bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ultrasonically guided chemical parathyroidectomy in patients with primary hyperparathyroidism: a follow‐up study
Authors: Karstrup Steen , Hegedüs Laszlo , Holm Hans Henrik 
Published: March 2008

SummaryOBJECTIVE We evaluated the long‐term results in two different groups of patients with primary hyperparathyroidism treated with ultrasonically guided percutaneous ethanol (96%) injection into parathyroid tumours.DESIGN A prospective long‐term follow‐up (more than 6 months). Ethanol (96%) was injected under ultrasonic guidance into biopsy verified solitary parathyroid tumours. Basic treatment included a maximum of three treatments with an interval of about 1 month (group 1) or 1 week (group 2). Dose of ethanol was half the volume of the parathyroid tumour.PATIENTS Two different groups of patients with only one ultrasonically detected and biopsy verified parathyroid tumour were treated. Group 1 (n= 18) were treated regardless of the severity of the hyperparathyroid disease. Group 2 (n= 14) were selected for treatment either due to severe hypercalcaemic symptoms (n= 3), a high surgical risk (n= 5), or refusal of surgery (n= 6).MEASUREMENTS The volume of the parathyroid tumours was measured as half the product of maximum length, width, and depth. Blood tests included measurements of ionized calcium, total calcium and PTH.RESULTS In group 1, 12 of 18 patients (66%) could be followed more than 6 months. Follow‐up ranged from 12 to 58 months (median 45 months). A significant decrease (P < 0 001) in serum concentrations of ionized calcium and total calcium was observed. Eight patients (44%) later underwent surgical parathyroidectomy. Injection therapy was regarded as successful in 10 of 18 patients (56%). In group 2,11 of 14 patients (79%) were followed more than 6 months. Follow‐up ranged from 18 to 50 months (median 39 months). A significant decrease (P <0 001) in serum concentrations of ionized calcium, total calcium and intact PTH (1–84) was observed. Treatment was successful in 11 of 14 patients (79%). Two patients required parathyroid surgery. Re‐examination with ultrasound showed a significant reduction in the volume of the treated parathyroid tumours. Fibrosis surrounding the parathyroid tumours was detected in eight of 10 patients who subsequently had operations. One patient from each group had a complication of a unilateral permanent vocal cord paralysis following injection therapy.CONCLUSION Partial or complete long‐term remission of primary hyperparathyroidism can be achieved using ultrasound‐guided chemical parathyroidectomy. However, the intervals between treatments should be short and the treatment should be reserved only for patients not fit for surgery.
Intracranial dissemination of a macroprolactinoma
Authors: Assies J. , Verhoeff N. P. L. G. , Bosch D. A. , Hofland L. J. 
Published: March 2008

SummaryA patient with a macroprolactinoma and extrasellar extension was treated by incomplete transfrontal surgery, external irradiation and additional bromocriptine (Br) treatment. After 4 years, partial bromocriptine resistance developed (a rare occurrence) together with the appearance of intracranial metastases. 123l‐lodobenzamide was helpful In evaluating the dopamine D2 receptor status of the metastatic tumour both in vivo using single‐photon emission computed tomography (SPECT) and in vitro. Prolactin release by the cultured metastatic tumour cells was more potently inhibited by CV 205–502 than by bromocriptine. The patient, treated by surgery, irradiation and CV 205–502, developed a ptosis of the left eye and a transient psychiatric delusional state, the latter probably an effect of the dopamine agonist. As the right frontal metastasis was markedly positive on SPECT with 111ln‐SMS, somatostatin treatment was added to the CV 205–502.
Thyroxine treatment increases circulating levels of insulin‐like growth factor binding protein‐1: a placebo‐controlled study
Authors: Angervo M. , Tiihonent M. , Leinonen P. , Välimaki M. , Seppälä M. 
Published: March 2008

SummaryOBJECTIVE Thyroid hormones affect carbohydrate metabolism in the liver, and hepatic insulin‐like growth factor binding protein‐1 (IGFBP‐1) participates in glucose counter‐regulation, so we studied the effects of oral thyroxine on serum IGFBP‐1.DESIGN The study was performed on a placebo‐controlled cross‐over basis covering 3 months’ thyroxine and 3 months’ placebo administration.PATIENTS Eight patients taking anticonvulsant medication and four patients with hypothalamic hypothyroidism were given thyroxine, 150–200 μg daily for 3 months, or placebo.MEASUREMENTS Serum IGFBP‐1, sex hormone binding globulin, free T3 and free T4, TSH and IGF‐I levels were measured after an overnight fast before treatment, and at the end of each 3‐month period.RESULTS Anticonvulsant medication had no significant effect on serum IGFBP‐1. After 3 months’ thyroxine treatment the serum IGFBP‐1 levels (69; 58‐167 μ g/l; median and interquartile range, respectively) were significantly higher than those after placebo treatment (44; 23‐58 μ g/l; P= 0 002), or the pretreatment levels (54; 19‐81 μ g/l, P= 0 005). The IGFBP‐1 levels rose in all 12 patients after thyroxine treatment, the median rise being 2.1‐fold compared to placebo levels. No change was found in serum IGF‐I concentrations.CONCLUSIONS Oral thyroxine produces a rise in serum IGFBP‐1 level without a change in serum IGF‐I concentration.
Gestational thyrotoxicosis and hyperemesis gravidarum: possible role of hCG with higher stimulating activity
Authors: Kimura Motoko , Amino Nobuyuki , Tamaki Haruo , Ito Eriko , Mitsuda Nobuaki , Miyai Kiyoshi , Tanizawa Osamu 
Published: March 2008

SummaryOBJECTIVE The thyroid gland is physiologically stimulated in normal early pregnancy. However, clinical thyrotoxicosis in normal pregnancy has not been well described. In order to clarify this we examined thyroid function and thyrotoxic symptoms in relation to emesis in normal pregnancy. We also investigated the possible mechanism of gestational thyrotoxicosis.DESIGN Thyroid function was evaluated in view of the clinical thyrotoxic symptoms and the severity of gestational emesis in early pregnancy of 51 normal women. Two pregnant women who showed clinical thyrotoxicosis were followed serially during and after pregnancy.MEASUREMENTS Serum free T4, free T3 and TSH were measured by radioimmunoassay and hCG by fluoroimmunoassay. Thyroid‐stimulating activity of pregnancy sera was measured by cAMP increase in cultured FRTL‐5 cells. RESULTS Fifty‐one pregnant women were divided into three groups: those without emesis (n= 24), with emesis (n= 19) and with hyperemesis (n= 8). Serum free T4 and free T3 were higher in the hyperemesis group (P<0.01) and the emesis group (P<0.01), and serum TSH was suppressed to less than 0 1 mU/l in both groups, while serum hCG was not significantly different among these three groups.However, serum thyroid‐stimulating activity was remarkably high in the hyperemesis group (P<0.01). Thus the ratio of thyroid‐stimulating activity to hCG was higher in the hyperemesis group (P < 0.05) and the emesis group (P < 0.05) compared with that in the group without emesis. These thyroid‐stimulating activities were abolished by treatment of the serum with anti‐hCG antibody. Two of eight women with hyperemesis, who had the highest free T4 and thyroid‐stimulating activity/hCG ratio, showed overt clinical symptoms of thyrotoxicosis; all the symptoms disappeared in association with a fall in thyroid‐stimulating activity and free T4.CONCLUSION Clinical thyrotoxicosis is caused by circulating hCG with higher biological activity in pregnant women with hyperemesis. A new clinical entity of‘gestational thyrotoxicosis’is proposed and tentative characteristics are discussed.
Age and gender influence the severity of thyroid‐associated ophthalmopathy: a study of 101 patients attending a combined thyroid‐eye clinic
Authors: Perros P. , Crombie A. L. , Matthews J. N. S. , Kendall‐Taylor P. 
Published: March 2008

SummaryBACKGROUND The pathogenesis of thyroid‐associated ophthalmopathy is thought to be autoimmune, although environmental and genetic factors are also considered to be important. As the morbidity of thyroid‐associated ophthalmopathy is considerable and treatment often unsatisfactory, there a need to identify possible predisposing factors.OBJECTIVE The study was undertaken in order to ascertain the relationship between age, gender and severity of thyroid‐associated ophthalmopathy.PATIENTS One hundred and one consecutive patients with thyroid‐associated ophthalmopathy who presented over a period of 5 years to a combined thyroid‐eye clinic.METHODS Patients were assessed by grading their inflammatory signs and degree of diplopia, and by measurement of exophthalmos, palpebral aperture, differential intraocular pressure, and visual acuity. On the basis of the above an ophthalmopathy index was devised to grade the overall severity of eye disease.RESULTS The mean age was 49.2 years (SD 13.4), the female‐to‐male ratio was 405, and mean ophthalmopathy index 6.49 (SD 3.3). Optic nerve compression was present in 9–9% of patients. There was a positive relationship between age and ophthalmopathy index (P<0.001); after correcting for age, males had an average ophthalmopathy index 41 % greater than that of females.CONCLUSION There is an association between severity of thyroid‐associated ophthalmopathy and (i) advancing age and (ii) female‐to‐male ratio, which has not been previously described. Patients over the age of 60 (particularly males) with Graves'disease appear to be at risk of developing severe eye disease.
Characterization of a novel mutant human thyroid hormone receptor β in a family with hereditary thyroid hormone resistance
Authors: Sakurai Akihiro , Miyamoto Takahide , Hughes Ieuan A. , DeGroot Leslie J. 
Published: March 2008

SummaryOBJECTIVE We wished to determine the abnormality responsible for Generalired Resistance to Thyroid Hormone in a family with this syndrome.DESIGN Molecular biological studies were performed on a mutant human thyroid hormone receptor beta (hTRβ) cloned from fibroblasts of the patient.PATIENTS The patient is from a previously reported family with typical features of Generalized Resistance to Thyroid Hormone, demonstrating goitre, elevated thyroid hormone levels, slightly elevated TSH, and retarded bone age.MEASUREMENTS A cDNA for hTRβ1 was cloned using specific oligonucleotide primers from fibroblast DNA. A mutant hTRβ1 expression vector was constructed, and an in‐vitro expressed mutant receptor was tested for T3 binding. Receptor binding to DNA was studied in a DNA cellulose assay and gel mobility shift assay.RESULTS Two mutations were found in the cloned hTRβ. One was silent but the second changed arginine 438 to histidine. The mutation was present in RNA and genomic DNA, as shown by allele‐specific amplification. The mutated receptor had reduced T3 binding affinity but demonstrated normal binding in a DNA cellulose assay and In a gel mobility shift assay. The receptor did not have altered heat sensitivity.CONCLUSIONS In the T sibship with Generalized Resistance to Thyroid Hormone, resistance to thyroid hormone is apparently produced by a substitution of a histidine for arginine at amino acid 438, which causes reduced binding of receptor to T3, although the receptor remains able to bind to DNA and, for this reason, functions as a dominant negative in affected subjects who are heterorygous with one normal and one mutated allele.
The early effects of radioiodine therapy for hyperthyroidism on biochemical indices of bone turnover
Authors: MacLeod Jean M. , McHardy K. C. , Harvey R. D. , Duncan A. , Reid I. W. , Bewsher P. D. , Robins S. P. 
Published: March 2008

SummaryOBJECTIVE We investigated the early changes following radioiodine therapy for hyperthyroidism, in biochemical indices of bone synthesis and degradation, and their relationship to circulating thyroid hormone concentrations.DESIGN Prospective follow‐up over the first 12 weeks after radioiodine therapy.PATIENTS Six women with clinical and biochemical evidence of hyperthyroidism.MEASUREMENTS Serum Concentrations of T4, free T3 and osteocalcin, and urinary excretion of the pyridinium cross‐links, pyridinaline and deoxypyridinaline, measured before and weekly for 12 weeks after administration of radioiodine therapy.RESULTS Biochemical indices of bone metabolism were elevated prior to treatment. There was a brisk reduction in circulating thyroid hormones levels paralleled by a similar fall In pyridinlum cross‐llnk excretion, which had returned to normal in five patients by the end of the study. There was a positive correlation between pyridinium cross‐link excretion and thyroid hormone concentrations. There was no significant change in serum osteocalcin.CONCLUSIONS Treatment of hyperthyroidism results in prompt correction of the associated increased rate of bone collagen degradation suggesting that effective early correction of hyperthyroidism is desirable to limit its detrimental effect on skeletal mass.
Influence of sex, age and adrenergic pathways on the growth hormone response to GHRP‐6
Authors: Peñalva A. , Pombo M. , Carballo A. , Barreiro J. , Casanueva F. F. , Dieguez C. 
Published: March 2008

SummaryOBJECTIVE His‐dTrp‐Ala‐Trp‐dPhe‐Lys‐NH2 (GHRP‐6) is a synthetic compound that releases GH in a dose‐related and specific manner in several species including man. To further characterize the effects of GHRP‐6 on GH secretion in normal human subjects, we assessed plasma GH levels following GHRP‐6 administration in normal male adult subjects, normal female adult subjects at different stages of their menstrual cycle and in normal prepubertal male and female children. We also studied the influence of adrenergic pathways on GHRP‐6 induced GH secretion in normal adult male subjects.DESIGN In a group of eight volunteers the following tests were carried out: GHRP‐6 alone (1 μg/kg i.v. at 0 minutes); propranolol(40 mg p.o. at −30 minutes) plus GHRP‐6; and (3 mg p.o. at −120 minutes) plus GHRP‐6. Another group of eight volunteers were studied with GHRP‐6 as above; clonidine alone (300 mg p.o. at −60 minutes); and clonidine plus GHRP‐6. A group of nine women were studied with 1 μg/kg i.v. of GHRP‐6 at 0 minutes, at different stages of their menstrual cycle. Finally, 12 children were studied with GHRP‐6 using the same dose and methods as above.PATIENTS Twenty‐five normal adult subjects (16 male and nine female) and 12 normal prepubertal children (six male and six female) wer studied after giving informed consent.EASUREMENTS Plasma GH levels were measured by radioimmunoassay.RESULTS No differences in GH responses to GHRP‐6 were found between children and normal adult male or female Subjects at different stages of their menstrual cycle. Administration of propranolol and clonidine did not modify the GH responses to GHRP‐6 in male adults. In contrast, prazosin administration induced an increase in plasma GH levels that was statistically different from that of GHRP‐6 alone (P>0.05 between area under curve).CONCLUSIONS GHRP‐6 exerts a potent stimulatory effect on GH secretion in adults and children. Its effects, at least at the dose studied, are Independent of sex and age. Noradrenergic pathways through α2 adrenergic receptors are unlikely to influence this response.
The relationship between peripheral immunoactive inhibin, human chorionic gonadotrophin, oestradiol and progesterone during human pregnancy
Authors: Tovanabutra S. , Illingworth P. J. , Ledger W. L. , Glasier A. F. , Baird D. T. 
Published: March 2008

SummaryOBJECTIVE The objective of this study was to investigate serial changes in the plasma concentration of inhibin in both the very early days of pregnancy following implantation and in late pregnancy. The timing of the changes in inhibin concentration relative to changes in the concentrations of other hormones of pregnancy was also investigated.DESIGN Serial observations of the peripheral concentrations of inhibin and other hormones in two groups of healthy volunteers in (a) early pregnancy and (b) late pregnancy.PATIENTS (a) Four healthy women recruited on cessation of contraception prior to conception. (b) Nine healthy women recruited at the antenatal clinic.MEASUREMENTS In the early pregnancy subjects, the concentrations of inhibin, progesterone, oestradiol and hCG were measured in plasma samples obtained three times per week from day 8 to day 10 of each menstrual cycle until 11 weeks after the last menstrual period in the conception cycle. In the late pregnancy subjects, plasma samples were obtained at 4‐week intervals from 12 weeks until term.RESULTS The concentration of inhibin, progesterone and oestradiol in conception cycles were similar to those in the preceding cycles until the mid/ to late‐luteal phase of the cycle when hCG was first measurable. By day 12 of the luteal phase the concentration of inhibin was significantly higher in the pregnancy cycle than in the non‐pregnancy cycle (P > 0.05) and progressively increased after the time of the missed menstrual period. The concentration of inhibin reached a peak (513.0 U/I, CI 442.1–595.3) by day 47 when the concentration of hCG was maximal. In early pregnancy the concentration of inhibin was correlated with that of hCG (r= 0.361; P>0.01) as well as progesterone (r= 0.584, P>0.001) and oestradiol (r= 0.602. P>0.001). After 12 weeks there was no significant correlation between hCG and lnhibin although significant correlations persisted with progesterone (r= 0.553, P>0.001) and oestradiol (r= 0.361, P>0.01).CONCLUSIONS The corpus luteum makes a significant contribution to the production of inhibin in early pregnancy while after 12 weeks the placenta is the major source.
Pituitary apoplexy and sudden blindness following the administration of gonadotrophin releasing hormone
Authors: Masson Ewan A. , Atkin Stephen L. , Diver Michael , White Michael C. 
Published: March 2008

SummaryPituitary apoplexy has been reported as a rare complication of combined tests and of TRH administration in prolactinomas. A 54‐year‐old man with a pituitary macro‐adenoma had a single injection of 100 μg GnRH. Twenty minutes later he complained of increasing headache and vomited. These symptoms settled spontaneously and were attributed to the pharmacological effects of GnRH. Five hours later he was found to be blind and disorientated without spontaneous complaint. Emergency CT showed a large adenoma with central necrosis, consistent with pituitary apoplexy. An urgent surgical decompression was carried out and necrotic haemorrhagic debris removed. Baseline bloods revealed non‐pulsatile FSH of 40 U/I with LH 0.3 U/I with no hormonal response to GnRH administration, but the sequence of events strongly suggests a causal relationship between this and pituitary apoplexy. To our knowledge this is the first time that GnRH administration has been associated with pituitary apoplexy of a glycoprotein secreting pituitary adenoma.
Five‐year follow‐up of growth hormone antibodies in growth hormone deficient children treated with recombinant human growth hormone
Authors: Massa Guy , Vanderschueren‐Lodeweyckx Magda , Bouillon Roger 
Published: March 2008

SummaryOBJECTIVE The aim was to investigate the long‐term evolution of circulating growth hormone antibodies (GH‐AB) during and after treatment with methionyl‐recombinant human growth hormone (met‐rhGH).DESIGN AND PATIENTS The investigation was performed on serum samples of 46 growth hormone deficient children, treated for at least 12 months with met‐rhGH. Twenty patients had never been treated with hGH (previously untreated patients, Group I). Twenty‐six subjects were previously treated with pituitary extracted hGH (treated patients, Group II).MEASUREMENTS Serum levels of GH‐AB were measured by radioimmunoassay using charcoal precipitation of free ligand.RESULTS Fifteen patients (75%) of Group I and three patients (12%) of Group II developed GH‐AB. In 15 GH‐AB positive patients the antibodies became detectable during the first year of treatment with met‐rhGH. In three patients, however, the GH‐AB appeared during the second year. Once present, the GH‐AB remained detectable throughout the period of treatment with met‐rhGH. In six patients in whom treatment with met‐rhGH was stopped, GH‐AB levels decreased rapidly. In nine patients in whom treatment with met‐rhGH was changed to rhGH, the levels of GH‐AB decreased and ultimately became undetectable. In two patients GH‐AB remained present during administration of rhGH. No effect of GH‐AB on the growth‐promoting effect of met‐rhGH could be documented, either during the first or during the second year of treatment.CONCLUSIONS This study confirms the high immunogenicity of met‐rhGH, especially in patients not treated earlier with hGH. Once present, the GH‐AB remain detectable throughout the period of treatment with met‐rhGH. After stopping met‐rhGH treatment or changing to rhGH the GH‐AB disappear rapidly in most patients. No effect of GH‐AB on the growth‐promoting effect of rhGH could be documented.
Different modes of growth hormone (GH) administration do not change GH binding protein activity in man
Authors: Ho Ken K. Y. , Jorgensen Jens O. L. , Valiontis Erefili , Waters Michael J. , Rajkovic Ivan A. , Christiansen Jens S. 
Published: March 2008

SummaryOBJECTIVE Studies in rodents have shown GH binding protein (GHBP) levels to be dependent on the mode of GH administration. The aim is to determine whether GHBP levels in man are also modulated by the pattern of GH administration.PATIENTS Six GH deficient subjects participated in a randomized study in which 2 IU GH were administered either as (i) a continuous 24‐hour infusion, (ii) two intravenous boluses or (iii) eight intravenous boluses every 3 hours. In a second study, six normal men received a single subcutaneous injection of 0 2 U/kg GH and GHBP activity was measured over 24 hours. Control data were obtained from an untreated group of six age‐matched normal men.MEASUREMENTS GHBP activity was measured by immunoprecipitation using a monoclonal antibody that recognizes the human GHBP, and expressed as percentage specific binding of 125I‐GH in 50 μl of serum.RESULTS GHBP activity was not significantly different between the GH deficient and normal subjects. GHBP activity did not rise significantly during GH administration with each of the three intravenous patterns of delivery nor were there any significant differences between treatments. in the second study, GHBP activity did not change significantly following subcutaneous GH injection nor did results differ from untreated normal controls.CONCLUSIONS The level of GHBP in man is not dependent on GH secretory status or altered by short‐term GH treatment or the mode of administration. These findings stand in contrast to GH treatment effects in rodents and suggest that GH regulation of GHBP may be different between species.