bluuebunny/crossref_metadata_2025_split huggingface dataset:
Is calculation of the dose in radioiodine therapy of hyperthyroidism worth while?
Authors: Jarløv Anne E. , Hegedüst Laszio , Kristensen Lars Ø. , Nygaard Birte , Hansen Jens M. 
Published: March 2008

SummaryOBJECTIVE The persistent controversy as to the best approach to radioiodine dose selection in the treatment of hyperthyroldism led us to perform a study in order to compare a fixed dose regime comprising doses of 185, 370 or 555 MBq based on gland size assessment by palpation only, with a calculated 131I dose based on type of thyroid gland (diffuse, multinodular, solitary adenoma), an accurate thyroid volume measurement, and a 24‐hour 131I uptake determination.DESIGN Prospective randomized study.PATIENTS Two hundred and twenty‐one consecutive hyperthyroid patients referred for 131I treatment. Four patlents who dled for reasons unrelated to hyperthyroidism, 7 lost to follow‐up and 47 who did not receive antithyroid drugs after treatment, were excluded. The remalnlng 163 patlents (143 women) were studied, dlvlded into subgroups accordlng to the type of gland. They all recelved antithyroid drugs prior to 131I treatment and this was resumed 7 days after treatment for a period of 3 weeks.MEASUREMENTS Thyroid function variables were determined approximately 2 weeks before 131I treatment, and again 1, 2, 3, 6, 9 and 12 months after treatment. Prior to 131I therapy the size of the thyroid gland was determined by ultrasound and a 24‐hour uptake of 131I was carried out. Thyroid in 78 of the 163 patients. Twelve months after the initial 131I dose patients could be classified as euthyroid, hyperthyrold or hypothyroid.RESULT Neither in the group of 163 patients nor within the three subgroups of hyperthyroidism could any significant difference in outcome between the two treatment regimes be demonstrated. Thirty‐two of 78 patients (41%) in the calculated dose group and 30 of 85 patients (35%, NS) in the fixed group were classified as hyperthroid. Seven of 78(9%) in the calculated dose group were classified as permanently hypothyroid. Finally, 39 of 78(50%) In the calculated dose group and 49 of 85(58%, NS) in the fixed group were enthyroid at 12 months after 131I treatment. One year after 131I therapy thyroid volume was deduced from 59.3 ± 9.2 (mean ± SEM) to 36.2 ± 6.6 ml (average reduction 39%) In the calculated dose group (P < 0.001). This reduction did not differ significantly from the fixed dose group where thyroid volume declined from 61.6 ± 6.1 to 41.17 ± 4.7 ml (average reduction 32%) (P < 0.001).CONCLUSIONS A semiquantitative approach is probably as good as the more elaborately calculated radiolodine dose for treatment of hyperthyroidism. It is clearly more cost effective and allows the use of predetermined standard doses.
Is previous hyperthyroidism still a risk factor for osteoporosis in post‐menopausal women?
Authors: Grant David J. , McMurdo Marion E. T. , Mole Patricia A. , Paterson Colin R. 
Published: March 2008

SummaryOBJECTIVE Hyperthyroidism is a risk factor for osteoporosis, but the relative contributions of the episode of hyperthroidism and thyroxine replacement for subsequent hypothroidism remain uncertain. In this study we have measured bone mineral density (BMD) in post‐menopausal women with a previous history of hyperthyroidism, comparing those requiring thyroxine therapy with those remaining euthyroid and with an historical local control population.DESIGN Cross‐sectional study.PATIENTS One hundred and SIX post‐menopausal women with a previous history of hyperthyroldism. These were divided Into four groups: treated with radiolodine, remaining euthyroid (group RU, n = 15); treated with radiolodine, receiving thyroxine for at least 5 years (group RT, n = 46); treated with surgery, remaining euthyrold (group SU, n = 21); treated with surgery, receiving thyroxine for at least 5 years (group ST, n = 24). There were 102 control subjects.MEASUREMENT Forearm bone mineral density at distal and ultradistal sites as measured by single‐photon absorptlometry.RESULTS Results were expressed as ‘2‐scores’ i.e. number of standard deviatlons from the mean of a 5‐year age‐band from the local control population. Mean Z‐scores at distal and ultradistal sites were as follows: −0.61 and −0.81 in group RU; −0.58 and −0.56 In group RT; −0.27 and −0.30 in group SU; −0.81 and −0.57 In group ST. Patients in groups RU, RT and ST but not SU had significantly lower BMD than controls.CONCLUSION Post‐menopausal women with previous hyperthyroidism treated with radioladine have reduced BMD, whether or not receiving thyroxine. They should be targeted for densitometry and protective therapy with oestrogen should be considered. Those treated with surgery appear to be at less risk; this may be because most are diagnosed and treated whilst premenopausal. Thyroxine may have a deleterious effect in this group; longitudinal studies would provide further clarification.
Vitamin D status in primary hyperparathyroidism in India
Authors: Harinarayan C. V. , Gupta N. , Kochupillai N. 
Published: March 2008

SummaryOBJECTIVES Primary hyperparathyroidism is a syndrome with variable clinical expression, presenting as asymptomatic hypercalcaemia in Western countries and with predominant bone disease in developing countries. Vitamin D deficiency has been implicated as the cause of bone disease. There is a paucity of information on the vitamin D (25‐OHD3) status of patients with primary hyperparathyroidism presenting with bone disease. The present study aims to evaluate the vitamin D status in patients with primary hyperparathyroidism and to correlate it with the bone disease.DESIGN Twenty consecutive patients with primary hyperparathyroidism admitted to the endocrinology and metabolism wards of the All India Institute of Medical Sciences were analysed to assess their clinical, radiological and biochemical features, as well as parathyroid hormone (mid‐molecular, PTH‐MM) and 25‐OHD3 levels.MEASUREMENTS PTH‐MM levels and 25‐OHD3 levels were measured using RIA kits.RESULTS Bone disease (osteitis fibrosa cystica) was the mode of presentation in 90%. Radiologically, sub‐periosteal resorption was present in 90% of the total group of patients, brown tumours in 60%, and pathological fractures in 40%. Renal stones and/or nephrocalcinosis was present in 50% of patients. Mean serum calcium, phosphate and alkaline phosphatase concentrations (mean of 3 days values) were 2.72 ± 0.24 mmol/l; 1.01 ± 0.28 mmol/l and 425 ± 249 IU/l respectively. The 24‐hour (mean of 3 days values) urine calcium and phosphate excretions were 8.0 ± 4.2 mmol and 19.0 ± 13mmol. Only 50% of the patients had hypercalcaemia (> 2.7 mmol/l). However, 90% of the whole group of patients had hypercalciurla. The mean serum creatinine concentration of patients with hypercalcaemia was 108 ± 38 μmol/l and of those with normocalcaemia 89 ± 33 pmol/l. The mean serum PTH‐MM was 438 ± 350 pmol/l (the detection limit for the kit was 34 pmol/l). Ultrasound examination detected adenomas in 72% of the cases and computerized tomography of the neck localized adenomas in 71 % of the cases. The median weight of the adenoma was 4.6 g (range 0.125–25 g). Two patients had coexistent hyperplasia of the other parathyroid glands and two had recurrent adenomas. 25‐OHD3 levels were assessed in all 20 patients under fasting conditions. The mean value of 25‐OHD3 observed (8.4 ± 51 μg/l) was comparable to the mean value measured in 14 healthy age and sex matched controls (83 ± 25 μg/l).CONCLUSION Patients with primary hyperparathyroidism in India presented with bone and renal diseases; half were normocalcaemic. All the patients had hypercalcuria despite the bone disease. The PTH‐MM levels were increased and 25‐OHD3 levels were low. The predominant bone disease is probably due to prolonged primary hyperparathyroidism coexisting with low calcium intake and/or 25‐OHD3 deficiency. The mean weight of the adenoma was higher than that reported for patients in the Western literature.
High prevalence of nodular thyroid disease in patients with Cushing's disease
Authors: Invitti C. , Manfrini R. , Romanini B. M. , Cavagnini F. 
Published: March 2008

SummaryOBJECTIVES In the recent past, we have noted a frequent Occurrence of thyroid nodules in our patients with Cushing's disease. We therefore elected to evaluate thyroid structure and function in these patients and also In patients with Cushing's syndrome of primary adrenal origin.PATIENTS AND METHODS In 33 of the 37 patients (30 women and 3 men aged 19–66 years) with endogenous hypercortisolism referred to our Institution during the last five years, measurement of T4, T3, FT4, FT3, TSH serum levels and thyroid ultrasonography were performed, at first admission in 15 cases and subsequently in the course of follow‐up in 18 cases. At the time of the study, 16 of the 33 patients had active Cushing's disease while 9 were in remission after successful surgery, 6 patients had an adrenal tumour and 2 patients had previously undergone unilateral adrenalectomy for an adrenal adenoma. Thyroid function and ultrasonography were also evaluated in 55 normal subjects, 40 women and 15 men aged 20–73 years.RESULTS In 25 patients with Cushing's disease, we found a significantly higher prevalence of thyroid nodular disease than that recorded in 55 control subjects (60.0 vs 20.0%, χ2= 10.779, P < 0.005) and comparable to that in patients with active disease (56.2%) and those in remission (66.6%). Multiple nodules were present in 8 Cushing's patients and in 4 normal subjects while a single nodule was detected in 7 patients and in 7 controls. A markedly lower Occurrence of thyroid abnormality was found in the 8 patients with adrenal tumours (25.0%, NS vs controls). In 9/17 (52.9%) patients with ultrasonographic evidence of thyroid nodules, these were palpable. As expected, serum thyroid hormone and TSH levels were reduced in patients with active Cushing's syndrome compared to normal controls.CONCLUSIONS We found a significantly higher prevalence of nodular thyroid disease in patients with Cushing's disease with respect to a group of controls in whom the prevalence of thyroid nodules was comparable to that reported for the general population in Europe. The possibility that glucocorticoid excess is responsible for the development of thyroid changes does not seem likely since in our small series of patients with adrenal tumours the prevalence was only slightly higher than that observed in control subjects. Other factors related to hyperactivity of the corticotrophic cell, or a growth factor stimulating both corticotroph and thyrocyte proliferation might be involved. Evaluation of a larger series of patients with adrenal tumours may help to distinguish between these possibilities.
The effect of an opiate antagonist on the hormonal changes induced by hexarelin
Authors: Korbonits Márta , Trainer Peter J. , Besser G. Michael 
Published: March 2008

SummaryOBJECTIVE Growth hormone‐releasing peptides (GHRPs) stimulate growth hormone (GH) release in vitro and in vivo in animals and in humans. GHRPs were developed by modification of the structure of met‐enkephalln but GHRP‐6 does not activate opioid receptors in animal studies. These agents may well have diagnostic and/or long‐term therapeutic potential in the future so their effects on opioid receptors need to be clarified in humans as well. Hexarelin is a recently developed six amino acid residue GHRP.DESIGN We have Investigated the effects of 100 μ g/kg I.v. dose of the opiate antagonist naloxone and 2 μ g/kg I.v. hexarelin or placebo on serum GH, prolactin, TSH, cortisol and plasma ACTH in 12 healthy volunteers in a double‐blind, randomized trial.RESULTS Hexarelin signiflcantly stimulated the peak serum levels and area under the curve for clrculating GH and this effect was not modulated by naloxone. Hexarelin also caused significant elevation of circulating prolactin, cortisol and ACTH but did not Influence circulating TSH levels. The effect of naloxone on cortisol and ACTH was stimulatory, while it did not influence prolactin, GH and TSH levels. The effect of the two drugs together on cortisol and ACTH was less than additive.CONCLUSIONS This study confirms that the activation of opiate receptors does not play a role in the GH‐releasing effect of growth hormone‐releasing peptides in humans.
Transient osteoporosis of the hip in pregnancy: natural history of changes in bone mineral density
Authors: Funk Janet L. , Shoback Dolores M. , Genant Harry K. 
Published: March 2008

SummaryA 31‐year‐old white female developed severe bilateral hip pain during the third trimester of pregnancy that persisted after parturition. Laboratory abnormalities (elevated alkaline phosphatase and erythrocyte sedimentation rate) and radiographic changes (faint demineralization of the femur in the more symptomatic hip on plain films with evidence of bone marrow oedema and small joint effusions bilaterally on MRI) in the absence of other causes of focal osteoporosis were consistent with the diagnosis of transient osteoporosis of the hip in pregnancy. Although loss of bone mineral density (BMD) characterizes this syndrome, serial BMD measurements in symptomatic transient osteoporosis of the hip in pregnancy have not previously been reported. In the case reported here, serial bone density measurements were obtained over a 4‐year period following the onset of symptoms. BMD in both femoral necks, which Initially was approximately 20% lower than the average for age matched controls, increased markedly during the first year, plateaued during the following year, and then rapidly increased again following cessation of lactation. Unexpectedly, BMD in the lumbar spine, an asymptomatic site, was also markedly decreased at the time of presentation (31% lower than the mean of age‐matched controls). Recovery of spinal density did not occur during the first year. However, spinal BMD did begin to increase during the second year and continued to rise after the cessation of lactation. In contrast to the marked reduction in bone density at these sites of trabecular bone, cortical bone density in the forearm was normal. Possible aetiologies of pregnancy associated osteoporosis are discussed.
Cushing's disease due to female gonadotroph adenoma of the pituitary
Authors: Ikeda Hidetoshi , Yoshimoto Takashi , Kovacs Kalman , Horvath Eva 
Published: March 2008

SummaryA 39‐year‐old woman presented with amenorrhoea, hyperprolactinaemia and sellar mass. Bromocrlptine normalized PRL levels but failed to suppress tumour growth. Subsequently, she developed clinical signs and elevated blood cortisol levels consistent with a diagnosis of Cushing's disease. A pituitary tumour was removed which was immunoreactive for ACTH. Electron microscopic examination, however, revealed a female gonadotroph adenoma indicating that adenoma cells regarded as gonadotrophs by ultrastructural analysis may occasionally secrete ACTH and cause Cushing's disease.
Further increase in forearm cortical bone mineral content after discontinuation of growth hormone replacement
Authors: Holmes Sarah J. , Whltehouse Richard W. , Economou Georgla , O'Halloran Domhnall J. , Adams Judith E. , Shalet Stephen M. 
Published: March 2008

SummaryOBJECTIVE Growth hormone replacement of adults with childhood onset GH deficiency results In an Increase In bone mineral density (BMD) after 6‐12 months of OH replacement. By measuring BMD 12 months after discontinuation of GH replacement we aimed to Investigate whether there is an effect of GH replacement on BMD persisting after GH has been withdrawn.DESIGN BMD was measured 13 ± 1 (mean ± SE, range 11‐16) months after discontinuation of OH replacement. PATIENTS Ten adults, age 23·;2 ±1·;4 (range 18·8‐32·4) years, with childhood onset isolated GH deficiency (2 idiopathic, 8 irradiation induced) who had previously completed a study of the effect of 12 months of OH replacement on BMD.MEASUREMENTS Forearm cortical bone mineral content (BMC) was measured using single‐photon absorptlometry at the proximal site of the distal forearm. Forearm integral BMC at the ultradistal site of the forearm and bone width at both proximal and ultradistal rites of the distal forearm were measured by the same technique. Vertebral trabecular BMD was measured using quantitative computed tomography.RESULTS Forearm cortical BMC was significantly greater than that measured at the time of discontinuation of OH (1·48 ±0·04 vs 1·44 ± 0·05 g/cm). There was no significant change in forearm integral BMC or in vertebral trabecular BMD after discontinuation of OH. There was no significant change in bone width at proximal and ultradistal sites of the distal forearm after discontinuation of GH.CONCLUSION After discontinuation of OH replacement the further increase In forearm cortical bone mineral content without a significant Increase In forearm bone width suggests that the Increase In cortical bone mineral content Is due to a persisting effect of previous GH replacement, and not to further spontaneous attainment of bone mass before peak bone mass lo reached. These findings emphasize the importance of continuing to monitor bone mass after the stimulus to Increase bone turnover has been withdrawn.
Somatostatin receptor imaging in persistent medullary thyroid carcinoma
Authors: Frank‐Raue K. , Bihl H. , Dörr U. , Buhr H. , Zlegler R. , Raue F. 
Published: March 2008

SummaryOBJECTIVE Somatostatin is secreted from thyroid C‐cells and seems to play an Important part In the regulation of calcitonin secretion. We therefore evaluated the usefulness of somatostatin receptor scintigraphy in the localization of tumour tissue in patients with persistent medullary thyroid carcinoma.DESIGN A prospective clinical study.PATIENTS The series consisted Of 26 patients with elevated calcitonin levels after total thyroldectomy for histologically proven medullary thyroid carcinoma.METHODS Somatostatin receptor scintigraphy using 111 In‐pentetreotide (Octreoscan) was performed in all patients and the results correlated with histology, ultrasonography, computerized tomography, magnetic resonance Imaging, plain radiography, bone scintigraphy and selective venous Catheterization. calcitonin and carcinoembryonic antigen levels were measured.RESULTS The sensitivity of somatostatin receptor scintigraphy for localization of persistent medullary thyroid carcinoma was 57% in patients with histologically proven disease. The results depended on tumour mass (low sensitivity (33%) in minimal residual disease) and on the location of metastases (Insensitive in detecting liver metastases).CONCLUSIONS Somatostatin receptor scintigraphy is of value as an additional diagnostic tool in localizing medullary thyroid carcinoma, especially pulmonary metastases. It is of minor importance in detecting minimal residual disease.
Loss of biological activity of arginine vasopressin during its degradation by vasopressinase from pregnancy serum
Authors: Gordge M. P. , Williams D. J. , Huggett N. J. , Payne N. N. , Nelld G. H. 
Published: March 2008

SummaryBACKGROUND AND OBJECTIVE Degradation of AVP by placental vasopressinase may precipitate gestational diabetes insipidus, which in some cases is accompanied by pre‐eciampsia. Abnormally elevated vasopressinase has also been reported in pre‐eciampsia without diabetes Insipidus. This association between excessive vasopressinase production and pre‐eciampsia might be explained if the products of AVP degradation by vasopressinase retained pressor activity even after anti‐diuretic activity had been destroyed. Recent evidence indicates that such products may raise blood pressure in rats. The objective of this study was, therefore, to purify vasopressinase and investigate its action on both the V1 and V2 receptor‐stimulating activity of AVP.DESIGN Vasopressinase was purified from pooled pregnancy serum by ammonium sulphate precipitation, followed by sequential Ion exchange, lentil lectin affinity and gel filtration chromatography. Purified enzyme was then used to degrade AVP and the loss of both immunoreactivity and biological activity monitored. Loss of V1 receptor‐stimulating activity and V2 receptor‐stimulating activity was compared by two‐way ANOVA.PATIENTS Blood was obtained from healthy women between week 34 and the end of pregnancy. Pooled serum from 20–30 patients was used as starting material for the purification of vasopressinase.MEASUREMENTS AVP immunoreactivity was measured by radioimmunoassay, V1 receptor‐stimulating activity by a platelet aggregation bioassay, and V2 receptor‐stimulating activity by adenylate cyclase stimulation in LLC‐PK1 target cells.RESULTS Purified vasopressinase was a dimeric protein of molecular weight 330 kDa, which cleaved the synthetic substrate S‐benzyl‐l‐cystelne‐4‐nitroanilide with a Km of 0·33 mM. Incubation of AVP (0·1 mm) with vasopressinase (0·66 g/I) at 37°C led to a parallel loss of both AVP immunoreactivity and biological activity. The rates of loss of V1 and V2 receptor mediated activities were not significantly different.CONCLUSIONS We report the first direct comparison between the loss of V1 and V2 receptor mediated activities of vasopresrinase degraded AVP. There was no significant retention of V1, relative to V2, receptor mediated activity. AVP degradation products are unlikely to be pathogenic in hypertensive pregnancy.
Megestrol‐induced Cushing's syndrome
Authors: Steer K. A. , Kurtz A. B. , Honour J. W. 
Published: March 2008

SummaryThis case describes the first report of a patient developing Cushing's syndrome whilst being treated with the synthetic progestogen, megestrol acetate (Megace).Drugs are the commonest cause of Cushing's syndrome. Some synthetic progestogens are known to have glucocorticoid activity at high doses. On structural grounds neither megestrol nor its major metaboiltes would be expected to interact with the glucocorticoid receptor, though the manufacturers report that it may have ‘weak glucocorticoid activity'.
Pseudo‐phaeochromocytoma after multiple drug interactions involving the selective monoamine oxidase inhibitor selegiline
Authors: Lefebvre H. , Noblet C. , Moore N. , Wolf L. M. 
Published: March 2008

SummaryA patient presented with paroxysmal hypertension and typical clinical features of phaeochromocytoma, but with a normal adrenal computed tomographic scan and much higher plasma noradrenaline than adrenaline concentrations. Urinary vanillyimandelic acid concentrations were only moderately elevated. This syndrome probably arose as a consequence of an interaction between the monoamine oxidase inhibitor selegiline, the sympathomimetic agent ephedrine, and a tricyclic antidepressant The mechanism of the interaction is thought to be related to increased sympathetic release of noradrenaline by ephedrine, inhibition of catabolism by selegiline, and inhibition of reuptake of noradrenaline by the tricyclic. Although newer selective monoamine oxidase inhibitors are considered to be safer than earlier non‐selective inhibitors, they can also contribute to drug intersections mimicking phaeochromocytoma.