Search Results
Search for other papers by Sonja Kunz in
Google Scholar
PubMed
Search for other papers by Xiao Wang in
Google Scholar
PubMed
Search for other papers by Uta Ferrari in
Google Scholar
PubMed
Search for other papers by Michael Drey in
Google Scholar
PubMed
Search for other papers by Marily Theodoropoulou in
Google Scholar
PubMed
Search for other papers by Katharina Schilbach in
Google Scholar
PubMed
Search for other papers by Martin Reincke in
Google Scholar
PubMed
KORA Study Centre, University Hospital of Augsburg, Augsburg, Augsburg, Germany
Search for other papers by Margit Heier in
Google Scholar
PubMed
German Centre for Cardiovascular Research (DZHK), Partner site Munich Heart Alliance, Munich, Germany
Search for other papers by Annette Peters in
Google Scholar
PubMed
German Heart Centre Munich, Technical University of Munich, Munich, Germany
Institute of Epidemiology and Medical Biometry, University of Ulm, Ulm, Germany
Search for other papers by Wolfgang Koenig in
Google Scholar
PubMed
German Centre for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Hamburg, Germany
Search for other papers by Tanja Zeller in
Google Scholar
PubMed
Search for other papers by Barbara Thorand in
Google Scholar
PubMed
Search for other papers by Martin Bidlingmaier in
Google Scholar
PubMed
Introduction Steroid hormones are signaling molecules involved in regulation of electrolyte concentrations, blood pressure, reproductive functions, and metabolism ( 1 ). A lack or an excess of steroids results from enzyme defects, adenomas, or
Search for other papers by Enrique Pedernera in
Google Scholar
PubMed
Search for other papers by Flavia Morales-Vásquez in
Google Scholar
PubMed
Search for other papers by María J Gómora in
Google Scholar
PubMed
Search for other papers by Miguel A Almaraz in
Google Scholar
PubMed
Universidad La Salle, Posgrado de la Facultad de Ciencias Químicas, Ciudad de México, México
Search for other papers by Esteban Mena in
Google Scholar
PubMed
Search for other papers by Delia Pérez-Montiel in
Google Scholar
PubMed
Search for other papers by Elizabeth Rendon in
Google Scholar
PubMed
Search for other papers by Horacio López-Basave in
Google Scholar
PubMed
Search for other papers by Juan Maldonado-Cubas in
Google Scholar
PubMed
Search for other papers by Carmen Méndez in
Google Scholar
PubMed
female reproductive events. Further, ovarian tumors are considered sensitive to sex steroid hormones, as they are mediated by specific androgen, estrogen, and progesterone receptors ( 3 ). Additionally, the steroid hormone receptor shows a particular
Search for other papers by Ruth Percik in
Google Scholar
PubMed
Search for other papers by Sherwin Criseno in
Google Scholar
PubMed
Search for other papers by Safwaan Adam in
Google Scholar
PubMed
Search for other papers by Kate Young in
Google Scholar
PubMed
Royal Marsden Hospital, London, UK
Search for other papers by Daniel L Morganstein in
Google Scholar
PubMed
regarding hormone replacement therapy. Whilst hormonal deficiencies require physiological replacement, rare cases of hypophysitis accompanied by severe oedema and pressure on the optic chiasm require treatment with high-dose steroids. A recent study
Search for other papers by Eleftherios E Deiktakis in
Google Scholar
PubMed
Search for other papers by Eleftheria Ieronymaki in
Google Scholar
PubMed
Search for other papers by Peter Zarén in
Google Scholar
PubMed
Search for other papers by Agnes Hagsund in
Google Scholar
PubMed
Search for other papers by Elin Wirestrand in
Google Scholar
PubMed
Search for other papers by Johan Malm in
Google Scholar
PubMed
Search for other papers by Christos Tsatsanis in
Google Scholar
PubMed
Imperial College London, Institute of Reproductive and Developmental Biology, London, UK
Search for other papers by Ilpo T Huhtaniemi in
Google Scholar
PubMed
Malmö University Hospital, Reproductive Medicine Center, Malmö, Sweden
Search for other papers by Aleksander Giwercman in
Google Scholar
PubMed
Search for other papers by Yvonne Lundberg Giwercman in
Google Scholar
PubMed
Introduction For decades, gonadotropin-releasing hormone (GnRH) agonists have formed the mainstay hormonal treatment of prostate cancer ( 1 ). While they generate suppression of testosterone due to persistent suppression of luteinizing hormone
Department of Public Health, Erasmus University Medical Center, Rotterdam, Netherlands
Search for other papers by Josephina G Kuiper in
Google Scholar
PubMed
Department of Endocrinology and Metabolism, Amsterdam Gastroenterology Endocrinology Metabolism (AGEM), Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands
Search for other papers by Aline C Fenneman in
Google Scholar
PubMed
Search for other papers by Anne H van der Spek in
Google Scholar
PubMed
Search for other papers by Elena Rampanelli in
Google Scholar
PubMed
Department of Endocrinology and Metabolism, Amsterdam Gastroenterology Endocrinology Metabolism (AGEM), Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands
Search for other papers by Max Nieuwdorp in
Google Scholar
PubMed
Search for other papers by Myrthe P P van Herk-Sukel in
Google Scholar
PubMed
Netherlands Comprehensive Cancer Organisation, Utrecht, Netherlands
Search for other papers by Valery E P P Lemmens in
Google Scholar
PubMed
Search for other papers by Ernst J Kuipers in
Google Scholar
PubMed
Department of Epidemiology and Data Science, Amsterdam UMC, Amsterdam, Netherlands
Search for other papers by Ron M C Herings in
Google Scholar
PubMed
Search for other papers by Eric Fliers in
Google Scholar
PubMed
.nivel.nl/nl/nivel-zorgregistraties-eerste-lijn/jaarcijfers-aandoeningen-incidenties-en-prevalenties ). Treatment of primary hypothyroidism consists of hormone substitution therapy with daily oral administration of the synthetic thyroid hormone levothyroxine. The majority of levothyroxine is absorbed in the upper gastrointestinal tract, ranging from 40 to 80
Department of Oncology, Comprehensive Cancer Centre, Helsinki University Hospital, Helsinki, Finland
Search for other papers by Hanna Karhapää in
Google Scholar
PubMed
Department of Oncology, Comprehensive Cancer Centre, Helsinki University Hospital, Helsinki, Finland
Search for other papers by Siru Mäkelä in
Google Scholar
PubMed
Department of Radiology, HUS Medical Imaging Centre, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
Search for other papers by Hanna Laurén in
Google Scholar
PubMed
Department of Radiology, HUS Medical Imaging Centre, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
Search for other papers by Marjut Jaakkola in
Google Scholar
PubMed
Endocrinology, Abdominal Centre, University of Helsinki and HUS, Helsinki, Finland
Search for other papers by Camilla Schalin-Jäntti in
Google Scholar
PubMed
Department of Oncology, Comprehensive Cancer Centre, Helsinki University Hospital, Helsinki, Finland
Search for other papers by Micaela Hernberg in
Google Scholar
PubMed
thyroid-stimulating hormone (TSH), free thyroxine (fT4), free triiodothyronine (fT3), and thyroid antibodies: TSH receptor antibodies (TSHRAb), thyroid peroxidase antibodies (TPOAb), and antithyroglobulin antibodies. Before treatment initiation, we also
Search for other papers by Orwa Dandash in
Google Scholar
PubMed
Search for other papers by James Allebone in
Google Scholar
PubMed
Search for other papers by Adam Mirabelli in
Google Scholar
PubMed
Search for other papers by Nicholas Russell in
Google Scholar
PubMed
Search for other papers by Mathis Grossmann in
Google Scholar
PubMed
Department of Florey Institute, University of Melbourne, Parkville, Victoria, Australia
Search for other papers by Andrea Gogos in
Google Scholar
PubMed
Search for other papers by Richard A Kanaan in
Google Scholar
PubMed
Introduction Androgen deprivation therapy (ADT) using gonadotropin-releasing hormone (GnRH) agonists is one of the mainstay therapies for prostate cancer ( 1 ). This therapy reduces circulating testosterone to castrate concentrations
Search for other papers by Anna Gorbacheva in
Google Scholar
PubMed
Search for other papers by Anna Eremkina in
Google Scholar
PubMed
Search for other papers by Daria Goliusova in
Google Scholar
PubMed
Search for other papers by Julia Krupinova in
Google Scholar
PubMed
Search for other papers by Natalia Mokrysheva in
Google Scholar
PubMed
cascades menin participates in ( 12 ). Menin in the development of bone disorders in MEN1 patients Parathyroid lesions in MEN1 manifest with PHPT, usually followed by hypersecretion of parathyroid hormone and hypercalcemia. Development of