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Endocrine Unit 2, Department of Clinical and Experimental Medicine, Laboratory of Chemistry and Endocrinology, University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy
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of SHPT, should be first to be excluded in the diagnostic workout of NPHPT. Other causes of SHPT, such renal failure, hypercalciuria, gastrointestinal diseases associated with malabsorption and other metabolic bone diseases that could affect PTH
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Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
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Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts, USA
Harvard Medical School, Boston, Massachusetts, USA
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). Glucocorticoids also have a negative impact on the Wnt/β-catenin pathway leading to an imbalance in bone formation and bone resorption, and thereby contributing to glucocorticoid-induced osteoporosis ( 1 , 3 , 10 , 11 , 12 , 13 ). In mice, glucocorticoids
Department of Endocrinology, Jiading Branch of Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
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Introduction Postmenopausal osteoporosis is related to aging and has serious health effects. Bone mineral density (BMD) is the most common diagnostic indicator of osteoporosis, and 60–80% of BMD variations are determined by genetic factors ( 1
F.I.R.M.O. Italian Foundation for the Research on Bone Diseases, Florence, Italy
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affected by tumor. In recent decades, some studies have shown that the premature loss of bone mass and osteoporosis represents early complications in MEN1 patients with PHPT ( 4 , 5 , 6 , 7 ), as a consequence of prolonged periods of increased levels
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Department of Paediatric Endocrinology, Royal Manchester Children’s Hospital, Central Manchester Foundation Hospitals NHS Trust, Manchester, UK
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Department of Paediatric Endocrinology, Royal Manchester Children’s Hospital, Central Manchester Foundation Hospitals NHS Trust, Manchester, UK
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Background
Higher 25(OH)D3 levels are associated with lower HbA1c, but there are limited UK interventional trials assessing the effect of cholecalciferol on HbA1c.
Aims
(1) To assess the baseline 25(OH)D3 status in a Manchester cohort of children with type 1 diabetes (T1D). (2) To determine the effect of cholecalciferol administration on HbA1c.
Methods
Children with T1D attending routine clinic appointments over three months in late winter/early spring had blood samples taken with consent. Participants with a 25(OH)D3 level <50 nmol/L were treated with a one-off cholecalciferol dose of 100,000 (2–10 years) or 160,000 (>10 years) units. HbA1c levels before and after treatment were recorded.
Results
Vitamin D levels were obtained from 51 children. 35 were Caucasian, 11 South Asian and 5 from other ethnic groups. 42 were vitamin D deficient, but 2 were excluded from the analysis. All South Asian children were vitamin D deficient, with mean 25(OH)D3 of 28 nmol/L. In Caucasians, there was a negative relationship between baseline 25(OH)D3 level and HbA1c (r = −0.484, P < 0.01). In treated participants, there was no significant difference in mean HbA1c at 3 months (t = 1.010, P = 0.328) or at 1 year (t = −1.173, P = 0.248) before and after treatment. One-way ANCOVA, controlling for age, gender, ethnicity, BMI and diabetes duration showed no difference in Δ HbA1c level.
Conclusion
We report important findings at baseline, but in children treated with a stat dose of cholecalciferol, there was no effect on HbA1c. Further studies with larger sample sizes and using maintenance therapy are required.
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for the cardiovascular system and in the skeleton ( 1 , 2 ). In this review we will discuss the current indication of TSH suppressive therapy in patients with DTC, the potential adverse effects on bones and their prevention. Thyroid hormone and
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. In MEN1, lesions of parathyroid glands have the highest penetrance; they manifest with primary hyperparathyroidism (PHPT). Conversely, PHPT is a powerful etiological factor that can lead to bone disorders including the significant decrease in bone
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people are reported to be obese ( 9 ). It is well established that overweight patients have a higher risk of bone fractures compared to healthy individuals ( 10 , 11 ). Previous research has highlighted the significant role of the Wnt pathway in bone
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disease ( 4 ). Most frequently affected organs include the bones, lungs, pituitary gland and skin while the lymph nodes, liver, spleen, intestine and central nervous system are less frequently involved. Clinical manifestations are various according to the
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(2) . Historically, bone metastases from NETs were considered to be extremely rare (3, 4) . As few as 50 case reports were identified in a recently published literature review on skeletal metastases from carcinoid tumors (5) . In a series of 145