bluuebunny/crossref_metadata_2025_split huggingface dataset:
AN ASSESSMENT OF POSTERIOR PITUITARY FUNCTION IN PATIENTS WITH SHEEHAN'S SYNDROME
Authors: JIALAL I. , DESAI R. K. , RAJPUT M. C. 
Published: March 2008

SUMMARYAntidiuretic hormone (ADH) function was assessed in a group of 16 patients with Sheehan's syndrome and 17 controls. All patients were on adequate cortisone and thyroxine replacement therapy before testing. During the dehydration test the patients revealed an impairment of ADH function. The maximum urine osmolalities and the urine‐plasma osmolality ratios were significantly lower in the patients with Sheehan's syndrome compared to controls (maximum urine osmolalities 633 ± 38 (SEM) and 873 ± 29 (SEM) mOsm/kg, respectively, P <0.001; urine‐plasma osmolality ratios 2.15 ± 0.14 (SEM) and 3.01 ± 0.10 (SEM), respectively, P < 0.001). Plasma osmolalities were significantly higher in the patients (296.1 ± 1.2 (SEM) and 290 ± 0.9 (SEM), respectively, P < 0.001). The patients took a longer period to achieve these maximum urine osmolalities. Three of the patients with Sheehan's syndrome were diagnosed as having diabetes insipidus since their maximum urine osmolalities were below 600 mOsm/kg and following desmopressin all three had an increment in urine osmolality which exceeded 9%. In addition these three patients had a maximum urine‐plasma osmolality ratio below 1‐9. Thus, it appears the patients with Sheehan's syndrome have an impairment of ADH function which manifests in some as diabetes insipidus.
THE PLACE OF INTRAVENOUS GHRH 1–40 STUDIES IN THE THERAPY OF GROWTH HORMONE‐DEFICIENT CHILDREN WITH GHRH
Authors: SMITH P. J. , BROOK C. G. D. 
Published: March 2008

SUMMARYWe studied GH responses to i.v. GH releasing hormone (GHRH) (1 jug/kg) before and during the treatment of 11 GH deficient children with s.c. nocturnal pulsatile GHRH 1‐10; seven for 9 months and four for 6 months. Each subject demonstrated GH stimulation at each i.v. study. There was a wide variation of response between subjects and in each subject on different occasions. Significant growth acceleration following s.c. GHRH was demonstrated in eight of 11 patients (73%). The sensitivity or true positive rate of the index GHRH study to predict a clinical response to s.c. treatment, regardless of the GH response achieved, was also 73%. When an index GH ‘cut‐off’ response of < 10 mU/1 was employed, the probability of an increase in growth rate to s.c. GHRH fell to 0‐50 (sensitivity 80%). The GHRH study was unhelpful, and in fact misleading, when assessed as a method of monitoring clinical progress and the outcome of pulsatile s.c. GHRH treatment. The growth response of a child to s.c. GHRH therapy is of far greater importance than the GH response following an i.v. bolus of GHRH. The index study gave no useful indication of either the potential GH pituitary reserve or which subjects would respond to treatment. Pretreatment and repeated GHRH studies are of limited value and should be interpreted with caution.
PREVALENCE, NATURAL HISTORY AND SURGICAL TREATMENT OF EXOPHTHALMOS
Authors: STREETEN D. H. P. , ANDERSON G. H. , REED G. F. , WOO P. 
Published: March 2008

SUMMARYThe 95% confidence limits of exophthalmometer measurements have been defined by a single observer in 105 individuals who had no known thyroid disease, and found to be 10.5‐18.8 mm. Measurements in 308 patients with thyrotoxicosis have shown that exophthalmos (>19 mm) of one or both eyes was present in 21‐3% of the patients. Among the 122 thyrotoxic patients whose exophthalmometer measurements could be performed annually for 3‐19 years after correction of the thyrotoxicosis (usually with 131I), exophthalmos remained stable in 78.7%, worsened in 15.6% and became less severe in 5.7% of the patients. Transantral decompression of the orbits was performed in 15 patients with rapid subjective improvement in all and reduction in exophthalmometer measurements of 3.6 ± 0.5 (mean ± SEM) mm, and no serious side‐effects. In view of these findings, transantral decompression should be considered more frequently in the treatment of severe or cosmetically damaging exophthalmos.
THE COEXISTENCE OF MALE PSEUDOHERMAPHRODITES WITH 17‐KETOSTEROID REDUCTASE DEFICIENCY AND 5α‐REDUCTASE DEFICIENCY WITHIN A TURKISH KINDRED
Authors: IMPERATO‐McGINLEY J. , AKGUN S. , ERTEL N. H. , SAYLI B. , SHACKLETON C. 
Published: March 2008

SUMMARYTwo distinct enzyme defects affecting androgen production and resulting in male pseudohermaphroditism were found in a Turkish kindred from a small isolated village in the Taurus mountains of southern Turkey. Pedigree analysis revealed the inter‐relationships of 9 male pseudohermaphrodites. Six affected subjects had adequate steroid hormone analysis. Two adult male pseudohermaphrodites had 17‐ketosteroid reductase deficiency with elevated concentrations of plasma androstenedione relative to testosterone, and elevated concentrations of urinary androsterone (A) and etiocholanolone (E) relative to tetrahydrocortisol (THF), 5α‐tetrahydrocortisol (5α‐THF) and tetrahydrocor‐tisone (THE). Four affected males (three adults, one child) had 5a‐reductase deficiency (elevated ratios of plasma testosterone/dihydrotestosterone and urinary 5β/5αC19 and C21 steroid metabolites). The homozygous state for both enzyme deficiencies was not demonstrable in the same affected subject, suggesting that the enzyme deficiencies are segregating separately within this kindred. Whether the mutant genes are segregating on allelic chromosomes or other autosomes cannot be determined from this study.
REDUCED GROWTH HORMONE RESPONSE TO GROWTH HORMONE‐RELEASING HORMONE IN CHILDREN WITH SIMPLE OBESITY: EVIDENCE FOR SOMATOMEDIN‐C MEDIATED INHIBITION
Authors: LOCHE S. , CAPPA M. , BORRELLI P. , FAEDDA A. , CRINÒ A. , CELLA S. G. , CORDA R. , MÜLLER E. E. , PINTOR C. 
Published: March 2008

SUMMARYWe have evaluated the plasma GH response to a single injection of 1μg/kg of GH‐releasing hormone (GHRH)‐40 in 15 obese children and 15 age‐matched control children. Most of the obese children showed a subnormal plasma GH response to GHRH and the mean plasma GH integrated area (IC‐GH) following stimulation was significantly smaller in obese than control children. Plasma somatomedin‐C (SM‐C) levels were significantly higher in obese than control children, and were negatively correlated with the peak plasma GH levels (r=−0.616, P<001) and the IC‐GH (r=−0.554, P<0.02) after GHRH. Non‐esterified fatty acids (NEFA) and fasting plasma insulin levels were also elevated in obese children, but did not correlate with the extent of plasma GH response to GHRH. These data confirm previous observations on the refractoriness of obese children to release GH after GHRH, and imply that it may be due to the feedback inhibition operated by the elevated plasma levels of SM‐C.
STILBOESTROL PRETREATMENT OF CHILDREN WITH SHORT STATURE DOES NOT AFFECT THE GROWTH HORMONE RESPONSE TO GROWTH HORMONE‐RELEASING HORMONE
Authors: ROSS R. J. M. , GROSSMAN A. , DAVIES P. S. W. , And M. O. SAVAGE , BESSER G. M. 
Published: March 2008

SUMMARYOestrogens are known to enhance both basal and stimulated GH secretion. To examine whether this effect is mediated through the hypothalamus or the pituitary we performed insulin tolerance and GH‐releasing hormone (GHRH) tests with and without oestrogen priming in a group of 14 short children. Pretreatment with stilboestrol increased basal levels of GH and both peak and incremental levels during insulin hypoglycaemia. In contrast, there was no effect of stilboestrol priming on the GH response to either an i.v. bolus of 100 μg or 0.1 μg/kg (range 2‐6 μg) of GHRH. The children had significantly higher GH responses to an unprimed GHRH than unprimed insulin tolerance test. We conclude stilboestrol priming acts through the hypothalamus presumably by increasing endogenous GHRH release, and that short children with a subnormal GH response to insulin hypoglycaemia show a greater response to GHRH; this suggests the presence of a hypothalamic cause for their decreased GH secretion.
ERYTHROCYTE OUABAIN BINDING IN PATIENTS RECEIVING THYROXINE
Authors: WILCOX A. H. , LEVIN G. E. 
Published: March 2008

SUMMARYThyroid hormone action at the cellular level was investigated in euthyroid women who were receiving replacement thyroxine, and whose plasma T4 levels were above the upper reference limit for healthy subjects. There is evidence that erythrocyte sodium pump sites are reduced in number in patients with hyperthyroidism. These sites were measured by the ouabain binding capacity. Plasma T4, free T3 and TSH were also measured, the latter by a high sensitivity fluoroimmunoassay. Three groups of women were investigated; 30 patients receiving T4 with elevated plasma T4 concentrations, 30 age‐matched healthy women, and 10 untreated thyrotoxic patients. Erythrocyte ouabain binding was significantly reduced in the thyroxine treated patients, although not to the degree observed in the thyrotoxic patients. Plasma free T3 concentration was increased in 12 of 30 treated patients. TSH was undetectable in 23 of 30 treated patients. The ouabain binding results provide some evidence for increased thyroid hormone action at cellular level in the thyroxine treated patients.
THE HUMAN LEUCOCYTE SODIUM PUMP IN ADRENOCORTICAL INSUFFICIENCY
Authors: NG L. L. , EVANS D. J. , BURKE C. W. 
Published: March 2008

SUMMARYIn view of the known effects of Cortisol and related compounds on sodium balance, we examined leucocyte 22Na+ efflux in patients with adrenocortical insufficiency. The ouabain‐sensitive 22Na+ efflux rate constant, which reflects sodium pump activity, was lowered in secondary hypoadrenalism (mean 1.95 ± SD 0.25 vs 2.33 ± 0.45 h‐1, P< 0.002, n= 6). Patients with hypoadrenalism also had higher intracellular sodium content (mean 34.9 ± SD 3.5 vs 27.8 ± 9.5 mmol/kg dry weight, P< 0.008) and lower intracellular potassium to sodium ratios (mean 9.7 ± SD 0.7 vs 12.9 ± 3.6, P<0.001). These defects in cellular sodium balance were corrected following replacement therapy with Cortisol, prednisolone or dexamethasone. In‐vitro incubation of normal leucocytes with 5‐20 nmol/1 dexamethasone led to an increase in the Na+/K+‐ATPase activity. The effect of Cortisol and related compounds on the distribution of sodium between intra‐ and extra‐cellular fluid may be mediated by their action on the sodium pump.
PHOSPHOLIPASE C ACTIVITY IN HUMAN ENDOMETRIUM: ITS SIGNIFICANCE IN ENDOMETRIAL PATHOLOGY
Authors: BONNEY R. C. , FRANKS S. 
Published: March 2008

SUMMARYPhospholipase C activity was measured in human endometrium using an assay based on the release of total labelled water soluble products (inositol, inositol phosphates) from L‐3‐phosphatidyl‐[2‐3H] inositol. The enzyme was shown to be calcium dependent and to have an optimum pH of 5.5. There was no difference between proliferative phase and secretory phase endometrium with respect to phospholipase C activity either in women with normal menstrual blood loss (proliferative phase: 3.7 ± 0.7 (mean ± SD), secretory phase: 4.5 ± 2.0 nmol/mg protein/min) or in those complaining of severe menorrhagia (proliferative phase: 5.8 ± 2.8, secretory phase: 7.0 ± 2.8 nmol/mg protein/min). However, women complaining of severe menorrhagia had significantly higher endometrial phospholipase C activity than those in the normal group (P<0.01 and P<0.02 for proliferative and secretory phases respectively). Endometrial phospholipase C activity was also elevated in the presence of other gynaecological disorders, e.g. dysmenorrhoea, adenocarcinoma of the cervix and endometrial hyperplasia. The results indicate that phospholipase C activity in human endometrium is not related to the stage of the menstrual cycle but that in the presence of menorrhagia and other gynaecological disorders, activity is increased. Phospholipase C could be implicated in the generation of arachidonic acid for prostaglandin synthesis which may in turn be associated with these abnormalities.
IMMUNOMODULATORY EFFECT OF THE TREATMENT OF GRAVES’DISEASE ON ANTIGEN‐SPECIFIC MONOCYTE PROCOAGULANT ACTIVITY PRODUCTION
Authors: IITAKA M. , IWATANI Y. , GERSTEIN H. C. , ROW V. V. , VOLPÉ R. 
Published: March 2008

SUMMARYThe monocyte procoagulant activity (PCA) production assay has been shown to be a good parameter of cell‐mediated immunity. We have studied antigen‐specific PCA production in peripheral blood mononuclear cells from patients with Graves’disease to determine the effect of the treatment on the cell‐mediated immune response. Peripheral blood mononuclear cells from patients with untreated or relapsed Graves’disease produced significantly greater PCA with thyroid antigen stimulation than those from normal subjects. Patients both on antithyroid drugs in the hyperthyroid state and within 3 months post‐131I therapy also produced significantly larger amount of PCA than normal subjects. However, there was no significant difference in PCA production with thyroid antigen stimulation between normal subjects and patients on anti‐thyroid drugs in the euthyroid state, or patients over 3 months post‐131I therapy. The ratio of positive to negative PCA production in patients on anti‐thyroid drugs in the euthyroid state or over 3 months post‐131I therapy was significantly lower than in untreated or relapsed Graves’disease patients. Mononuclear cells from patients on propylthiouracil responded to propylthiouracil in vitro by production of PCA. Cells from normal subjects, untreated Graves’disease patients, or patients with Hashimoto's thyroiditis did not produce PCA with propylthiouracil stimulation. Mononuclear cells from patients who were on propylthiouracil for more than 3 months produced greater PCA than those on the drug for less than 3 months, suggesting sensitization of lymphocytes to propylthiouracil during the course of treatment. However, after 131I therapy, they gradually became unresponsive to propylthiouracil. This study has shown that the activity of the antigen‐specific response assessed by PCA production in mononuclear cells from Graves’disease patients declined after treatment, suggesting that the treatment exerted immunomodulatory effects.
LONG‐TERM TREATMENT OF HYPERPROLACTINAEMIA WITH BROMOCRIPTINE: EFFECT OF DRUG WITHDRAWAL
Authors: WANG C. , LAM K. S. L. , MA J. T. C. , CHAN T. , LIU M. Y. , YEUNG R. T. T. 
Published: March 2008

SUMMARYFifty‐one patients with hyperprolactinaemia (23 with macroadenoma, 23 with microadenoma, and five with idiopathic hyperprolactinaemia) were treated with bromocriptine for 2‐12 years (4.9 ± 2.9 years, mean ± SD). During therapy, the serum PRL levels were suppressed into the normal range in all but five patients. In these five patients, despite the high circulating PRL, gonadal function returned to normal in three, while in the other two gonadotrophin reserve was impaired even before therapy. Gel chromatography showed that one of these patients had a high proportion of a large molecular weight form of PRL. Twenty‐four patients received bromocriptine as the sole method of treatment for over 2 years (3.4 ± 2.3 years). In five out of the 24 subjects (21 %), serum PRL remained normal with no clinical symptoms after prolonged drug withdrawal (1‐4 years). Twenty‐one patients received radiotherapy in conjunction with bromocriptine therapy. Of these 11 had prior surgery. After a follow‐up of 6.0 ± 3.0 years after radiotherapy, serum PRL remained within the normal range in 6 out of 21 subjects (29%), 1‐4 years after bromocriptine withdrawal. One of the patients had impaired GH response to insulin hypoglycaemia developing after radiotherapy. We conclude that prolonged bromocriptine treatment is an effective treatment for prolactinomas.
AN IMMUNOCHEMILUMINOMETRIC ASSAY FOR SERUM FREE THYROXINE
Authors: STURGESS M. L. , WEEKS I. , EVANS P. J. , MPOKO C. N. , LAING I. , WOODHEAD J. S. 
Published: March 2008

SUMMARYAn immunochemiluminometric assay has been developed for the measurement of free T4 concentrations in serum. The assay uses chemiluminescent acridinium ester labelled monoclonal antibodies which react with free T4 in the sample. A T4‐rabbit immunoglobulin G conjugate competes for antibody binding sites, immune‐complexes containing this being isolated using an anti‐immunoglobulin G antibody coupled to paramagnetic particles. Associated chemiluminescence intensity is thus dependent on the free T4 concentration. The assay distinguishes patients with primary thyroid disease from euthyroid subjects and is unaffected by abnormal binding proteins which compromise the diagnostic accuracy of radiolabelled analogue immunoassays. The test yields results which accurately reflect the clinical thyroid status of euthyroid patients with a variety of acute and chronic non‐thyroid illnesses. This is again in marked contrast to the aberrant results seen using certain radiolabelled analogue procedures.
THE SIGNIFICANCE OF ELEVATED LEVELS OF GASTRIN IN PATIENTS WITH PITUITARY ADENOMA
Authors: FONSECA M. E. , ZARATE A. 
Published: March 2008

SUMMARYSix patients were studied with pituitary adenomas and elevated concentrations of gastrin similar to those found in cases of benign antral gastrinoma syndrome. Chromatography of the serum using Sephadex‐G50 revealed different molecular forms of gastrin according to the type of adenomas. In those cases of acromegaly and gonadotrophinoma, gastrin‐34 and unsulphated gastrins constitute the predominant forms. In contrast, in cases of Cushing's disease, gastrin‐17, sulphated as well as non‐sulphated were the predominant types; the chromatographic pattern was similar to that observed in two patients with antral gastrinoma syndrome who acted as controls. These findings demonstrate that pituitary adenomas might secrete gastrin. Taking into account that gastrin‐34 and unsulphated gastrins were the predominant forms in cases of acromegaly, gonadotrophinoma and non‐functioning adenoma, it is assumed that those molecular forms are mainly produced in the anterior lobe of the hypothysis. Conversely, gastrin‐17 was the principal molecular form in cases of Cushing's disease confirming the close relationship of the synthesis of gastrin and corticotrophin peptides. The cases with Cushing's disease exhibited a serum gastrin pattern similar to that observed in the two cases with antral syndrome in which the predominant immunoreactive form of gastrin in gastrin‐17 exhibiting a degree of sulphation corresponding to that of antral gastrin. It is concluded that the circulating excess of gastrin originated in the pituitary tumour tissue and the molecular form varied with the type of pituitary adenoma.
THYROTROPHIN RECEPTOR BLOCKING ANTIBODIES: INCIDENCE, CHARACTERIZATION AND IN‐VITRO SYNTHESIS
Authors: KRAIEM Z. , LAHAT N. , GLASER B. , BARON E. , SADEH O. , SHEINFELD M. 
Published: March 2008

SUMMARYThe prevalence and characteristics of TSH receptor blocking activity were examined in patients with different thyroid disorders. Studies were also performed on the in‐vitro synthesis and immunoregulation of the blocking antibody. Blocking activity was tested by measuring the inhibition of TSH‐stimulated cAMP production of cultured human thyroid cells by patient immunoglobulin (Ig) preparations. The following patients were investigated (number of cases in parentheses): Hashimoto's thyroiditis (33); primary myxoedema (17); euthyroid ophthalmopathy (8); active Graves’disease (19); cold nodule (5); non‐toxic goitre (14); toxic adenoma (8); toxic multinodular goitre (9) and 22 normal controls. TSH receptor blocking activity was only detected in primary hypothyroidism with the following characteristics: (i) Such activity was present in only 16% of the patients (both goitrous, i.e. Hashimoto's thyroiditis, and non‐goitrous, i.e. primary myxoedema), and in three patients with previously active Graves’hyperthyroidism who had become hypothyroid. (ii) Blocking activity seems to be associated with the Ig fraction of serum as indicated by protein A adsorption, (iii) The block‐positive samples did not bind l25I‐TSH, which seems to rule out an antibody directed against TSH. (iv) The specificity of the blocking activity seems to be directed towards the TSH‐(thyroid stimulating immunoglobulin, TSI) receptor‐mediated cAMP response since no inhibition of prostaglandin E1‐stimulated cAMP production was found. Moreover, all cases in which an inhibitory effect was demonstrated towards TSH also exhibited blocking of TSI‐stimulated cAMP, with a high correlation between the degree of inhibition of the TSH to that of the TSI response (r= 0.89, P<0.001, n= 11). The blocking activity may contribute to the pathogenesis of some cases of primary hypothyroid autoimmune thyroiditis, both goitrous and non‐goitrous, as well as in the evolution of hyper‐ to hypothyroidism. By culturing peripheral blood lymphocytes, as well as B/T lymphocyte co‐cultures isolated from three patients with blocking activity present in serum, the in‐vitro synthesis of the blocking antibody was demonstrated for the first time. Moreover, in‐vitro secretion of the antibody by patients B lymphocytes, as well as T cell regulation of autoantibody production, were also shown.
PREVENTION OF HYPOGLYCAEMIA IN A PATIENT WITH PANCREATIC MICROADENOMATOSIS BY A LONG‐ACTING SOMATOSTATIN ANALOGUE SMS 201‐995
Authors: KUNG A. W. C. , MA J. T. C. , WANG C. , FU K. H. , LAM K. S. L. , YEUNG R. T. T. , BOEY J. 
Published: March 2008

SUMMARYAcute suppression of insulin secretion from pancreatic insulinomas by long‐acting somatostatin analogue SMS 201‐995 has been documented. We report the chronic use of the drug in a patient with persistent hypoglycaemia due to benign pancreatic microadenomatosis with satisfactory control of plasma glucose level and reduction of insulin production. There was no tachyphylaxis or untoward side‐effect noted during the 6‐month treatment period.
GROWTH HORMONE AND PROLACTIN SECRETION AFTER GROWTH HORMONE‐RELEASING HORMONE ADMINISTRATION, IN ANOREXIA NERVOSA PATIENTS, NORMAL CONTROLS AND TAMOXIFEN‐PRETREATED VOLUNTEERS
Authors: CASANUEVA F. F. , BORRAS C. G. , BURGUERA B. , LIMA L. , MURUAIS C. , TRESGUERRES J. A. F. , DEVESA J. 
Published: March 2008

SUMMARYAnorexia nervosa is associated with several abnormalities in GH secretion elicited by different stimuli. To investigate the precise mechanism of this alteration, GHRH was administered to 14 women: a group of eight anorexia nervosa patients in the acute phase of their illness and a control group of six age‐matched volunteers. As patients with anorexia nervosa have chronic low oestrogen values, the volunteer women of the control group underwent a second GHRH test after pretreatment with the oestrogen receptor blocker tamoxifen. GHRH 1‐29 (1 μg/kg i.v.) induced a GH peak (mean±SEM) of 28.2 ±5.1 ng/ ml (GH ng/ml ± 2 = mU/l) at 30 min in the anorectic patients. This value was no different from the GHRH‐stimulated GH peak in the control women (28.1 ± 100 ng/ml). Tamoxifen pretreated women had a GH peak after GHRH of 35.6 ± 9.7 ng/ml, not significant versus control test. Compared with the control group, oestrogen levels were significantly lower in anorectic patients and higher in tamoxifen‐treated women. GHRH administration induced a small PRL peak at 15 min that was similar in the three groups tested. After this 15 min peak, PRL in both anorexic and tamoxifen‐treated women returned toward basal values steadily. However, in untreated control women a second PRL peak was evident at 60 min. In conclusion, GHRH‐induced GH secretion in anorexia nervosa patients was similar to that in control subjects and in controls under oestrogen receptor blockade.