underlying mechanisms of PCOS are not fully understood yet though obesity and insulin resistance are regarded as major risk factors for hyperandrogenism in PCOS due to abnormal sex steroid production in ovaries and adrenals ( 2 ). Especially, the differential
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Thomas Reinehr, Alexandra Kulle, Juliane Rothermel, Caroline Knop-Schmenn, Nina Lass, Christina Bosse, and Paul-Martin Holterhus
María J Gómora, Flavia Morales-Vásquez, Enrique Pedernera, Delia Perez-Montiel, Horacio López-Basave, Antonio R Villa, Azucena Hernández-Martínez, Esteban Mena, and Carmen Mendez
that can increase the incidence as well as tumor aggressiveness ( 8 , 9 , 10 ). Sexual steroid hormones acting through their receptors regulate signaling pathways related to cell proliferation, epithelial–mesenchymal transition, apoptosis, cell
Johanna Christina Penell, Mark M Kushnir, Lars Lind, Jonatan Bergquist, Jonas Bergquist, P Monica Lind, and Tord Naessen
inter-variation than estradiol ( 7 , 12 ), which declines with the onset of menopause. Estradiol levels are very low in postmenopausal women ( 7 ) but play an important role for physiological functions. Although data on endogenous sex steroid
Fidéline Bonnet-Serrano, Maxime Barat, Anna Vaczlavik, Anne Jouinot, Lucas Bouys, Christelle Laguillier-Morizot, Corinne Zientek, Catherine Simonneau, Etienne Larger, Laurence Guignat, Lionel Groussin, Guillaume Assié, Jean Guibourdenche, Ioannis Nicolis, Marie-Claude Menet, and Jérôme Bertherat
-24 stimulation test is not only used to make the diagnosis of adrenal insufficiency, characterized by an insufficient response of cortisol, but is also very useful to detect partial enzymatic deficiency, characterized by an explosive response of the steroid
Henrik H Thomsen, Holger J Møller, Christian Trolle, Kristian A Groth, Anne Skakkebæk, Anders Bojesen, Christian Høst, and Claus H Gravholt
Soluble CD163 (sCD163) is a novel marker linked to states of low-grade inflammation such as diabetes, obesity, liver disease, and atherosclerosis, all prevalent in subjects with Turner syndrome (TS) and Klinefelter syndrome (KS). We aimed to assess the levels of sCD163 and the regulation of sCD163 in regards to treatment with sex hormone therapy in males with and without KS and females with and without TS. Males with KS (n=70) and age-matched controls (n=71) participating in a cross-sectional study and 12 healthy males from an experimental hypogonadism study. Females with TS (n=8) and healthy age-matched controls (n=8) participating in a randomized crossover trial. The intervention comprised of treatment with sex steroids. Males with KS had higher levels of sCD163 compared with controls (1.75 (0.47–6.90) and 1.36 (0.77–3.11) respectively, P<0.001) and the levels correlated to plasma testosterone (r=−0.31, P<0.01), BMI (r=0.42, P<0.001), and homeostasis model of assessment insulin resistance (r=0.46, P<0.001). Treatment with testosterone did not significantly lower sCD163. Females with TS not receiving hormone replacement therapy (HRT) had higher levels of sCD163 than those of their age-matched healthy controls (1.38±0.44 vs 0.91±0.40, P=0.04). HRT and oral contraceptive therapy decreased sCD163 in TS by 22% (1.07±0.30) and in controls by 39% (0.55±0.36), with significance in both groups (P=0.01 and P=0.04). We conclude that levels of sCD163 correlate with endogenous testosterone in KS and are higher in KS subjects compared with controls, but treatment did not significantly lower levels. Both endogenous and exogenous estradiol in TS was associated with lower levels of sCD163.
Muriel Houang, Thao Nguyen-Khoa, Thibaut Eguether, Bettina Ribault, Séverine Brabant, Michel Polak, Irène Netchine, and Antonin Lamazière
, respectively, with positive predictive values (PPVs) of 12.0 and 16.1%, respectively. Different factors could explain such a low PPV: (i) cross-reactive detection of 17-OHP with its steroid precursors and their sulphated conjugates, which are present in the
Amit Kumar, Maria Ghosh, and Jubbin Jagan Jacob
levels >10 mg/dL (100 g/L) were excluded. Patients receiving mannitol infusions were excluded. Other exclusion criteria included patients with blood glucose values >400 mg/dL (22.2 mmol/L), those who received oral or i.v. steroids within the last 6 months
I Savchuk, M L Morvan, J P Antignac, K Gemzell-Danielsson, B Le Bizec, O Söder, and K Svechnikov
Introduction Steroid hormones produced by the human fetal adrenal glands (HFA) have been proposed to regulate intrauterine homeostasis and the maturation of certain organs required for extrauterine life ( 1 ). In this case, appropriate
Roberto Cosimo Melcangi, Livio Casarini, Marco Marino, Daniele Santi, Samantha Sperduti, Silvia Giatti, Silvia Diviccaro, Maria Grimoldi, Donatella Caruso, Guido Cavaletti, and Manuela Simoni
of erection was produced ( 18 ). PFS etiopathogenesis remains elusive. Three different clinical studies ( 18 , 25 , 26 ) demonstrated that finasteride treatment not only affects the steroids directly related with the enzyme 5α-R but has broad
Lesley A Hill, Zeynep Sumer-Bayraktar, John G Lewis, Eva Morava, Morten Thaysen-Andersen, and Geoffrey L Hammond
Introduction Corticosteroid-binding globulin (CBG) transports steroids in the blood and regulates their access to tissues and cells ( 1 , 2 ). Crystal structure analyses show that CBG contains a single hydrophobic steroid-binding site ( 3
