ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1991.tb00928.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1991.tb00929.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARYobjectiveThe aim was to study the effect of growth hormone (GH) on new markers of bone resorption (fasting urinary excretion of pyridinium cross‐links (pyridinoline and deoxypyrWlnoline)) in GH‐deficient adultsdesignRandomized, double‐blind, placebo‐controlled cross‐over study. The treatment periods (GH 2 IU/in2subcutaneously, or placebo daity for 4 months) were separated by a 4‐month washout period.patientsTwenty GH‐deficient adults (aged 18–39)measurementsBlood and fasting urine samples were collected at the end of each 4‐month treatment period. Plasma bone Gla protein was measured by radioimmunoassay and urine pyridinoline and deoxypyrfdinoline were measured by spectrofluorometry after high performance liquid chromatography and corrected for urinary creatinineresultsGH increased fasting urinary excretion of pyridinoline (287 ± 123%,P>0·001) and deoxypyridinoline (313 ± 140%,P>0·001). The GH‐induced Increment In these parameters correlated with the increase seen in plasma bone Gla protein (r= 0·83–0·86,P>0·001).conclusionFour months of GH substitution in GH‐deficient adults increases bone resorption as well as bone formation. The effect on b

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1991.tb00930.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARYobjectiveTo study whether modulation of the GABAergic system (with sodium valproate) affects pulsatile LH secretion in the late follicular phase of normal womendesignFifteen normal women volunteers were studied over an 8‐hour period in the late follicular phase of two successive menstrual cycles. On each occasion, blood samples were taken every 10 minutes between 1000 and 1800 h. Nine of the volunteers—the short treatment group—were administered 400 mg of sodium valproate every 8 hours on the two days preceding their second session, and a further 400 mg at 0900 h on the day of the session. The other six—the long treatment group—were administered 400 mg of sodium valproate every 8 hours on the seven days preceding their second session and at 0900 and 1400 h on the day of the sessionmeasurementsLH, oestradiol and progesterone were determined by radloimmunoassay, and sodium valproate by repolarization fluorescence spectrophotometry. Pulse detection was carried out both by the program ULTRA and by a method developed by the authorsresultsThere were no significant differences In LH pulse amplitude or relative pulse amplitude between records taken in the first and second menstrual cycles, i.e. without or with prior sodium valproate treatment. Short treatment did change interpulse interval and mean secretlon period, but the changes, though statistically significant, were small (about 10 minutes), so that the values for both post‐treatment and control sessions were within the normal range; these parameters were unaffected by long treatmentconclusionsActivation of the GABAergic system with sodium valproate had no biologically significant effect on the late follicular phase pulsatile LH secretion of these

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1991.tb00931.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARYobjectiveIn normal subjects, cortlcosterolds stimulate growth hormone (GH) secretion at 3 hours. Obesity is associated with blunted GH secretion. In order to clarify both the deranged mechanism of GH secretion In obesity and the corticosterold mechanism of action we have assessed In normal and obese subjects the effects of dexamethasone, pyridostigmine (a drug capable of suppressing somatostatln release) and GHRH. We also compared in normal subjects the stimulatory effect of three different cortlcosterolds on plasma GH levelsdesignIn both normal and obese subjects the following tests were carried out: placebo; dexamethasone alone (4 mg l.v. at 0 minutes); and dexamethasone plus pyridostigmine (120 mg p.o. at 60 minutes)In normal subjects we also studied the effects of hydrocortisone (100 mg l.v. at 0 minutes) and deflazacort (a corticosteroid that does not cross the blood‐brain barrier) (60 mg l.v. at 0 minutes). In obese subjects we also assessed the effect of dexamethasone plus GHRH (100μg l.v. at 150 minutes) on plasma GH levels.patientsTen normal subjects and 22 obese subjects were studied. Normal controls were within 10% of their ideal body weight. Obese subjects had a body mass Index of 37·1±1·1 (mean ± SEM)measurementsPlasma GH levels were measured by radioimmunoassay.resultsDexamethasone‐induced GH secretion In normal subjects (28·6±7·8 mμ/l,P>0·05). Cortlcosterolds did not alter GH levels In obese subjects. Pretreatment with pyridostigmine increased dexamethasone‐induced GH release in normal subjects (40·8±6·8 mμ/l) but this did not achieve statistical significance. Dexamethasone plus pyridostigmine did not alter GH levels In obese subjects (8·0±1·6 mU/l). In some subjects, dexamethasone protreatment potentiated GHRH‐stimulated GH secretion, while In half the subjects the basal GH levels were not altered.In control subjects, hydrocortisone and deflazacort caused GH release similar to dexamethasoneconclusionsCorticosteroids are a new and selective stimulus of GH secretion. They do not cause GH release in obese subjects. Their relative independence from chollnergic control suggest that they act by reduci

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1991.tb00932.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARYobjectivesWe aimed to investigate both nocturnal spontaneous and morning growth hormone (GH)‐releasing hormone (GHRH)‐induced GH secretion in children on daily glucocorticoid treatment after liver transplantation and to evaluate the effect of pyridostigmine (an acetylcholinesterase inhibitor thought to reduce hypothalamic somatostatin tone) on GH secretion in these patientsdesignWe performed a randomized, single‐blind, crossover studypatientsWe studied three male and three female Juvenile patients, within a year of orthotopic liver transplantation and under immunosuppressive glucocorticoid therapy (mean dose ± SEM, 5·92·0±63 mg/day) and five normal children (four males, one female)measurementsBoth nocturnal spontaneous and morning GHRH‐induced GH secretion were evaluated after administration of placebo, 1 tablet P.O., or pyridostigmine, 2 mg/kg p.oresultsSpontaneous GH. Placebo: in liver transplanted children nocturnal GH secretion (mean GH level 10·8±2·0 mU/l) was not significantly different with respect to normal children (mean GH level 12·8±1·2 mU/l); pyridostigmine: nocturnal GH secretion was significantly Increased as compared to placebo In subjects with liver transplantation but not In normal children. GHRH test. Placebo: liver transplanted patients showed a blunted GH response to GHRH with respect to normal children; pyridostigmine: the GH responses to GHRH (P>0·05) Increased as compared to placebo and did not differ sign If Icantly In the two groups.conclusionsOur data suggest a steroid‐mediated increase in hypothalamic somatostatin tone in liver

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1991.tb00933.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARYobjectiveWe wished to examine the effects of ambient glycaemla on hypothalamic somatostatlnerglc tone In Insulin‐dependent diabetes mellitusdesignAfter 6‐hour periods of either euglycaemla (15 mmol/l) or hyperglycaemia (15 mmol/l), exercise‐induced GH secretion was measuredpatientsSeven insulin dependent diabetics with no evidence of complications were recruitedresultsThere was no significant difference between basal GH levels during euglycaemla and hyperglycaemia (5·50vs5·53 mU/l). Nor was there a significant difference when mean Δ GH levels (33·9vs27·4 mU/l) or mean area under GH curve (2331vs4038 mU min/l) during euglycaemia or hyperglycaemia were compared.conclusionsWe find no evidence therefore to support short‐term effects of ambient glucose concentration on GH responsiveness, and by inference no direct effect of short‐term changes in glycaemic control on hypothalamic release of somatostatln in the aetiology of GH hypersecretion In insulin‐dependent

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1991.tb00934.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARYobjectiveTo evaluate whether the supposed physiological interaction between serotoninergic and opioidergic pathways in the modulation of PRL release is preserved in human obesity, a pathological condition in which these two systems are greatly impaireddesignAccording to a single‐blind randomized procedure, three tests were performed: test A (oral placebo + saline infusion over 5 hours), test B (fenfluramine, a well known serotoninergic drug, 60 mg orally + saline infusion over 5 hours) and test C (fenfluramine at the same dose + naloxone, an opiate receptor antagonist, infusion over 5 hours at a dose of 3 mg/h)patientsTen obese women (body mass index 34·4±2·3 kg/m2, mean ± SE) and ten normal‐weight sex and age‐matched subjects (body mass index 22·3±2·4 kg/m2) volunteered for the study.measurementsAt each test, blood samples for PRL determination were collected in basal conditions (time 0) and every hour for 5 hours. Plasma PRL was determined by radiolmmunoassayresultsIn controls, naloxone significantly reduced the clear‐cut PRL increase induced by fenfluramine. In obese patients, serotoninergic stimulation caused an increment in PRL levels similar to that in the controls, but oplold receptor blockade by naloxone did not affect this responseconclusionsThese findings confirm that there is a physiological relationship between the serotoninergic and the opfoiderglc systems in the control of PRL secretion and show that this interaction is not present in obese subjects. Our data provide indirect proof of the functional impairment of these two systems i

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1991.tb00935.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARYobjectiveWe wished to assess the contributions of Insulin secretion, insulin sensitivity and glucose‐mediated glucose disposal to glucose tolerance in subjects exposed to chronic glucocorticoid excess. DESIGN Patients with Cushing's disease were subjected to a frequently sampled intravenous glucose tolerance test before and at least 3 months after curative surgery and compared to a control grouppatientsSeven patients with clinical and biochemically proven pituitary dependent Cushing's disease and 10 healthy control subjects were studiedmeasurementsPaired glucose and insulin plasma profiles were analysed by the Minimal Model method of Bergman, which provided simultaneous estimates of the glucose decay rate, Insulin secretion, insulin sensitivity and glucose‐mediated and non‐insulin‐mediated glucose disposal. Data were evaluated by non‐parametric statistical analysis and reported as median and interquartile rangesresultsBasal glucose, insulin, C‐peptlde and glucagon levels were significantly raised preoperatively and fell towards normal post‐operatlvely. Glucose tolerance assessed as glucose decay rate was reduced significantly preoperatively (pre: 1·3 (0·8–2·0)vspost: 1·6 (1·5–2·6) per min x 102,p>0·05). First phase insulin release was similar in the Cushing's disease and control subjects. In contrast, second phase insulin release was significantly greater preoperatively and remained high post‐operatlvely compared to control subjects (pre: 18·8 (16·7–23·6)vspost: 16·7 (8·5–18·8)vscontrol 11·1 (4·5–15·4) mU/g/min2x 10‐2,P>0·002). Median insulin sensitivity was reduced by 60% preoperatively in the Cushing's disease subjects compared to the post‐operative Cushing's disease and control subjects (pre: 2·1 (1·3–4·2)vspost: 5·0 (3·2–7·3) vs control 5·1 (2·2–7·2) per min/mU/l x 104). Median glucose‐mediated glucose disposal was reduced by 40% In the pre and post‐operative Cushing's disease subjects compared to the control group (pre: 1·1 (0·6–2·1)vspost: 1·1 (0·6–2·1)vscontrol 1·9 (1·4–2·6) per min x 102), but this was not statistically significant. However, non‐insulin‐mediated glucose disposal was significantly reduced In the preoper‐atlve Cushing's disease subjects (pre: 0·55 (0·08–1·59)vscontrol 1·43 (0·94–2·27) per min x 102,p>0·05). In the Cushing's disease subjects, glucose tolerance correlated with both Insulin sensitivity (rs= 0·84,P>0·01) and non‐insulin‐mediated glucose disposal (rs= 0·56,P>0·05). The fractional clearance rate of insulin was unaltered by Cushing's disease.conclusionsCushing's disease subjects are characterized by impaired glucose tolerance due to both reduced in

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1991.tb00936.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARYobjectiveSerum thyroglobulin (Tg) should be undetectable in patients successfully treated for thyroid carcinoma. We have examined the course of disease in 19 patients with raised serum Tg (<5μg/l) on initial measurement but no other evidence of residual, recurrent or metastatic cancer.design416 patients from several centres were followed for periods between 1 and 9 years. Serum Tg was measured at 6–12‐month intervalspatientsAll had differentiated thyroid cancer, treated by partial or total thyroldectomy and/or131I ablation, and were receiving suppressive thyroxine therapy.measurementSerum Tg was measured and clinical, X‐ray and scan assessment made of presence or absence of residual, recurrent or metastatlc cancerresultsOf 416 patients initially assessed, only 19 had Tg<5μg/l but no clinical or radiological evidence of disease. At follow‐up, 11 patients had developed overt signs of malignancy; one had been treated with131I with a subsequent fall in Tg; five had Tg between 5 and 20μg/l with incompletely suppressed TSH levels; two subjects remained with slightly elevated Tg and undetectable TSH.conclusionPatients with elevated Tg require careful follow‐up even in the apparent absence of disease. Moderate elevation of serum Tg may be due to inadequate thyroxine suppression therapy, assessed by detectable TSH values measured in a se

ISSN:0300-0664    

DOI:10.1111/j.1365-2265.1991.tb00937.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY