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Adriano N Cury, Verônica T Meira, Osmar Monte, Marília Marone, Nilza M Scalissi, Cristiane Kochi, Luís E P Calliari, and Carlos A Longui

-line treatment in children (11) . Thus, long-term experience with significantly more patients who undergo RAI therapy is needed to determine its safety profile in children and adolescents. There is also concern with regard to its potential carcinogenic effects

Open access

H Vlaardingerbroek, E L T van den Akker, and A C S Hokken-Koelega

children and adults with obesity, an underlying hormonal or genetic cause can be found. In the last decades, the unraveling of genetic and molecular mechanisms of obesity progresses steadily, especially due to whole-exome sequencing by which single

Open access

Shenglong Le, Leiting Xu, Moritz Schumann, Na Wu, Timo Törmäkangas, Markku Alén, Sulin Cheng, and Petri Wiklund

substantially during puberty ( 6 , 7 ). Along these lines, low serum SHBG level has been associated with increased adiposity and insulin resistance in children and adolescents ( 3 , 8 , 9 , 10 , 11 , 12 ); therefore, it has been hypothesized that SHBG

Open access

Maria Lola Evia-Viscarra, Edel Rafael Rodea-Montero, Evelia Apolinar-Jiménez, and Silvia Quintana-Vargas

percentile, at 14.6% among children (5–11 years) and 13.3% among adolescents (12–19 years) (1) . These prevalence rates are similar to those reported in other high-prevalence countries (2) . Pediatric obesity is accompanied by various conditions: orthopedic

Open access

Werner F Blum, Abdullah Alherbish, Afaf Alsagheir, Ahmed El Awwa, Walid Kaplan, Ekaterina Koledova, and Martin O Savage

Introduction The growth hormone (GH)–insulin-like growth factor (IGF)-I axis is the principle endocrine system regulating linear growth in children ( 1 ). Linked to the nutritional status of the individual, GH is a potent stimulator of IGF

Open access

Ekaterina Koledova, George Stoyanov, Leroy Ovbude, and Peter S W Davies

Introduction Recombinant human growth hormone (GH) is approved for use in the treatment of children with various aetiologies, including growth hormone deficiency (GHD), Turner syndrome (TS) and born small for gestational age (SGA) with no

Open access

Athanasios Zervas, George Chrousos, and Sarantis Livadas

fact that the majority of them were overweight or obese would rule out insufficient nutrient intake ( 18 ). Iatrogenic causes could, of course, also be ruled out as well as constitutional delay of growth and puberty granted that children with the latter

Open access

Stine Linding Andersen and Stig Andersen

hypothesis of fetal programming by maternal hypothyroidism is biological plausible from experimental evidence and from the description of cretinism with profound mental and physical deficits in children born to mothers with severe hypothyroidism caused by

Open access

Kristian Almstrup, Hanne Frederiksen, Anna-Maria Andersson, and Anders Juul

epigenetic studies. We have previously published one of the first studies demonstrating changes in DNA methylation patterns with the onset of puberty in healthy children ( 12 ) and identified the promotor of the thyroid hormone receptor interactor 6 gene

Open access

Agnès Linglart, Martin Biosse-Duplan, Karine Briot, Catherine Chaussain, Laure Esterle, Séverine Guillaume-Czitrom, Peter Kamenicky, Jerome Nevoux, Dominique Prié, Anya Rothenbuhler, Philippe Wicart, and Pol Harvengt

Introduction Phosphate wasting ineluctably leads to hypophosphatemia and numerous consequences including mineralization defects. In children, hypophosphatemia is revealed by vitamin D-resistant rickets and results in variable degrees of delayed