摘要:

SUMMARY131I‐meta‐iodobenzylguanidine scanning was performed in 14 patients with phaeochromocytomas. In all but one patient scintigraphy successfully localized the lesion(s). The results confirm that scintigraphic imaging with131I‐meta‐iodobenzylguanidine, a noninvasive method, is a valid and reliable procedure for imaging and localization of adrenal and extra‐adrenal phaeochromocytomas, both benign and

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb00054.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYThe modulation of pulsatile gonadotrophin release by endogenous ovarian steroids during the normal menstrual cycle may be involved in the initiation of the following menstrual cycle. The absence of this cyclical variation may, in some cases, be the cause of, or contribute to the cause of, amenorrhoea. To assess this the modulatory effect of gonadal steroid administration on the pulsatile release of gonadotrophins was studied in fourteen amenorrhoeic and four oligomenorrhoeic women. Pulsatility was assessed by samples collected at 10 min intervals during a 4 h morning period before and after treatment with either progesterone or micronized oestradiol or a sequential combination of both.Ten patients with intact positive oestrogen‐gonadotrophin feedback responded to progesterone treatment by both a significant reduction in LH pulse frequency, from a mean of 4·1 to a mean of 2·1 pulses within the 4 h study period and an increase in pulse amplitude. Progesterone therapy did not affect mean LH concentrations but there was a significant reduction in mean FSH concentrations. In the eight patients with absence of positive feedback, none of the treatment regimes elicited significant changes in LH release. No definable FSH pulses were detected before or after treatment in either group.Both the changes in LH and FSH concentrations and their release observed in this study, support the concept that cycle initiation may be related to a reduced pituitary exposure to LHRH associated with elevated progesterone concentration in the luteal phase of the cycle. This selectively induces FSH synthesis and storage. Release of this stored FSH may occur as a result of failure of the corpus luteum and falling progesterone concentrati

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb00055.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYHuman red blood cells (RBC) have been shown to have highly specific insulin receptors. We have studied the binding characteristics of insulin to these receptors in erythrocytes from normal male and female subjects on their usual diet and physical activity. There were no significant differences in insulin binding in erythrocytes from females between the two phases of the menstrual cycle. However, the receptor concentration was higher in the 2nd half of the cycle accompanied by a reduction in affinity.Binding curves of125‐I‐insulin to RBC from males were higher than females in either phases of the menstrual cycle, primarily due to an increase in receptor concentration when compared to females in the follicular phase and mediated by an increased affinity at low receptor occupancy when compared to females in the luteal phase.We speculated that the differences in the binding characteristics of125I‐insulin to RBC insulin receptors are mediated by differences in the levels of sex hor

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb00056.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYThe serum T3 assay has been regarded as the most sensitive single test for hyperthyroidism although impaired conversion of T4 to T3 in non‐thyroidal illness (NTI) might decrease its diagnostic sensitivity. The present report gives experience from the T3 assay in middle‐aged females under conditions similar to those in a general health survey. The assays were performed during two periods with an interval of six years.In 1974–75 we studied a representative sample (n= 1283) of women of ages 44, 52, 56, 60 and 66 years in Göteborg, Sweden. Individuals with serum T3 concentration>mean + 2·5 SD were selected for a follow‐up study (n= 21). Of 16 individuals with no previous thyroid disease and no present treatment with thyroid hormones or oestrogens, 14 were subjected to a TRH‐stimulation test giving a normal TSH response in 10 cases having T3 concentrations up to mean + 3·5 SD. Four women with serum T3 concentration ≥ mean + 3·5 SD had previously unrecognized autonomous function thyroid function, of whom two developed hyperthyroidism after two years.The original population sample was reinvestigated after six years in 1980‐81 (n= 1138) together with an additional sample of women giving a total sample of 1422 women of ages 26, 38, 50, 58, 62, 66 and 72 years. Of the females studied in 1974–75 eight had developed hyperthyroidism between the two studies; three of these had raised serum T3 at the investigation in 1974–75. No case of hyperthyroidism had been missed by the T3 assay in the 1974–75 study. Of individuals with serum T3≥mean + 2·5 SD selected for a follow‐up (n= 29) at least five were found to have previously unrecognized thyroid autonomy.We found a raised serum T3 to be associated with hyperthyroid (n= 2) and euthyroid GRAVES' disease, autonomously functioning thyroid adenoma(s), possible painless subacute thyroiditis, possible thyrotoxicosis factitia, diminished thyroid reserve and thyroid substitution therapy.Since we did not correct for variations in protein binders a number of individuals with oestrogen‐associated rise of total T3 were identified, but the rises were usually modest. The incidence of hyperthyroidism for the original sample as calculated for the six‐year period was 1.3 cases/1000 women/year whereas the prevalence by 1980‐81 was 13 cases/1000 women.We conclude that a single T3 determination will in most cases be sufficient for the diagnosis of clinical hyperthyroidism in a non‐hospitalized population. Our study indicates some of the problems associated with the follow‐up of a general screening for hyperthyroidism, the possible

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb00057.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYIn postmenopausal women with breast carcinoma, plasma and urinary oestrogens remain detectable following surgical adrenalectomy or hypophysectomy. These residual oestrogens could result from absorption of exogenous steroids, from endogenous production, or from a combination of these two sources. To determine whether endogenous production contributes to this oestrogen pool, we administered a potent steroidogenesis inhibitor, aminoglutethimide (AG), to women with breast carcinoma following hypophysectomy or adrenalectomy. Plasma and urinary oestrogens were measured with radioimmunoassays developed to provide appropriate sensitivity. In five women treated after initial hypophysectomy (hypox), plasma oestrone fell from 66·28 pg/ml (hypox) to 9·1 ± 2·4 pg/ml (hypox and AG) and oestradiol decreased from 8·3 ± 1·8 pg/ml to 2·5 ± 0·69 pg/ml. Similar decrements in urine oestrone (U‐E1) and ostradiol (U‐E2) were observed (U‐E1hypox: 2·25 ± 0·71 μg/24 h and 0·071·0±015 μg/24 h hypox and AG; U‐E20·47 ± 0·12 μg/24 h hypox to 0·124 ± 0·015 hypox and AG,P<0·05 for all). Similar significant reductions in plasma oestrone and oestradiol were observed in four women treated with aminoglutethimide following surgical adrenalectomy. While the levels of urinary oestrogens also fell in these patients, the differences were not statistically significant. In response to the decrements in oestrogen levels induced by AG, 2/5 women in the post‐hypophysectomy group and 2/4 in the post‐adrenalectomy group experienced partial objective tumour regression. These observations indicated that the residual oestrogens produced after surgical adrenalectomy or hypophysectomy, even though made in small quantities, were nonetheless biologically active. We conclude that endogenous production of oestrogens in extragonadal and extra‐adrenal sit

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb00058.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYThe role of dopaminergic mechanisms in the control of gonadotrophin secretion in normal and hyperprolactinaemic subjects is controversial. Whilst bromocriptine, a potent dopamine agonist, has been used to restore normal gonadotrophin secretion in subjects with pathological hyperprolactinaemia (PHP), dopamine and dopamine agonists have been reported to suppress basal and stimulated gonadotrophin release. We therefore investigated the importance of dopaminergic control of gonadotrophin secretion by studying LH, FSH and PRL responses in normal and PHP subjects to central dopamine synthesis inhibition using monoiodotyrosine (MIT) and to a 4 h dopamine infusion designed to elevate peripheral plasma dopamine concentration to levels reported for pituitary portal plasma (1–6 ng/ml). MIT administration resulted in a significant release of PRL (peak increment 520 ± 84% above basal) but not of LH or FSH in normal subjects. In PHP subjects there was a blunted PRL response (peak 13·3 ± 3·5%) to MIT administration and significant LH (P<0·05) but not FSH release. Dopamine infusion (0·5 μg/kg/min) resulted in suppression of PRL (min 19 ± 3% of basal) but not of LH or FSH. A rebound of PRL (peak 188 ± 68% of basal) but not LH or FSH occurred on cessation of dopamine. There was an apparent rise in LH (P<0·02 vs. normals) but not FSH in PHP patients during dopamine infusion. Plateau dopamine levels achieved during the infusion were 2·9 ± 0·3 ng/ml and 5·9 ± 0·8 ng/ml in normal and PHP subjects respectively. The responses to MIT show that dopamine functions as an inhibitor of PRL but not of LH or FSH in normal subjects. In PHP patients the responses suggest increased dopaminergic inhibition of LH release but loss of inhibitory control of PRL release. Physiological concentrations of plasma dopamine do not significantly inhibit LH or FSH release in normal subjects but paradoxically results in an apparent release of LH in PHP patients. We conclude that dopamine mechanisms do not play a significant role in modulating gonadotrophin release in normal subjects. In PHP pati

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb00059.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYPlasma glucose, immunoreactive somatomedin‐C (Sm‐C), GH, insulin (IRI) and T3 were measured daily in 20 obese subjects before and during a 9‐day fast. Control levels of Sm‐C were normal and exhibited no significant correlation with any of the other parameters investigated. During fasting there were no consistent variations in GH, but significant decreases occurred in blood glucose, IRI, T3 and Sm‐C levels. While individual Sm‐C patterns varied widely, as a group the fasting Sm‐C values showed a positive correlation with the fasting IRI and T3 levels, and with control body weight. These findings suggest that the decrease in Sm‐C which occurs during caloric deprivation may be the result of concomitant decreases occurring in T3

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb00060.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYSynthetic CRF‐41 has been given to 43 patients with hypothalamic, pituitary or adrenal diseases and contrasted with the responses in 20 normal subjects. In the normal subjects the mean increment in serum cortisol (± SE) was 276 ± 38 nmol/l; the increments showed a significant negative correlation with the basal serum cortisol levels (r= ‐0·56;P<0·02). The mean peak serum cortisol was 662 ± 34 nmol/1 and the mean peak corticosterone was 28·6 ± 3·8 nmol/1. There was a significant positive correlation between the peak serum corticosterone and cortisol concentrations (r= 0·84;P<0·0001). Dexamethasone pretreatment abolished the rise in cortisol in response to CRF‐41. The peak serum cortisol following CRF‐41 was not significantly different between the normal subjects and those patients with pituitary disease who had normal cortisol responses to insulin‐induced hypoglycaemia. However, in individual patients the peak cortisol levels induced by hypoglycaemia were greater than, but significantly correlated with, those induced by 100 μg of CRF‐41. Seven patients were ACTH deficient in response to hypoglycaemia, and of these six responded normally to CRF‐41. Only one of these patients had a lesion clearly originating in the hypothalamus; four had pituitary tumours with suprasellar extensions and the remaining patient had idiopathic GH and ACTH deficiency. Our data suggest that these patients have a functional defect of ACTH secretion due to the failure of CRF to reach the corticotroph. Of the four patients with pituitary‐dependent Cushing's disease who were on no treatment at the time of testing, three showed an exaggerated and one a normal response to CRF‐41. These normal or enhanced responses of hypercortisolaemic patients with Cushing's syndrome contrast with the complete inhibition of the responses to CRF‐41 in normal subjects given dexamethasone. In the treated p

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb00061.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYFasting serum calcitonin levels were measured in 54 postmenopausal women who had for 10 years been taking part in a double blind trial to assess the effect of the synthetic oestrogen, mestranol, on postmenopausal bone loss. There were no differences in calcitonin levels between mestranol treated and placebo groups, Fifteen of the women were challenged with a calcium infusion to measure the secretory reserve of calcitonin. Oestrogen treatment did not increase the calcitonin response to calcium infusion. The three patients who exhibited the greatest responses were placebo treated. Bone density was measured by γ‐ray absorptiometry over the ten year period and the annual rate of change of bone density calculated. No correlation could be found between basal calcitonin level or calcitonin reserve and change in bone density. Our results indicate that postmenopausal osteoporosis is not caused by a deficiency of calcitonin and that the action of oestrogen therapy to prevent bone loss does not involve calciton

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb00062.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYThe practical application of a simple, reproducible androgen receptor assay using dispersed fibroblasts is described for the investigation of patients with the androgen insensitivity syndrome (AIS). The concentration of androgen receptors (Bmax) in genital skin fibroblasts derived from normal subjects is 814 ± 168 ×−18moles/μg DNA (mean ± SD) and the binding affinity (Kd) is 0·91 ± 0·26 × 10±10M at 37°C, using [3H]‐5α‐dihydrotestosterone (DHT) as the labelled ligand. Studies in patients with phenotypic signs of complete or partial AIS showed either absent (receptor‐negative), decreased (receptor‐deficient) or normal/increased (receptor‐positive) specific binding of DHT to the receptor. In some mutant cell lines, there was evidence of thermolability and increased rate constant of dissociation of the androgen‐receptor complex, suggesting a possible structural abnormality of the receptor protein. This simple receptor assay can be used to delineate quantitative and qualitative defects of the androgen receptor in a significant number of patients with a wide spectrum of phenotypic abnormalities associated

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb00063.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY