Center for International Health, University of Bergen, Bergen, Norway
Search for other papers by Kjersti S Bakken in
Google Scholar
PubMed
Department of Microbiology, Innlandet Hospital Trust, Lillehammer, Norway
Search for other papers by Kristina Randjelovic Nermo in
Google Scholar
PubMed
Department of Clinical Science, University of Bergen, Bergen, Norway
Search for other papers by Bjørn Gunnar Nedrebø in
Google Scholar
PubMed
Search for other papers by Tim I M Korevaar in
Google Scholar
PubMed
Department of Research, Innlandet Hospital Trust, Lillehammer, Norway
Search for other papers by Tor A Strand in
Google Scholar
PubMed
–20 weeks and is therefore dependent on maternal thyroid hormones ( 10 , 11 ). Although Norway has been considered iodine sufficient, pregnancy is a state of increased iodine demand and recent evidence suggests that mild and moderate iodine deficiency is
Search for other papers by David S McLaren in
Google Scholar
PubMed
Search for other papers by Aarani Devi in
Google Scholar
PubMed
Search for other papers by Nikolaos Kyriakakis in
Google Scholar
PubMed
Search for other papers by Michelle Kwok-Williams in
Google Scholar
PubMed
Division of Cardiovascular and Diabetes Research, Leeds Institute of Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, UK
Search for other papers by Robert D Murray in
Google Scholar
PubMed
hormone deficiencies is not fully understood but may result from a combination of damage to hypothalamic nuclei, portal vasculopathy, pituitary fibrosis, or the development of pituitary atrophy secondary to hypothalamic damage. HP dysfunction can present
Department of Endocrinology, Department of Molecular Medicine and Surgery, Metabolism and Diabetology, Karolinska University Hospital, 171 76 Stockholm, Sweden
Search for other papers by Charlotte Höybye in
Google Scholar
PubMed
Search for other papers by Erik Wahlström in
Google Scholar
PubMed
Search for other papers by Petra Tollet-Egnell in
Google Scholar
PubMed
Search for other papers by Gunnar Norstedt in
Google Scholar
PubMed
(3) . Adult growth hormone deficiency (GHD) syndrome is a well-defined clinical entity, including abnormal body composition, poor quality of life, dyslipidaemia and increased cardiovascular risk and mortality (4, 5) . GH has systematically been given
Search for other papers by Athanasios Zervas in
Google Scholar
PubMed
National and Kapodistrian University of Athens Medical School, ‘Aghia Sophia’ Children’s Hospital, Athens, Greece
Search for other papers by George Chrousos in
Google Scholar
PubMed
Search for other papers by Sarantis Livadas in
Google Scholar
PubMed
retardation, etc.) • Rheumatological (chronic juvenile arthritis, systemic lupus erythematosus, etc.) Endocrine diseases • Growth hormone/IGF-1 deficiency or insensitivity • Hypothyroidism • Hypercortisolism • Precocious puberty
Search for other papers by Lukas Plachy in
Google Scholar
PubMed
Search for other papers by Lenka Petruzelkova in
Google Scholar
PubMed
Search for other papers by Petra Dusatkova in
Google Scholar
PubMed
Search for other papers by Klara Maratova in
Google Scholar
PubMed
Search for other papers by Dana Zemkova in
Google Scholar
PubMed
Search for other papers by Lenka Elblova in
Google Scholar
PubMed
Search for other papers by Vit Neuman in
Google Scholar
PubMed
Search for other papers by Stanislava Kolouskova in
Google Scholar
PubMed
Search for other papers by Barbora Obermannova in
Google Scholar
PubMed
Search for other papers by Marta Snajderova in
Google Scholar
PubMed
Search for other papers by Zdenek Sumnik in
Google Scholar
PubMed
Search for other papers by Jan Lebl in
Google Scholar
PubMed
Search for other papers by Stepanka Pruhova in
Google Scholar
PubMed
familial short stature ( 6 ). Growth hormone deficiency (GHD) type II ( GH1 gene) is one example. Another possibility is rare AD inheritance of mutations in genes affecting pituitary morphogenesis and differentiation (e.g. POU1F1 , GLI2 , LHX4 , PITX2
Search for other papers by A Bergougnoux in
Google Scholar
PubMed
INSERM Unité 1203 (DEFE), Université de Montpellier, Montpellier, France
Search for other papers by L Gaspari in
Google Scholar
PubMed
Search for other papers by M Soleirol in
Google Scholar
PubMed
Search for other papers by N Servant in
Google Scholar
PubMed
Search for other papers by S Soskin in
Google Scholar
PubMed
Search for other papers by S Rossignol in
Google Scholar
PubMed
Search for other papers by K Wagner-Mahler in
Google Scholar
PubMed
Search for other papers by J Bertherat in
Google Scholar
PubMed
Search for other papers by C Sultan in
Google Scholar
PubMed
Search for other papers by N Kalfa in
Google Scholar
PubMed
Département d'Endocrinologie et de Gynécologie Pédiatrique, Hôpital Arnaud de Villeneuve, Université de Montpellier, Montpellier, France
INSERM Unité 1203 (DEFE), Université de Montpellier, Montpellier, France
Search for other papers by F Paris in
Google Scholar
PubMed
MM New MI Ten S Sultan C & Bhangoo A . The clinical and molecular heterogeneity of 17βHSD-3 enzyme deficiency . Hormone Research in Paediatrics 2010 74 229 – 240 . ( https://doi.org/10.1159/000318004 ) 10 Hiort O Marshall L Birnbaum
Search for other papers by Qiu-ming Yao in
Google Scholar
PubMed
Search for other papers by Bin Wang in
Google Scholar
PubMed
Search for other papers by Xiao-fei An in
Google Scholar
PubMed
Search for other papers by Jin-an Zhang in
Google Scholar
PubMed
Search for other papers by Liumei Ding in
Google Scholar
PubMed
T2DM are still necessary to copy with the epidemic of T2DM. There is evidence to indicate that endogenous sex hormones play a vital role in the pathogenesis of T2DM ( 4 ). Some studies proposed that testosterone was possibly linked with T2DM risk
Department of Endocrinology, The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK
Search for other papers by Sophie Howarth in
Google Scholar
PubMed
Search for other papers by Luca Giovanelli in
Google Scholar
PubMed
Search for other papers by Catherine Napier in
Google Scholar
PubMed
Department of Endocrinology, The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK
Search for other papers by Simon H Pearce in
Google Scholar
PubMed
or biochemically manifest ( 4 ). A proportion (~50%) of these patients progress to adrenal cortical destruction ( 5 ) but are able to compensate by adrenocorticotrophic hormone (ACTH)-driven hypertrophy of unaffected areas, as demonstrated by case
Search for other papers by Kevin D Cashman in
Google Scholar
PubMed
also in non-skeletal processes ( 1 ), all of which can be compromised by vitamin D deficiency. Around a decade ago, we performed a detailed analysis of persistent knowledge gaps and research needs in vitamin D nutrition and public health, with
Search for other papers by Marc Blondon in
Google Scholar
PubMed
Search for other papers by Emmanuel Biver in
Google Scholar
PubMed
Search for other papers by Olivia Braillard in
Google Scholar
PubMed
Search for other papers by Marc Righini in
Google Scholar
PubMed
Search for other papers by Pierre Fontana in
Google Scholar
PubMed
Search for other papers by Alessandro Casini in
Google Scholar
PubMed
disability-adjusted life-years in both high- and low-income countries. With this massive burden, prevention efforts may yield important positive effects on the population’s health. In observational studies, vitamin D deficiency is associated with increased