Department of Pediatric Endocrinology and Metabolic Diseases, Mofid Children Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Search for other papers by Farzaneh Rohani in
Google Scholar
PubMed
Search for other papers by Mohammad Reza Alai in
Google Scholar
PubMed
Search for other papers by Sedighe Moradi in
Google Scholar
PubMed
Search for other papers by Davoud Amirkashani in
Google Scholar
PubMed
have a slow pattern of growth during childhood and adolescence. The patients are identified with short stature, delay bone age and puberty. Their bone age lags behind their chronological age, which is providing an indication of remaining the growth
Search for other papers by Kaiyu Pan in
Google Scholar
PubMed
Search for other papers by Chengyue Zhang in
Google Scholar
PubMed
Search for other papers by Xiaocong Yao in
Google Scholar
PubMed
Search for other papers by Zhongxin Zhu in
Google Scholar
PubMed
Introduction Calcium (Ca) is the primary nutrient of interest in bone health. It is essential to ensure adequate Ca intake to support the accelerated growth spurt during childhood and adolescence when bone accumulates and grows at a rapid rate
Department of Nutrition, Institute of Life Sciences, Federal University of Juiz de Fora, Governador Valadares, Minas Gerais, Brazil
Department of Nutrition, Faculty of Health and Medical Sciences, University of Surrey, University of Surrey, Guildford, UK
Search for other papers by Marcela Moraes Mendes in
Google Scholar
PubMed
Search for other papers by Patricia Borges Botelho in
Google Scholar
PubMed
Search for other papers by Helena Ribeiro in
Google Scholar
PubMed
Introduction Vitamin D is vital to bone health, and prolonged severe deficiency can lead to rickets in children and osteomalacia/osteoporosis in adults ( 1 , 2 , 3 ). Vitamin D is an exceptional nutrient in that its primary source is the
Search for other papers by Shu-Meng Hu in
Google Scholar
PubMed
Search for other papers by Yang-Juan Bai in
Google Scholar
PubMed
Search for other papers by Ya-Mei Li in
Google Scholar
PubMed
Search for other papers by Ye Tao in
Google Scholar
PubMed
Search for other papers by Xian-Ding Wang in
Google Scholar
PubMed
Search for other papers by Tao Lin in
Google Scholar
PubMed
Search for other papers by Lan-Lan Wang in
Google Scholar
PubMed
Search for other papers by Yun-Ying Shi in
Google Scholar
PubMed
closely associated with bone fracture, graft loss, cardiovascular events and all-cause death after KT ( 2 , 3 , 4 ). Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone produced by osteocytes and osteoblasts. By binding to FGF receptor 1
Search for other papers by M Ahmid in
Google Scholar
PubMed
Search for other papers by C G Perry in
Google Scholar
PubMed
Search for other papers by S F Ahmed in
Google Scholar
PubMed
Search for other papers by M G Shaikh in
Google Scholar
PubMed
research over the past two decades that has demonstrated deficits in bone health and cardiac function, together with impaired quality of life in adults with CO-GHD after completion of childhood treatment ( 3 , 4 , 5 , 6 ), has questioned this practice
Search for other papers by Zhiyan Yu in
Google Scholar
PubMed
Search for other papers by Yueyue Wu in
Google Scholar
PubMed
Search for other papers by Rui Zhang in
Google Scholar
PubMed
Search for other papers by Yue Li in
Google Scholar
PubMed
Search for other papers by Shufei Zang in
Google Scholar
PubMed
Search for other papers by Jun Liu in
Google Scholar
PubMed
Introduction Osteoporosis is a systemic bone disease characterized by decrease in bone mass and damage to the microstructure of bone tissue, resulting in increased bone fragility and susceptibility to fracture ( 1 ). Pain due to osteoporosis
Search for other papers by Nobuo Matsuura in
Google Scholar
PubMed
Search for other papers by Tadashi Kaname in
Google Scholar
PubMed
Search for other papers by Norio Niikawa in
Google Scholar
PubMed
Search for other papers by Yoshihide Ooyama in
Google Scholar
PubMed
Search for other papers by Osamu Shinohara in
Google Scholar
PubMed
Search for other papers by Yukifumi Yokota in
Google Scholar
PubMed
Search for other papers by Shigeyuki Ohtsu in
Google Scholar
PubMed
Search for other papers by Noriyuki Takubo in
Google Scholar
PubMed
Search for other papers by Kazuteru Kitsuda in
Google Scholar
PubMed
Search for other papers by Keiko Shibayama in
Google Scholar
PubMed
Search for other papers by Fumio Takada in
Google Scholar
PubMed
Search for other papers by Akemi Koike in
Google Scholar
PubMed
Search for other papers by Hitomi Sano in
Google Scholar
PubMed
Search for other papers by Yoshiya Ito in
Google Scholar
PubMed
Search for other papers by Kenji Ishikura in
Google Scholar
PubMed
metacarpals are common in patients with ACRO, Turner syndrome, PHP and other congenital skeletal abnormalities ( 11 ). In the pediatric endocrine clinic, we usually take hand X-rays for the evaluation of bone age in patients with congenital hypothyroidism
Search for other papers by Enrique Soto-Pedre in
Google Scholar
PubMed
Department of Endocrinology and Diabetes, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK
Search for other papers by Paul J Newey in
Google Scholar
PubMed
Search for other papers by John S Bevan in
Google Scholar
PubMed
Department of Endocrinology and Diabetes, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK
Search for other papers by Graham P Leese in
Google Scholar
PubMed
relationship between prolactin and all-cause cancer or breast cancer have also given inconsistent results ( 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 ). Similarly, there are no consistent correlations reported between prolactin levels and bone loss or
Search for other papers by Imane Benabbad in
Google Scholar
PubMed
Search for other papers by Myriam Rosilio in
Google Scholar
PubMed
Search for other papers by Maité Tauber in
Google Scholar
PubMed
Search for other papers by Emmanuel Paris in
Google Scholar
PubMed
Search for other papers by Anne Paulsen in
Google Scholar
PubMed
Search for other papers by Lovisa Berggren in
Google Scholar
PubMed
Search for other papers by Hiren Patel in
Google Scholar
PubMed
Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Universitaire Robert-Debré, Department of Pediatric Endocrinology and Diabetology, and Centre de Référence des Maladies Endocriniennes Rares de la Croissance, Paris, France
Search for other papers by Jean-Claude Carel in
Google Scholar
PubMed
Search for other papers by the Phoenix Study Group in
Google Scholar
PubMed
were at puberty onset. It was hypothesised that the addition of leuprorelin for 2–3 years would delay progression of puberty and bone maturation, allowing prolonged efficacy of GH and increased adult or near-adult height (NAH). After commencement of the
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
Objective
Vitamin D deficiency is associated with increased risks of arterial and venous cardiovascular events. Hypothetically, supplementation with vitamin D may lead to a less prothrombotic phenotype, as measured by global coagulation assays and fibrin clot structure.
Methods
In this prospective cohort study, we enrolled adult outpatients attending the Primary Care Division of the Geneva University Hospitals with a severe vitamin D deficiency (25-hydroxyvitamin-D3 (25-OHD) <25 nmol/L), excluding obese patients or with a recent acute medical event. We evaluated changes in coagulation times, thrombin generation assay, clot formation and clot lysis time, 25-OHD and parathormone before and 1–3 months after cholecalciferol oral supplementation with one-time 300,000 IU then 800 IU daily. Paired t-tests with a two-sided alpha of 0.05 compared absolute mean differences.
Results
The 48 participants had a mean age of 43.8 ± 13.8 years. After supplementation, 25-OHD levels increased from 17.9 ± 4.6 nmol/L to 62.5 ± 20.7 nmol/L 6.4 ± 3.0 weeks after inclusion. Endogenous thrombin potential and thrombin generation peak values both decreased significantly (−95.4 nM × min (95%CI −127.9 to −62.8), P < 0.001; −15.1 nM (−23.3 to −6.8), P < 0.001). The maximum absorbance by turbidimetry decreased significantly (P = 0.001) after supplementation. There was no change in clot lysis time, coagulation times or plasminogen activator inhibitor-1 and homocysteine levels.
Conclusions
In severe vitamin D deficiency, a high-dose cholecalciferol supplementation was associated with a reduction in thrombin generation and an average decreased number of fibrin protofibrils per fibers and fibrin fiber size measured by turbidimetry. This suggests that severe vitamin D deficiency may be associated with a potentially reversible prothrombotic profile.
