摘要:

SUMMARYA patient with congenital adrenal hypoplasia (AH) and hypogonadotrophic hypogonadism was treated with pulsatile subcutaneous GnRH therapy for 16 weeks in an attempt to induce puberty. No rise in serum LH or FSH concentrations occurred despite increasing doses of GnRH (2.8 μg/pulse‐22.4 μg/pulse). In contrast a similar programme of therapy successfully initiated the biochemical changes of puberty in a patient with Kallmann's syndrome. Both patients before therapy had low basal serum LH and FSH concentrations with blunted LH and FSH responses to GnRH stimulation. After 1 week, serum LH and FSH rose into the normal adult range in the patient with Kallmann's syndrome. This study fails to confirm a previous report which suggested that intermittent low dose GnRH therapy may be of value in inducing puberty in AH. The reasons for the difference of pituitary responsiveness to GnRH in AH and Kallmann's syndrome are unclear at pres

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb01401.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYIn a previous study we have analysed serum free T4 concentrations in a representative population of 70‐year‐old men. In the present study the effect of previous or present tobacco smoking on free T4, T4, T3, rT3, TSH and thyroid hormone binding proteins was analysed in 181 of the 460 men, excluding those with past or present goitre, those who were obviously ill or had died between 70 and 75 years of age and those who had any disease or medication influencing free T4 concentrations. Smokers had higher T4 and rT3 levels, and lower TSH levels but T3 levels no different from non‐smokers. The difference in T4 levels, but not rT3 or TSH levels, between smokers and non‐smokers could be attributed to differences in body mass and also to differences in TBG levels. The results indicate that tobacco smoking is associated with long‐term alterations in thyroregulatory

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb01402.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYAn alteration of the hypothalamic dopaminergic regulation of LH secretion has been implicated in the abnormal LH secretion of polycystic ovarian syndrome (PCOS). To investigate this, the acute effect of dopamine (DA) receptor blockade on LH, FSH, PRL and TSH secretion was determined. No effect was observed on either LH or FSH secretion in the PCOS patients or in normal women and LH pulsatility appeared to be maintained. When the PCOS patients were divided into those who ovulated in the preceding cycle and those who were anovulatory, it was observed that the ovulatory patients had a normal PRL and TSH response; whereas in the anovulatory patients, the PRL rise was blunted and the TSH response was absent. We conclude that this study gives no evidence to support the hypothesis of altered hypothalamic DA regulation of LH secretion in PCOS. The lack of LH response to DA blockade suggests that a physiological role of DA in the control of LH secretion seems unlikely as determined under these experimental conditions. The differences in PRL and TRH response may reflect anovulation rather than a fundamental abnormality in PCOS.

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb01403.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYNineteen patients thought to have Cushing's disease were treated by trans‐sphenoidal microsurgery; the type of operation performed depended upon the findings in the individual patient. Seventeen patients remitted. Failures occurred in a patient with an invasive macroadenoma and in a patient who was subsequently found to have a thymic carcinoid tumour secreting ACTH. One patient who remitted suffered a recurrence during pregnancy, 30 months after operation. The ten patients (Group I) who had a selective removal of a microadenoma or a limited resection of the gland were often GH deficient, but seven regained cortisol reserve and all ten regained normal pituitary‐thyroid and pituitary‐gonadal responses. By contrast abnormalities of pituitary function were common in nine patients who had a radical or total hypophysectomy. We conclude that transsphenoidal microsurgery is the best treatment for Cushing's disease and that, when feasible, a selective microadenomectomy is the most appropriate oper

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb01404.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYTwenty‐three endemic goitrous subjects (goitre grade: III and IV) that were living in a chronic iodine‐deficient area (iodine intake: less than 40 μg I/d) were submitted to clinical and laboratory evaluation within 3–8 weeks of arrival at the metropolitan area of São Paulo, where daily iodine intake is estimated to be 150–200 μg I/d. Eight patients developed a mild thyrotoxic state (T4 = 14.7 ± 2.3 μg/dl, T3 = 279 ± 55 ng/dl, no TSH response to TRH). Five additional subjects, although euthyroid, had a blunted TSH‐response to TRH, and the remaining ten patients were euthyroid and had a normal TSH response to TRH. Thyrotoxicosis was associated with larger goitres (mean thyroid weight: 133 ± 46 g), with high thyroid uptake of RAI (mean 24 h131I uptake: 40 ± 15%) but not with increased urinary iodine excretion. Serum Tg levels were more elevated in the first two groups of patients (respectively, geometric means 68 and 72 ng/ml), than in the euthyroid, TRH‐responsive group (52 ng/ml). Thyrotoxicosis resolved spontaneously after three to six months without the need for any specific medication. It was concluded that a relatively small and normal iodide intake due to regular consumption of iodized salt and industrialized foods may induce a transient form of thyrotoxicosis in endemic goitre patients arrivi

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb01405.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYThe effect of adrenergic denervation on the metabolic and hormonal responses to a standard meal was studied in six tetraplegic subjects (pre‐ganglionic sympathectomy) and compared with six normal subjects. Gastric emptying, estimated by isotope scintiscanning, was similar in both groups. Following the meal the mean blood glucose and plasma insulin rose in both groups, but were higher and remained elevated for longer in the tetraplegic subjects. There were no significant differences in the secretion of pancreatic glucagon, enteroglucagon, gastric inhibitory peptide (GIF) and neurotensin between the two groups. The mean basal and post‐prandial levels of pancreatic polypeptide and motilin were significantly higher in the tetraplegic group. This study confirms the presence of mild glucose intolerance in tetraplegic subjects which is not explicable on the basis of abnormal insulin or pancreatic glucagon secretion or abnormal gastric emptying. In addition the results provide evidence for a sympathetic inhibitory influence on the secretion of pancreatic polypeptide and motilin in man, which is probably adrenergically‐med

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb01406.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYProstaglandins and prostaglandin synthesis inhibitors are known to influence the secretion of a number of hormones. More specifically, sodium salicylate is known to increase insulin secretion in Type II diabetics in response to a glucose stimulus. To challenge the hypothesis that prostaglandins may be instrumental in a generalized defect of glucose recognition in Type II diabetics, the effect of sodium salicylate on the hormonal counter‐regulatory response to insulin‐induced hypoglycaemia was examined. Before salicylate treatment, seven Type II diabetics had brisk increases (mean ± SEM) in circulating adrenaline (time 0 = 50 ± 7 pg/ml; peak = 1630 ± 330 pg/ml), noradrenaline (time 0 = 260 ± 46 pg/ml; peak = 770 ± 140pg/ml), glucagon (time 0 = 38 ± 6 pg/ml; peak = 75 ± 10 pg/ml) and pancreatic polypeptide (time 0 = 149 ± 30 pg/ml; peak = 1170 ± 180 pg/ml) in response to insulin‐induced hypoglycaemia. In contrast to previous studies in normal subjects, treatment with sodium salicylate failed to augment hypoglycaemia‐induced secretion of adrenaline, noradrenaline or pancreatic polypeptide in Type II diabetics. The glucagon response to hypoglycaemia was augmented by sodium salicylate when the data were expressed as the incremental area under the glucagon vs. time curve, but not when peak response was used for analysis. These results are inconsistent with a prostaglandin‐related generalized defect in glucose recognition in Type II diabetics and suggest that augmentation of hormone secretion in these patients by sodium salicylate may be specific for glucose‐induc

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb01407.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYThe mechanism for the hyperinsulinaemia in cirrhosis was investigated using two different approaches. In the first study, the metabolic clearance rate of insulin was measured at steady state in 13 cirrhotic and 13 weight‐matched control subjects. With comparable insulin infusion rates (1.00 ± 0.19 versus 1.07 ± 0.15 mU/kg/min), steady‐state plasma insulin concentrations (104 ± 25 versus 87 ± 12 μU/ml; P>0.5) and MCRIRI(13.6 ± 1.6 versus 15.4 ± 2.0 ml/kg/min; P>0.5) were similar. In the second study, fasting and oral glucose stimulated C‐peptide/insulin ratios were compared in 16 cirrhotic and 18 weight matched control subjects. Although fasting glucose levels were significantly higher in the cirrhotic groups, all values were in the normal range (5.5 ± 0.3 versus 4.8 ± 0.1 mmol/l, P<0.02). However, fasting insulin (0.171 ± 0.02 versus 0.068 ± 0.004 nmol/l) and C‐peptide (1.02 ± 0.13 versus 0.42 ± 0.02 nmol/l) were strikingly higher (P0.3). This suggests that beta cell hypersecretion was the principal cause of the fasting hyperinsulinaemia, rather than decreased insulin hepatic extraction. Following the glucose load in 13 of the control and seven of the cirrhotic group, the C‐peptide/insulin ratio fell in both groups but was significantly lower in the cirrhotic compared to control subjects at 30, 60 and 120 min, consistent with possible impairment of hepatic insulin extraction. We conclude that, in cirrhosis, fasting hyperinsulinaemia is due to beta cell hypersecretion, whereas at higher insulin secretion rates following a glucose load, reduced hepatic insulin extraction may also contribut

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb01408.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYInsulin‐induced hypoglycaemia, which stimulates gastric acid secretion, is associated with an increase in circulating somatostatin levels in man. In order to assess the mechanisms involved in this rise, six normal volunteers connected to a Biostator for continuous glucose monitoring were studied, on three separate occasions. On each occasion after basal blood sampling, 0.15 i.u. /kg body weight of insulin was administered i.v. and further samples were obtained intermittently over 150 min. On one occasion, dextrose was infused by the Biostator to prevent hypoglycaemia, while on the other two, a constant infusion of either normal saline or the specific H2antagonist cimetidine was administered. Insulin plus dextrose caused no significant changes in circulating somatostatin levels, whereas insulin plus saline was associated with a marked, sustained and significant rise in all subjects; insulin plus cimetidine also produced a rise but it was delayed; the area under the curve was significantly (P<0.05) greater with insulin plus saline than with insulin plus cimetidine. These results show that in man insulin itself does not stimulate somatostatin secretion directly, but indirectly via hypoglycaemia. Further, the inhibition of gastric acid secretion with cimetidine reduces somatostatin release during insulin‐induced hypoglycaemia. This suggests that gastric acid may mediate somatostatin secretion associated with insulin‐induced hypoglyc

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb01409.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY

摘要:

SUMMARYReceptor and post‐receptor abnormalities of insulin action and their possible role in the insulin resistance of cirrhosis were examined in eight biopsy‐proven cirrhotic subjects and eight age‐weight matched healthy volunteers. To this end, oral glucose tolerance tests (OGTT), insulin dose response curves and insulin binding to circulating monocytes were determined for each subject. The dose‐response curves for the cirrhotic subjects were significantly shifted to the right compared to the control subjects, indicating the presence of insulin insensitivity (ED50223 ± 30 versus 64 ± 8 mU/l respectively; P<0.001). The magnitude of the right shift of the insulin‐dose response curves correlated significantly (P<0.001) with the OGTT 2 h insulin levels (r = 0.74) and the insulin areas under the OGTT curves (r = 0.86). In contrast, insulin responsiveness was marginally elevated in the cirrhotic group (maximal glucose disposal 680 ± 47 versus 574 ± 21 ml/m2/min; P<0.05). Insulin binding to circulating monocytes was normal in the cirrhotic subjects. It is concluded that the insulin resistance of cirrhosis is due to a post‐receptor defect in insulin action which reduces insulin sensitivity but not insulin

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1984.tb01410.x

出版商:Blackwell Publishing Ltd    

年代:1984

数据来源: WILEY