bluuebunny/crossref_metadata_2025_split huggingface dataset:
FENCLOFENAC‐SECONDARY EFFECTS UPON THE PITUITARY THYROID AXIS
Authors: TAYLOR R. , HUTTON C. , WEEKE J. , CLARK F. 
Published: March 2008

SUMMARYTo elucidate the mechanism of suppression of TSH responsiveness to TRH induced by the initiation of fenclofenac therapy, the early period of drug administration was examined in detail and the effect of the drug during a thyrotrophin releasing hormone infusion was assessed. In addition, the effect of fenclofenac upon the response of ACTH, cortisol, growth hormone and prolactin to insulin‐induced hypoglycaemia was examined. The effect of fenclofenac upon an equilibrium dialysis method for estimating free thyroid hormones was evaluated and was found to be insignificant within the therapeutic concentration range of the drug. A sharp, short‐lived rise in free thyroxine (21·7 ± 2·0 to 26·8 ± 1·9 pmol/1; P <0·03) was observed 60 min after the first dose of fenclofenac. Repeated peaks of free thyroxine during chronic fenclofenac treatment, superimposed upon the previously described steady decline of free and total serum thyroxine, are postulated to cause the observed suppression of TSH release which is present only until free and total serum thyroxine levels reach their nadir. The time course of the changes seen during thyrotrophin releasing hormone infusion suggested that the pituitary suppression was secondary to a rise in free thyroxine. The responses to hypoglycaemia of those pituitary hormones examined were not affected by fenclofenac.
EFFECT OF FENFLURAMINE ON PROLACTIN SECRETION IN OBESE PATIENTS: EVIDENCE FOR SEROTONINERGIC REGULATION OF PROLACTIN IN MAN
Authors: BARBIERI C. , MAGNONI V. , RAUHE W. G. , ZANASI SILVIA , CALDARA R. , FERRARI C. 
Published: March 2008

SUMMARYThe present investigation was carried out to study the effect of serotoninergic stimulation on prolactin (PRL) secretion in man. Fenfluramine (60 mg, orally), an anorexiant drug which under acute circumstances stimulates the serotoninergic system, was administered to eight obese patients. Compared with placebo, drug administration increased PRL significantly (P < 0.05 at 180 and 300 min, P < 0.01 at 240 min). No significant changes were observed after fenfluramine in blood pressure, plasma aldosterone (PA), plasma cortisol, plasma renin activity, serum electrolytes or growth hormone. Since it has been reported that dopaminergic blockade raises PA concentration, the lack of change in PA in obese patients treated with fenfluramine suggests that the observed increase in PRL induced by fenfluramine is likely to be mediated by serotoninergic stimulation.
LONGTERM PERGOLIDE TREATMENT OF ACROMEGALY
Authors: KENDALL‐TAYLOR PAT , UPSTILL‐GODDARD GILL , COOK D. 
Published: March 2008

SUMMARYThe effect of pergolide mesylate, a new potent longacting dopamine agonist, was investigated in eight patients with active acromegaly, none of whom had received pituitary irradiation. Patients were assessed at different dose levels for clinical response and biochemical response by measuring mean fasting growth hormone (GH), mean ambulant GH and glucose‐induced GH response. Six patients had definite clinical improvement. No major side effects were noted. All patients showed a statistically significant reduction in GH, although in two reduction was not below 75% of pretreatment levels. On 500 μg pergolide daily the overall response for the group of eight patients was a reduction of fasting serum GH, mean ambulant GH and of GH response to glucose to 55% of pretreatment values. When the daily dose was increased to 1000 μg there was a further significant reduction in GH in some patients; on this dose the response for the group was a decrease in fasting serum GH and mean ambulant GH to 40% of pretreatment values. In three patients GH concentrations of 5 mU/1 or less were achieved. In two patients the daily dose was increased to 1500 μg but no extra benefit was obtained. We conclude that pergolide given once daily has a beneficial effect in acromegaly, with significant reduction in serum GH; it promises to be a useful therapeutic agent.
INFLUENCE OF OBESITY ON BASAL GLUCAGON LEVELS IN NON‐DIABETIC AND DIABETIC NAURUANS
Authors: ALFORD F. P. , ZIMMET P. , CHISHOLM D. J. , WHITEHOUSE S. 
Published: March 2008

SUMMARYBasal plasma glucagon (IRG), insulin (IRI) and glucose levels were measured in normal weight (Body Mass Index (BMI) < 30) and obese (BMI < 30) non‐diabetic and diabetic Micronesians (n= 30) on Nauru Island. This population has a high prevalence of diabetes mellitus. IRG levels were significantly higher (P < 0.02) in the non‐diabetic obese, compared to the non‐diabetic lean subjects (109 ± 19 vs 44 ± 12 SEM pg/ml, respectively) and there was a significant positive correlation between basal IRG and BMI (r= 0.79, P < 0·001). IRG levels were similar in diabetic obese and diabetic lean subjects. The pathophysiological significance of the hyperglucagonaemia in these obese subjects is not known, although it may be related to the frequent development of diabetes in this unique population.
PSEUDOHYPOPARATHYROIDISM: INHERITANCE AND EXPRESSION OF DEFICIENT RECEPTOR‐CYCLASE COUPLING PROTEIN ACTIVITY
Authors: FISCHER J. A. , BOURNE H. R. , DAMBACHER M. A. , TSCHOPP F. , DE MEYER R. , DEVOGELAER J.‐P. , WERDER E. A. , DE DEUXCHAISNES C. NAGANT 
Published: March 2008

SUMMARYPseudohypoparathyroidism, Type I (PSP‐I) is a familial disorder characterized by secondary hyperparathyroidism, resistance of urinary cyclic adenosine‐3′,5′‐monophosphate (cAMP) excretion to exogenous parathyroid hormone (PTH), and by effects upon other hormones, including thyrotrophin (TSH) hyperresponsiveness to thyroliberin (TRH). In the present study, 12 PSP‐I patients in five families exhibited partial deficiency of receptor‐cyclase coupling protein (N protein) in blood cells, in association with the skeletal findings of Albright's hereditary osteodystrophy. In one father and six mothers of PSP‐I patients, deficient N protein activity was associated with normal urinary cAMP responses to PTH. In this group of seven parents, five had Albright's osteodystrophy, two exhibited secondary hyperparathyroidism, and two had TSH hyperresponsiveness to TRH. In a sixth family with none of the features of Albright's osteodystrophy, N protein deficiency did not correlate with urinary cAMP responsiveness to PTH. In this kindred, one mother with N protein deficiency, but normal urinary cAMP responsiveness to PTH had raised serum levels of immunoreactive PTH. We conclude that in the majority of families with PSP‐I the urinary cAMP response to PTH is an inadequate indicator of the genetic defect. In such families, deficiency of N activity more consistently points to metabolic defects, including secondary hyperparathyroidism and TSH hyperresponsiveness, even when urinary cAMP responses are normal.
CHANGES IN CYCLIC AMP AND ELECTROLYTES AFTER PARATHYROIDECTOMY IN PRIMARY HYPERPARATHYROIDISM
Authors: KOHRI KENJIRO , KATAOKA KIYONORI , YACHIKU SUNAO , KURITA TAK‐ ASHI , SONODA TAKAO 
Published: March 2008

SUMMARYChanges in the excretion of urinary cyclic AMP, calcium and phosphate, and serum calcium, ionized calcium, and magnesium were studied after parathyroidectomy for primary hyperparathyroidism. Urinary cyclic AMP decreased rapidly and 8 of 11 patients had a significant reduction 1 h postoperatively, but changes in serum calcium and ionized calcium were delayed. Serum calcium concentrations closely parallelled those of serum ionized calcium and phosphate excretion returned to normal almost 7 h later than that of cyclic AMP. Excretion of urinary calcium rose rapidly at 4 h after surgery because calcium clearance improved after the reduction in circulating parathyroid hormone. The fall in urinary calcium at about 24 h was due to the subsequent reduction in serum calcium.
MEASUREMENT OF SEX HORMONE BINDING GLOBULIN IN HUMAN AMNIOTIC FLUID: ITS RELATIONSHIP TO PROTEIN AND TESTOSTERONE CONCENTRATIONS, AND FETAL SEX
Authors: HAMMOND G. L. , LEINONEN P. , BOLTON N. J. , VIHKO R. 
Published: March 2008

SUMMARYSex hormone binding globulin (SHBG) has been identified and quantified in human amniotic fluid. Identification was based on its electrophoretic mobility on polyacrylamide gels and its steroid binding characteristics, which were identical to those attributed to SHBG in pregnancy serum. Amniotic fluid SHBG binding capacity was measured by competitive saturation analysis using [3H]‐5α‐dihydrotestosterone as the labelled ligand, after removal of endogenous steroids with dextran‐coated charcoal. Similar amniotic fluid SHBG binding capacities were found in samples taken during early (13–20 weeks, 8.5 ± 5.1 (SD) nmol/l, n= 10) and late (36–37 weeks, 8.7 ± 3.0 nmol/l, n= 28) pregnancy. In comparison with pregnancy serum SHBG levels (390 ± 140 nmol/l, n= 5), amniotic fluid SHBG was not enriched in relation to the relative concentrations of total proteins, albumin or transferrin. Amniotic fluid is therefore not a better source for the purification of SHBG than pregnancy serum. There were no differences in amniotic fluid SHBG levels with respect to fetal sex, but positive correlations were observed between SHBG binding capacities and testosterone concentrations in amniotic fluid from both male (r= 0.68, P < 0.001) and female (r= 0.53, P < 0.05) fetuses. It is suggested that SHBG may sequester free testosterone in amniotic fluid, and that measurements of SHBG in amniotic fluid may help to more accurately identify fetal sex in cases where borderline amniotic fluid testosterone concentrations are found.
HYPOGONADOTROPHIC HYPOGONADISM RESISTANT TO hCG AND RESPONSIVE TO LHRH: REPORT OF A CASE
Authors: DONALD R. A. , WHEELER M. , SÖNKSEN P. H. , LOWY C. 
Published: March 2008

SUMMARYThe treatment of hypogonadotrophic hypogonadism with gonadotrophin releasing hormone (LHRH) has proved difficult in the past because of a progressive decline in the pituitary gonadotrophin response. These early studies generally used large relatively infrequent doses of natural LHRH (Davies et al., 1977) or analogues with a prolonged action (Smith et al., 1979).Recently, several reports have indicated that the lack of gonadotrophin response to LHRH can be overcome by frequent administration of low doses of natural LHRH in a pulsatile fashion (Belchetz et al., 1978; Crowley et al., 1980; Jacobson et al., 1979; Schoemaker et al., 1981; Valk et al., 1980). However, it is not known whether those patients with hypogonadotrophic hypogonadism who fail to respond to human chorionic gonadotrophin (hCG) (Bardin et al., 1969) are capable of responding to LHRH. In this case report of a patient with hypogonadotrophic hypogonadism who was resistant to prolonged hCG therapy, normal pituitary gonadotrophin and testosterone responses were obtained following pulsatile LHRH administration. The sperm count rose to 11 ± 106/ml. His wife became pregnant and was delivered of a normal healthy female infant after an uneventful pregnancy.
OPIATE PEPTIDES CONTROL GROWTH HORMONE THROUGH A CHOLINERGIC MECHANISM IN MAN
Authors: DELITALA G. , GROSSMAN A. , BESSER G. M. 
Published: March 2008

SUMMARYOpiate peptides are known to elevate circulating GH in man, and data in other animals suggest that acetylcholine may be involved. We have administered the long‐acting met‐enkephalin analogue DAMME to 6 normal males, and have shown that the resulting elevation in GH is blocked by the specific cholinergic antagonist, pirenzipine. It seems likely that a cholinergic mechanism may interact with opiate‐induced changes in GH in man.
DETECTION OF THYROID TUMOURS USING RADIO‐LABELLED ANTI‐THYROGLOBULIN
Authors: FAIRWEATHER D. S. , BRADWELL A. R. , WATSON‐JAMES S. F. , DYKES P. W. , CHANDLER S. , HOFFENBERG R. 
Published: March 2008

SUMMARYIgG antibody to human thyroglobulin was labelled with 131Iodine (131I) and used to locate deposits of thyroid follicular and papillary tumours with a gamma camera. Of twelve patients studied a total of 40 tumour‘areas’were detected by a variety of clinical and radiological techniques. Sixteen of these were detected using conventional 131I uptake scans whereas 34 were positive on the antibody scans. The difficulty of assessing diffuse pulmonary lesions (3 areas) and the possibility that free 131I from labelled antibody may have contributed to the antibody scan results in six areas left 31 definite areas for scan comparison. Twenty seven (87%) areas were positive on the antibody scan, nine (29%) were positive on conventional 131I scans whilst 24 (77%) areas were detected by a combination of clinical and other radiological criteria. Five areas were positive on the antibody scan alone but there was evidence, albeit indefinite, that these areas contained tumour. Four of the 31 areas were not detected by the antibody scans.The results indicate that anti‐thyroglobulin scanning is more sensitive than conventional 131I‐iodide scans and may contribute to the staging and management of thyroid cancer.
CLINICAL APPLICATIONS OF LHRH AND ITS ANALOGUES
Authors: SANDOW J. 
Published: March 2008

SUMMARYThe physiological requirement for activation of pituitary gonadotrophin secretion by pulsatile LHRH stimulation is discussed, and compared with the effect of pituitary stimulation by LHRH agonists. Initial stimulation is followed by a phase of progressive pituitary and gonadal inhibition. This inhibition is fully reversible at the end of agonist treatment. Clinical applications of high dose suppression are the treatment of precocious puberty and hormone‐dependent tumours (mammary and prostatic carcinoma). In women, agonist administration by nasal spray is a reversible method of inhibiting ovulation, and may also be useful in the treatment of endometriosis. Clinical advantages of agonist therapy are favourable biological tolerance, lack of side effects and rapid reversibility.
SERUM THYROGLOBULIN AFTER MANTLE IRRADIATION FOR HODGKIN'S DISEASE
Authors: HOLT G. , GALLIGAN J. , WINSHIP J. , ROESER P. , MORTIMER R. 
Published: March 2008

SUMMARYThyroid function and serum thyroglobulin levels were studied in 66 subjects whose Hodgkin's disease had been previously treated by cervical, mediastinal and axillary lymph node (mantle) irradiation. Three patients were already undergoing treatment for thyroid disorders (one for primary hypothyroidism, two for Graves’disease) and a fourth was found to have euthyroid Graves’disease. 36 (Group I) of the remaining 62 patients had normal free thyroxine indices, normal basal thyrotrophin (TSH) levels and normal TSH response to thyrotrophin releasing factor (TRH). In 20 patients (Group II) free thyroxine indices were normal but either basal TSH levels were raised or normal basal TSH levels were associated with an exaggerated response to TRH. In 6 patients (Group III) free thyroxine indices were subnormal. Although results of thyroid function tests in group I lay within the normal range, the mean free thyroxine index was significantly lower and mean basal and peak TSH levels were significantly higher than those of a group of 35 normal subjects, indicating mild thyroid hypofunction. Elevated thyroglobulin levels were demonstrated in 11 irradiated subjects (18%). Mean thyroglobulin levels were significantly raised in each of the three groups of irradiated subjects. Significant positive correlations were found between log serum thyroglobulin and log basal TSH (r = 0.453, P<0.001) and log peak TSH (r = 0.515, P<0.001) levels. Mild thyroid hypofunction is common after mantle irradiation for Hodgkin's disease and raised serum thyroglobulin levels are a sensitive indicator of TSH stimulation of the damaged thyroid gland.
INCREASED SECRETION OF INSULIN BUT UNCHANGED SECRETION OF GROWTH HORMONE IN HYPERGLYCAEMIC TYPE II DIABETICS TREATED WITH ACETYL‐SALICYLIC ACID
Authors: VIERHAPPER H. , BRATUSCH‐MARRAIN P. , WALDHÄUSL W. , NOWOTNY P. , PANZER S. 
Published: March 2008

SUMMARYThe effect of acetyl‐salicylic acid (ASA, 3 g/d for three days) on basal and arginine‐stimulated concentrations of insulin and growth hormone was studied in seven type II diabetics. From 120 min before until 120 min after the infusion of arginine‐hydrochloride (30 g/30 min) blood glucose concentrations were clamped at hyperglycaemic levels both during treatment with ASA (blood glucose: 12.7 ± 1.2 mmol/l) and during a control experiment without ASA (blood glucose: 12.9 ± 1.3 mmol/l). Concentrations of serum insulin in the hyperglycaemic state prior to arginine infusion were increased during treatment with ASA, whereas increments of serum insulin induced by i.v. arginine were unaffected. No difference was seen in either basal or stimulated concentrations of growth hormone. Thus, ASA enhances glucose‐induced secretion of insulin in type II diabetics but fails to potentiate the glucose‐dependent suppression of arginine‐stimulated growth hormone release. In contrast to the pancreatic β‐cell the glucose‐sensitive regulatory mechanism of growth hormone release appears to be unaffected by the inhibition of endogenous prostaglandin synthesis.
DYDROGESTERONE INCREASES SERUM LACTALBUMIN CONCENTRATION IN THE PUERPERIUM
Authors: MARTIN R. H. , EL SHEIKH M. A. A. , CHAPMAN C. 
Published: March 2008

SUMMARYEight women taking oral dydrogesterone 10 mg twice daily for the first 10 d of the puerperium, had significantly (P < 0.01) greater levels of serum lactalbumin than controls (n= 9), from day 4. No difference was observed in prolactin concentrations between groups.
THE ASSAY OF GRAVES’IMMUNOGLOBULINS: A COMPARISON OF DIFFERENT METHODS
Authors: HARDISTY C. A. , KENDALL‐TAYLOR PAT , ATKINSON S. , HUMPHRIES HAZEL , MUNRO D. S. 
Published: March 2008

SUMMARYA multiplicity of techniques has arisen for the measurement of the immunoglobulins specifically associated with Graves’hyperthyroidism, which has led to difficulty in assessing the clinical significance of these immunoglobulins. In this study of untreated toxic Graves’disease we have taken two assays (LATS protector and thyrotrophin binding inhibiting immunoglobulin, TBII) which depend upon the measurement of binding to thyroid cell membranes, and correlated them with a bioassay which measures as the index of activity the biologically relevant end point of T3 secretion from thyroid tissue.The frequency of positive responses obtained with each method was similar to that of previous studies; combining the results a positive response was found in 100%. No significant correlation was found between any of these three assays. We have also correlated the results of each assay with the serum T4 and serum T3 to assess which method relates most closely to circulating thyroid hormone levels in vivo. A highly significant correlation was obtained for TSAb measured by T3 secretion with both total serum T3 and total serum T4 levels. A positive correlation was also found for LATS protector, but not for TBII.We conclude that although these assays are specific for Graves’immunoglobulins, they are measuring closely related but not identical immunoglobulin activities.
IMMUNOCYTOCHEMICAL GROWTH HORMONE AND PROLACTIN IN PITUITARY ADENOMAS CAUSING ACROMEGALY AND THEIR RELATIONSHIP TO BASAL SERUM HORMONE LEVELS AND THE GROWTH RESPONSE TO THYROTROPHIN RELEASING HORMONE
Authors: KRUSEMAN A. C. NIEUWENHUIJZEN , BOTS G. Th. A. M. , ROELFSEMA F. , FRÖLICH M. , VAN DULKEN H. 
Published: March 2008

SUMMARYBasal prolactin levels and the dynamics of growth hormone secretion in response to intravenous TRH in 34 untreated acromegalic patients were compared with immunocytochemical localization of growth hormone and prolactin in the adenoma cells.The serum prolactin level was elevated in 13 patients. All adenomas contained growth hormone detectable by immunocytochemistry. Twelve adenomas contained prolactin as well; of these only six were associated with hyperprolactinaemia. In six patients with a mixed adenoma the serum prolactin levels were in the normal range. In 17 patients the growth hormone value more than doubled after TRH. Eight of these patients had hyperprolactinaemia, and in only six did the adenomas contain immunoreactive prolactin; eight were associated neither with hyperprolactinaemia nor with positive immunostaining for prolactin. Eight adenomas had suprasellar extension, six of these were associated with hyperprolactinaemia. Of the seven adenomas with hyperprolactinaemia but no adenomatous prolactin immunoreactivity, four had supprasellar extension. In three patients hyperprolactinaemia was associated neither with prolactin immunoreactivity in the adenoma cells nor with suprasellar extension of the tumour.It is concluded that in acromegalics (1) there is no relation between hyperprolactinaemia, and the presence of prolactin in the adenoma cells; (2) the hyperprolactinaemia may be due either to adenomatous prolactin secretion or possibly suprasellar mass interference of hypothalamic control of normal prolactin cells; and (3) the presence of hyperprolactinaemia or immunocytochemically defined adenomatous prolactin does not correlate with the reactivity of the adenomatous growth hormone cells to TRH.
THE EFFECTS OF CHRONIC TREATMENT WITH LHRH ON GONADOTROPHIN SECRETION AND PITUITARY RESPONSIVENESS TO LHRH IN WOMEN WITH SECONDARY HYPOGONADISM
Authors: WILLIAMS C. A. VAUGHAN , McNEILLY A. S. , BAIRD D. T. 
Published: March 2008

SUMMARYTwenty women with secondary hypogonadism and four normal women in the early follicular phase of the cycle were treated for 7 days with 10, 50 or 100 μg synthetic LHRH administered intramuscularly at 4 h intervals. Concentrations of pituitary and ovarian hormones in plasma were measured at intervals during the treatment period. The episodic pattern of LH secretion and the gonadotrophin responses to acute stimulation with LHRH were evaluated before and after treatment.In normal women the concentrations of gonadotrophins and the LH response to LHRH remained unchanged, whilst the FSH response to LHRH was reduced after treatment. Concentrations of oestradiol rose progressively in response to treatment, indicating follicular development.In hypogonadal subjects with unimpaired pituitary function, treatment with LHRH induced a marked but transient increase in the concentrations of LH and FSH in plasma and a progressive rise in that of oestradiol. The concentration of progesterone was increased in four of the 11 subjects. However, the amplitude of LH pulses and the responses of FSH and LH to LHRH after treatment were suppressed below pretreatment values.Women with hypogonadotrophic hypogonadism and diminished pituitary responses to LHRH exhibited a sustained increase in the concentrations of LH, FSH and oestradiol in plasma to normal follicular phase levels. The amplitude of LH pulses and the LH response to LHRH were increased after treatment but did not reach normal values. The FSH response to LHRH was further reduced after treatment. Treatment of similar subjects with 10 μg LHRH induced a small increase in the concentration of gonadotrophins but not of ovarian steroids.
HYPERTHYROIDISM DUE TO A THYROTROPHIN‐SECRETING MICROADENOMA
Authors: KELLETT HILARY A. , WYLLIE A. H. , DALE B. A. B. , BEST J. J. K. , TOFT A. D. 
Published: March 2008

SUMMARYWe report a 63‐year‐old female with a TSH‐secreting pituitary adenoma causing hyperthyroidism. This case is apparently unique, and challenges the present concept of dividing patients with inappropriate TSH secretion into tumour and non‐tumour groups on the basis of conventional pituitary fossa radiology.