS OF CALCITONIN ON GH RESPONSE TO PYRIDOSTIGMINE IN COMBINATION WITH hGHRH (1–29) NH2 IN NORMAL ADULT SUBJECTS
Authors: GIUSTINA ANDREA , BODINI CORRADO , BOSSONI SIMONETTA , DOGA MAURO , GIRELLI ANGELA , PIZZOCOLO GIUSEPPE , WEHRENBERG WILLIAM B. 
Published: March 2008

SUMMARYStudies in man demonstrated that salmon calcitonin (sCT) administration blunts the pituitary GH response to GH‐releasing hormone (GHRH). However, the mechanisms underlying this inhibitory action of CT in man are unclear. Pyridostigmine (PD), an acetylcholinesterase inhibitor, is hypothesized to enhance the GH response to GHRH in normal subjects probably via a decrease in the somatostatinergic tone. The aim of the present study was to investigate the mechanism of the inhibitory action of sCT on the GH response to human GHRH (1–29) NH2 by concomitant PD administration in normal humans. The GH response to GHRH was significantly suppressed by prior administration of sCT. Pretreatment of subjects with PD significantly enhanced the GH response to GHRH but did not alter the inhibitory actions of sCT. We conclude that sCT is able to inhibit GHRH‐stimulated GH secretion in man without influencing the hypothalamic somatostatinergic tone.
SERUM FORMS OF TESTOSTERONE IN MEN AFTER AN hCG STIMULATION: RELATIVE INCREASE IN NON‐PROTEIN BOUND FORMS
Authors: COOKE R. R. , MCINTOSH R. P. , MCINTOSH J. G. A. , DELAHUNT J. W. 
Published: March 2008

SUMMARYA postulated function of steroid binding proteins in serum is to smooth changes in steroid levels. To test this, testosterone levels in six normal men were increased by injecting 6000 IU hCG i.m., and changes in serum forms of testosterone were measured. Blood was collected every 10 min for 2.5 h and then once a day for 4 days. By day 4 the mean serum testosterone level had risen to 178%±13% (SEM) of a mean basal level (first five samples). This rise was less than that in free testosterone (221%±18%), which was in turn less than the rise in the non‐SHBG‐bound fraction (255%±19%). The concentrations of SHBG and albumin were constant. Thus, two putative bioactive fractions of testosterone, the free and non‐SHBG‐bound, increased to a greater extent than did total testosterone. Because the binding protein concentrations were constant, this implies they may act not as a buffer, but as an enhancer of active testosterone over this time interval.
THYROTOXICOSIS DUE TO PITUITARY RESISTANCE TO THYROID HORMONES. SUCCESSFUL CONTROL WITH D THYROXINE: A STUDY IN THREE PATIENTS
Authors: DOREY F. , STRAUCH G. , GAYNO J. P. 
Published: March 2008

SUMMARYSelective pituitary resistance to thyroid hormone (PRTH) is responsible for thyrotoxicosis due to inappropriate secretion of TSH. The TSH suppressive action of D‐thyroxine (DT4) has been previously documented in euthyroid and hypothyroid subjects. This prompted us to treat with DT4 three patients with PRTH uncontrolled by anti‐thyroid drugs (ATD) alone or supplemented with bromocriptine, and whose follow‐up had been complicated by atrial fibrillation in two patients. Because of 100% cross‐reactivity between the D and L isomers of T4 and T3 in our RIAs, thyroglobulin (Tg) was used as an index of thyroid secretion. Under ATD, TSH and Tg levels were respectively: 35 mIU/l and 670.5 pmol/1 (patient 1), 87 mIU/1 and 453 pmol/1 (patient 2) and 110 mIU/1 and 906 pmol/1 (patient 3). When DT4 was added (patient 1, 3 mg daily; patients 2 and 3, 2 mg daily) to the same dose of ATD, plasma TSH and Tg levels fell but were still over the upper limit of normal and thyrotoxicosis persisted as illustrated by a recurrence of atrial fibrillation in one patient. When ATD were withdrawn and DT4 given alone (2 mg daily) all symptoms subsided within 1 month while TSH and Tg levels fell within the normal range. TSH normalization was documented within 1 week in one patient. After 16‐27 months of follow‐up the patients remained clinically euthyroid and plasma TSH and Tg levels were normal (patient 1, 0.65 mIU/1 and 5.6 pmol/l; patient 2, 1.4 mIU/1 and 49.8 pmol/l; patient 3, 0.83 mIU/1 and 104.2 pmol/l, respectively) as were the peripheral indexes of thyroid hormones actions serum enzymes, SHBG, ferritin and echocardiographic parameters. We conclude that DT4 at a daily dose of 2 mg is able to control safely thyrotoxicosis due to PRTH. DT4 could be tried as the first treatment of PRTH.
THE GROWTH HORMONE INDEPENDENT INSULIN‐LIKE GROWTH FACTOR‐I BINDING PROTEIN BP‐28 IS ASSOCIATED WITH SERUM INSULIN‐LIKE GROWTH FACTOR‐I INHIBITORY BIOACTIVITY IN ADOLESCENT INSULIN‐DEPENDENT DIABETICS
Authors: TAYLOR A. M. , DUNGER D. B. , PREECE M. A. , HOLLY J. M. P , SMITH C. P. , WASS J. A. H. , PATEL S. , TATE V. E. 
Published: March 2008

SUMMARYThe relationship between the growth hormone independent insulin‐like growth factor binding protein (BP‐28) and serum insulin‐like growth factor‐I (IGF‐I) inhibitory bioactivity observed in diabetic serum was investigated in five poorly controlled adolescent type I diabetics. We have measured the in‐vitro effects of purified BP‐28 from amniotic fluid on serum IGF‐I stimulated and basal cartilage sulphation and compared serum IGF‐I bioactivity obtained from 24‐h serum profiles from each diabetic subject with serum concentrations of BP‐28 and IGF‐I measured by specific radioimmunoassays. Purified BP‐28 inhibited serum IGF‐I stimulated and basal cartilage sulphation in vitro, in a dose‐dependent manner. Serum IGF‐I bioactivity of diabetic sera showed a change in activity over the 24‐h period, with peak inhibitory bioactivity observed in each subject between 0800 and 1000 h. BP‐28 concentrations in each individual showed a marked circadian rhythm with maximum peak levels occurring at 0800 h. Long‐acting insulin administered in the evening in two of the diabetic subjects blunted the maximum peak level attained compared to the three diabetics who had long‐acting insulin administered in the morning. IGF‐I concentrations did not change over the 24‐h period in each individual. The data shows that BP‐28 inhibits serum IGF‐bioactivity on cartilage in vitro. The changes in inhibitory bioactivity observed in diabetic serum are associated with similar changes in serum concentrations of BP‐28. We propose that BP‐28 is one of the IGF‐I inhibitors observed in diabetic serum and that it may play a role in retarded growth and delayed puberty often seen in the adolescent diabetic.
PRESENCE OF BOTH STIMULATING AND BLOCKING TYPES OF TSH‐RECEPTOR ANTIBODIES IN SERA FROM THREE PATIENTS WITH PRIMARY HYPOTHYROIDISM
Authors: KASAGI K. , TAKEDA K. , GOSHI K. , TAKAMATSU J. , HIDAKA A. , HATABU H. , MISAKI T. , IIDA Y. , KUMA K. , KONISHI J. 
Published: March 2008

SUMMARYA case report of three patients with primary hypothyroidism who had potent TSH‐binding inhibitor immunoglobulins (TBII) and both thyroid stimulating (TSAb) and thyroid stimulation‐blocking antibodies (TSBAb) has been described. Two patients displayed symptoms and signs indistinguishable from those in primary myxoedema (cases 1 and 2), and another patient had a history of Graves'disease (case 3). TBII, TSAb and TSBAb activities were 90.0, 1084.2 and 94.5% in case 1, 91.5, 826.6 and 95.8% in case 2, 76.0, 230.0 and 95.0% in case 3, respectively (normal range, < 11.0%, < 145.0 and < 22.0%, respectively. The results indicate that both stimulating and blocking types of TSH‐receptor antibodies exist in these patients. The possible mechanism whereby hypothyroidism developed has been discussed.