bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transcavernous surgery; an effective treatment for pituitary macroadenomas
Authors: Matsuno Akira , Sasaki Tomio , Saito Nobuhito , Mochizuki Toshihiro , Fujimaki Takamitsu , Kirino Takaaki , Takakura Kintomo 
Published: December 2008

Matsuno A, Sasaki T, Saito N, Mochizuki T, Fujimaki T, Kirino T, Takakura K. Transcavernous surgery; an effective treatment for pituitary macroadenomas. Eur J Endocrinol 1995:133:156–65. ISSN 0804–4643
The endocrinological outcome in four patients with pituitary macroadenomas laterally invading the cavernous sinus, who were treated surgically by the transcranial transcavernous approach, was compared with that in four patients with macroadenomas that had been removed transsphenoidally. The decrease in the elevated serum levels of anterior pituitary hormones after transcavernous surgery ranged from 58.4% to 90.1%, whereas after transsphenoidal surgery it ranged from 0% to 46.1%. The responsiveness of pituitary hormones to stimulation tests was restored and maintained after transcranial transcavernous surgery. Transsphenoidal surgery achieved neither sufficient tumor reduction nor produced a satisfactory endocrinological remission. When cavernous sinus invasion is suspected by magnetic resonance imaging, even if it cannot be confirmed with certainty, transcranial transcavernous surgery is recommended. It is a useful surgical procedure for obtaining a sufficient degree of tumor extirpation and satisfactory endocrinological improvement in patients with macro-adenomas laterally invading the cavernous sinus, particularly somatotroph or corticotroph macro-adenomas. Postoperatively, mild cranial nerve paresis may occur, but this may resolve in 1–4 months.
Akira Matsuno, Department of Neurosurgery, Teikyo University Ichihara Hospital, 3426-3 Anegasaki, Ichihara City, Chiba 299-01, Japan
Altered adrenocorticotropin and cortisol response to corticotropin-releasing hormone in HIV-1 infection
Authors: Biglino Alberto , Limone Paolo , Forno Brunella , Pollono Annamaria , Cariti Giuseppe , Molinatti Gian Michele , Gioannini Paolo 
Published: December 2008

Biglino A, Limone P, Forno B, Pollono A, Cariti G, Molinatti GM, Gioannini P. Altered adrenocorticotropin and cortisol response to corticotropin-releasing hormone in HIV-I infection. Eur J Endocrinol 1995;133:173-9. ISSN 0804-4643
Alterations of the hypothalamic-pituitary-adrenal (HPA) axis are common in HIV infection. To characterize further the site of these derangements and their possible causes, eight male drug addicts with symptomatic HIV infection (stage IV C2) underwent the following investigations: repeated baseline determinations of cortisol, adrenocorticotropin (ACTH), interleukin 1β (IL-1β), IL-6 and interferon alpha (IFN-α): and ovine corticotropin-releasing hormone (CRH) test (100 μg IV) for ACTH and cortisol determinations. Baseline cortisol levels were either normal or elevated in all patients. A significant positive linear correlation was found between baseline levels of cortisol and both IL-6 (r=0.955; p<0.001) and IL-1β (r=0.863; p<0.005), but not between cortisol and ACTH or between ACTH and circulating cytokines. Both ACTH and cortisol responses to CRH were nearly absent in six out of eight patients, and delayed in the others. The areas under the curves of both ACTH and cortisol after CRH were significantly lower in HIV patients than in a group of eight healthy control subjects (p=0.0157 for ACTH and p=0.046 for cortisol). Our data suggest the possibility of an inappropriate stimulation of the HPA axis in symptomatic HIV infection by HIV-induced release of cytokines, with a blunted pituitary and adrenal response to CRH.
Paolo Limone, Institute of Internal Medicine, University of Torino, C.so AM Dogliotti 14, 10126 Torino, Italy
Reduced bone mineral density in adults with growth hormone (GH) deficiency: increased bone turnover during 12 months of GH substitution therapy
Authors: Degerblad Marie , Bengtsson Bengt-Åke , Bramnert Margareta , Johnell Olof , Manhem Per , Rosén Thord , Thorén Marja 
Published: December 2008

Degerblad M, Bengtsson B-Å, Bramnert M, Johnell O, Manhem P, Rosén T, Thorén M. Reduced bone mineral density in adults with growth hormone (GH) deficiency: increased bone turnover during 12 months of GH substitution therapy. Eur J Endocrinol 1995;133:180–8. ISSN 0804–4643
To evaluate the consequences of growth hormone (GH) deficiency on bone mineral density and to evaluate the effects of GH substitution therapy, 68 adults (25 females and 43 males) aged 22–61 (mean 44.2 ± 1.2) years with GH deficiency (GHD) were studied. Fifty-eight patients had panhypopituitarism, three had isolated GHD and in seven patients at least one additional pituitary function was affected. Twenty-one patients had childhood onset GHD. The patients were randomized to receive either GH in daily injections (0.125 IU · kg−1 · week−1 for the first 4 weeks and subsequently 0.25 IU · kg−1 · week−1) or placebo for 6 months. The trial continued as an open study with GH treatment for 6 or 12 months, with data presented as compiled data of 12 months of GH treatment in 64 patients. Bone mineral density (BMD) was measured by dual energy x-ray absorptiometry and bone turnover was assessed by serum markers of bone metabolism (osteocalcin, procollagen I peptide, crosslinked telopeptide of type I collagen and alkaline phosphatase activity). In women with adult onset GHD (N = 19) and in men with childhood onset GHD (N = 15), total body, spine and hip BMD was significantly reduced at baseline compared to Swedish age- and sex-matched control material. In men with adult onset of GHD (N = 28), BMD did not differ from male controls. During the placebocontrolled period, GH induced decreased total body and spine BMD, probably due to an expansion of the remodelling space, whereas all serum markers of bone turnover increased. Compiled GH data showed similar results after 6 months of treatment. After 12 months of GH treatment, BMD did not differ from basal values except for total body BMD, which was lower, whereas the serum markers of bone metabolism were still increased as compared to basal values. Two-thirds of the patients experienced fluid retention with peripheral oedema and arthralgias on the higher GH dosage. One obese patient developed non-insulin-dependent diabetes mellitus and was withdrawn from the study. These results demonstrate that GHD has negative effects on BMD and that GH substitution induces increased bone turnover. Continued long-term observations will reveal if there is a positive effect of GH substitution on bone mass in the adult GHD patient.
Marie Degerblad, Department of Endocrinology and Diabetology, Karolinska Hospital, S-17176 Stockholm, Sweden
Acute and chronic effects of octreotide on thyroid axis in growth hormone-secreting and clinically non-functioning pituitary adenomas
Authors: Colao Annamaria , Merola Bartolomeo , Ferone Diego , Marzullo Paolo , Cerbone Gaetana , Longobardi Salvatore , Di Somma Carolina , Lombardi Gaetano 
Published: December 2008

Colao A, Merola B, Ferone D, Marzullo P, Cerbone G, Longobardi S, Di Somma C, Lombardi G. Acute and chronic effects of octreotide on thyroid axis in growth hormone-secreting and clinically non-functioning pituitary adenomas. Eur J Endocrinol 1995;133:189–94. ISSN 0804–4643
The effect of somatostatin on thyroid function was studied in 12 patients with growth hormone (GH)-secreting and eight patients with clinically non-functioning adenomas (NFA) and normal pituitary/ thyroid axis; the patients were subjected to the administration of octreotide (OCT), which is a longacting somatostatin analog. All the patients received an acute test with 100 μg of OCT, both short term (1 month) and long term (6 months), with doses ranging from 300 to 600 μg/day, Serum thyroxine (T4). triiodothyronine (T3), free T4, free T3, thyroglobulin and basal and thyrotropin (TSH)-releasing hormone (TRH)-stimulated TSH were evaluated before and after 1 and 6 months of therapy. Circulating GH and insulin-like growth-factor I (IGF-I) in acromegalics and GH, IGF-I and α-subunit in NFA were assessed at baseline and every month. The acute administration of 100 μg of OCT significantly reduced the TSH response to TRH (p < 0.01) in both acromegalics and NFA. In all the patients OCT administration caused a significant decrease of GH, IGF-I and α-subunit levels (p < 0.01). In addition, after 1 month of therapy both baseline and TRH-induced TSH secretion were decreased significantly in acromegalics and NFA. After 6 months of therapy, baseline and TRH-induced TSH was still reduced in NFA. Conversely, in acromegalics, baseline TSH levels were increased while TSH response to TRH was inhibited. No change of T4, T3, free T4 and free T3 was observed in NFA, whereas a slight but significant increase of T4 and decrease of T3 was recorded in acromegalics. In conclusion, OCT does seem to possess long-term suppressive effects on TSH response to TRH, both in acromegalics and NFA. The lack of basal TSH level inhibition in acromegalics could depend on the restored peripheral conversion of T4 into T3 due to the normalized GH levels during long-term OCT administration.
Annamaria Colao, Corso Europa 63, 80127 Napoli, Italy
Relationship between sex hormones, body composition and metabolic risk parameters in premenopausal women
Authors: Pedersen Steen B , Børglum Jens D , Brixen Kim , Richelsen Bjørn 
Published: December 2008

Pedersen SB, Borglum JD, Brixen K, Richelsen B. Relationship between sex hormones, body composition and metabolic risk parameters in premenopausal women. Eur J Endocrinol 1995;133: 200–6. ISSN 0804–4643
The metabolic complications associated with obesity are dependent upon the degree of obesity and the distribution of adipose tissue. In order to evaluate the associations between sex hormone status, metabolic risk parameters, obesity and distribution of adipose tissue, 25 premenopausal women with a wide range of body mass index (19.3–48.1 kg/m2 were studied. Body composition was determined by dual-energy x-ray absorptiometry scan and anthropometric measurements; in addition, lipid and sex hormone status were determined and an oral glucose tolerance test was performed. We found that sex hormone-binding globulin was correlated negatively with total fat mass (r = –0.77, p < 0.001) and especially with abdominal localization of adipose tissue (r = –0.85, p < 0.001). Free testosterone was correlated positively with total fat mass (r = 0.40, p < 0.05) and with abdominal fat accumulation (r = 0.64, p < 0.001). Free estrogen was correlated negatively with total amount of adipose tissue (r = –0.40, p < 0.05) but not with the distribution of adipose tissue, Finally, total fatness, abdominal localization of adipose tissue and free testosterone were all associated with elevated metabolic risk factors. However, multiple regression analysis revealed that only abdominal localization of adipose tissue was independently associated with a higher risk profile, whereas the effects of sex hormones or total fatness disappeared when abdominal localization of adipose tissue was included in the analysis. In conclusion, these findings in premenopausal women indicate that the connection between sex hormones and metabolic risk factors might be indirect, probably operating through alterations in the amount of adipose tissue in the abdominal region.
SB Pedersen, University Clinic of Endocrinology and Internal Medicine, Aarthus, Amtssygehus, Tage Hansensgade, DK-8000 Aarhus C, Denmark
Urinary iodine excretion in Belarus children
Authors: Mityukova TA , Astakhova LN , Asenchyk LD , Orlov MM , VanMiddlesworth L 
Published: December 2008

Mityukova TA, Astakhova LN, Asenchyk LD, Orlov MM, VanMiddlesworth L. Urinary iodine excretion in Belarus children. Eur J Endocrinol 1995;133:216–7. ISSN 0804–4643.
Casual urine samples were collected to determine iodine excretion of 1680 Belarus children during 1990–1994. The subjects, 8–16 years old, were from nine different regions of Belarus; 60% were from the Gomel oblast, which has been associated with relatively high levels of radioiodine fallout and increased incidence of thyroid cancer. Most of the median values indicate borderline/low iodine intake or mild iodine deficiency. Ranges were wide but 163 children excreted < 20 μgI/l urine and they should be considered severely deficient in iodine.
L VanMiddlesworth, Dept. of Physiology and Biophysics, University of Tennessee, 894 Union Avenue, Memphis, TN 38163, USA
Modification of pancreatic digestive function by pituitary grafting in mice
Authors: Matsuda Manabu , Mori Takao , Park Min K , Kawashima Seiichiro 
Published: December 2008

Matsuda M, Mori T, Park MK, Kawashima S. Modification of pancreatic digestive function by pituitary grafting in mice. Eur J Endocrinol 1995;133:221–6. ISSN 0804–4643
The effect of prolactin on the digestive potency of the acinar pancreas was examined in pituitary-grafted hyperprolactinemic mice, because our previous experiment showed that a marked proliferation of pancreatic acinar cells was induced by pituitary grafting in mice. To know whether the digestive function is modified, the tissue contents of pancreatic digestive enzymes, such as chymotrypsin, lipase, α-amylase and ribonuclease, were measured in the hyperprolactinemic mice. Pituitary grafting significantly increased the contents of chymotrypsin and lipase in the pancreas on day 12 after the operation without affecting intake of food, when compared to those in the sham-operated controls. On day 30, however, the differences between pituitary-grafted and control mice were no more discernible. Thus, the digestive enzyme activities are easily modified soon after the increase of circulating prolactin level. This effect of prolactin on the function of the pancreas may be responsible for "homeorhetic" control of nutrients during lactation. In another set of experiments in adrenalectomized–castrated or castrated mice, pituitary grafting induced an increase in the weight of the pancreas. In addition, adrenalectomy in combination with castration did not alter the pancreatic contents of chymotrypsin and lipase but decreased the amylase content. These results taken together seem to indicate that the effect of prolactin on the exocrine pancreas is not mediated by gonadal and adrenal steroid hormones.
Manabu Matsuda, Zoological Institute, Graduate School of Science, University of Tokyo, Bunkyo-ku, Tokyo 113, Japan
Myocardial production of prostaglandins: its role in atrial natriuretic peptide release
Authors: Azizi Chafik , Barthélemy Christiane , Masson Françoise , Maistre Geneviéve , Eurin Joëlle , Carayon Alain 
Published: December 2008

Azizi C, Barthélemy C, Masson F, Maistre G, Eurin J, Carayon A. Myocardial production of prostaglandins: its role in atrial natriuretic peptide release. Eur J Endocrinol 1995;133:255–9. ISSN 0804–4643
In recent years, considerable evidence has been accumulated on prostaglandins (PG) in modulating atrial natriuretic peptide (ANP) release. In the current study we investigated whether eicosanoids promote isoproterenol-induced ANP secretion from superfused rabbit sliced atria. Inclusion of the cyclooxygenase inhibitor indomethacin (10 μmol to the superfusing medium abolished isoproterenol-induced ANP release. Next, PGE2, but not PGF2α or PGI2 (10 μmol), increased ANP release. Furthermore, isoproterenol-induced PGE2 formation was fully attenuated by indomethacin. Dibutyl-cAMP (0.5 mmol) had no effect on PGE2 formation, and the protein kinase A (PKA) inhibitor H89 (20 μmol) did not alter isoproterenol-induced PGE2 formation. On the other hand, indomethacin led to a significant decrease in isoprotrenol-induced cAMP production. In addition, PGE2 enhanced basal cAMP concentration in superfusates. Superfusion of sliced atria by forskolin (10 μmol) or by dibutylcAMP (0.5 mmol) produced a significant rise in ANP release. Finally, H89 was ineffective on basal ANP release but abolished the increase of ANP release in response to isoproterenol or to PGE2. We conclude that: the effect of isoproterenol on ANP release is sensitive to indomethacin and H89; PGE2, but not PGF2α or PGI2, increases ANP release; isoproterenol promotes myocardial PGE2 formation independently of adenylate cyclase and PKA activation pathways; and PGE2-induced ANP release is mediated by cAMP production and subsequent PKA activation. These results suggest that isoproterenol-induced ANP release appears to be mediated at least partly by PGE2 with underlying cAMP formation and PKA activation.
C Azizi, Service de Biochimie, CHU Pitié-Salpêtrère, 91 boulevard de l'hôpital, 75634 Paris Cedex 13, France
Amniotic fluid and plasma levels of parathyroid hormone-related protein and hormonal modulation of its secretion by amniotic fluid cells
Authors: Dvir Rina , Golander Avraham , Jaccard Niva , Yedwab Gideon , Otremski Itzhak , Spirer Zvi , Weisman Yosef 
Published: December 2008

Dvir R, Golander A, Jaccard N, Yedwab G, Otremski I, Spirer Z, Weisman Y. Amniotic fluid and plasma levels of parathyroid hormone-related protein and hormonal modulation of its secretion by amniotic fluid cells. Eur J Endocrinol 1995;133:277–82. ISSN 0804–4643
Parathyroid hormone-related (PTHrP), the major mediator of humoral hypercalcemia of malignancy, may also regulate placental calcium flux, uterine contraction and fetal tissue development. In the present study, we demonstrated that the mean immunoreactive PTHrP concentrations in amniotic fluid at mid-gestation (21.2 ± 3.7 pmol/l) and at term (19.0 ± 2.7 pmol/l) were 13-16-fold higher than levels measured in either fetal (1.6 ± 0.1 pmol/l) or maternal plasma (1.4 ± 0.3 pmol/l) at term and equal to levels found in plasma of patients with humoral hypercalcemia of malignancy. In vitro studies pointed to three possible sources of PTHrP in amniotic fluid: cultured amniotic fluid cells, cells derived from the amniotic membrane overlying the placenta and placental villous core mesenchymal cells. Treatment of cultured amniotic fluid cells with human prolactin, human placental lactogen (hPL) or human growth hormone (100 μg/l) increased PTHrP secretion after 24 h by 43%, 109% and 90%, respectively. Insulin-like growth factors I and II(100 μg/l), insulin (100 μg/l) and epidermal growth factor (EGF) (10 μg/l) increased PTHrP secretion by 53%, 46%, 68% and 118%, respectively. The stimulation of PTHrP secretion by EGF or by hPL was both time- and dose-dependent. In contrast, calcitriol and dexamethasone (10 nmol/l) decreased PTHrP secretion by 32% and 75%, respectively. Estradiol, progesterone, dihydrotestosterone and human chorionic gonadotropin had no effect on PTHrP secretion. These findings support the notion that PTHrP may play a physiological role in the uteroplacental unit and demonstrate that human amniotic fluid cells could be a useful model for studying the regulation of PTHrP production and secretion by hormones and growth factors.
Y Weisman, Bone Disease Unit, Tel Aviv Medical Center, 6 Weizman Street, Tel Aviv 64239, Israel
Presence of heterogeneous thyroid-stimulating antibodies in sera from individual Graves' patients as shown by synthesized thyrotropin receptor peptide application: evidence showing two independent epitopes and a possible recognition of two epitopic regions by one antibody molecule
Authors: Sugawa Hideo , Akamizu Takashi , Kosugi Shinji , Ueda Yoshimichi , Ohta Chizuko , Okuda Jyoji , Mori Toru 
Published: December 2008

Sugawa H, Akamizu T, Kosugi S, Ueda Y, Ohta C, Okuda J, Mori T. Presence of heterogeneous thyroidstimulating antibodies in sera from individual Graves' patients as shown by synthesized thyrotropin receptor peptide application: evidence showing two independent epitopes and a possible recognition of two epitopic regions by one antibody molecule. Eur J Endocrinol 1995;133:283–93. ISSN 0804–4643
To define the epitope(s) of stimulating thyrotropin receptor antibody (TSH-R-Sab), we synthesized 19 oligopeptides covering almost all amino acids of the extracellular domain of the human TSH-R and studied these effects on the inhibition of one TSH-R-Sab activity. Four of the 19 peptides encompassing residues 31–50 (P31-20), 91–119 (P91-29), 287–304 (P287-18) and 354–367 (P354-14) were found to show significant TSH-R-Sab inhibition and to have similar effects on the other three Graves' immunoglobulins. When these peptides were applied in combination with P354-14 only P287-18 revealed additional effects but the other two combinations did not. Furthermore, sequential addition of these peptide pairs confirmed the additional effects of P287-18 and P354-14. Sequential peptideaffinity gel studies were then performed. Most of the TSH-R-Sab activity in the unabsorbed fraction from P287-18 gel was absorbed to a subsequent P354-14 gel and the eluted fraction from P287-18 mostly remained unabsorbed by the P354-14 gel. On the other hand, most of the unabsorbed fraction from P91-29 gel remained unabsorbed even by the subsequent P354-14 gel. When a P354-14 affinity gel-purified TSH-R-Sab immunoglobulin was labeled and evaluated for its binding to FRTL-5 cells, additions of original immunoglobulin, P354-14 and P91-29 resulted in significant inhibition of the binding but P287-18 did not affect either. From these results, it was concluded that most of the individual Graves' immunoglobulins contain at least two heterogeneous moieties with TSH-R-Sab activity, one of which binds P354-14 and the other binds P287-18. Further, P354-14 and P91-29 were indicated to bind the same molecule of TSH-R-Sab immunoglobulin.
Toru Mori, Department of Laboratory Medicine, Kyoto University School of Medicine, 54 Shogoin Kawaharacho, Sakyo-ku, Kyoto 60601, Japan