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Tomás P Griffin Centre for Endocrinology, Diabetes and Metabolism, Saolta University Health Care Group (SUHCG), Galway University Hospitals (GUH), Galway, Ireland
Regenerative Medicine Institute at CÚRAM SFI Research Centre, School of Medicine, National University of Ireland Galway (NUIG), Galway, Ireland

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Caroline M Joyce Department of Clinical Biochemistry, Cork University Hospital, Cork, Ireland

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Sumaya Alkanderi Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK

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Liam M Blake Department of Clinical Biochemistry, SUHCG, GUH, Galway, Ireland

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Derek T O’Keeffe Centre for Endocrinology, Diabetes and Metabolism, Saolta University Health Care Group (SUHCG), Galway University Hospitals (GUH), Galway, Ireland

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Delia Bogdanet Centre for Endocrinology, Diabetes and Metabolism, Saolta University Health Care Group (SUHCG), Galway University Hospitals (GUH), Galway, Ireland

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Md Nahidul Islam Regenerative Medicine Institute at CÚRAM SFI Research Centre, School of Medicine, National University of Ireland Galway (NUIG), Galway, Ireland
Department of Clinical Biochemistry, SUHCG, GUH, Galway, Ireland

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Michael C Dennedy Centre for Endocrinology, Diabetes and Metabolism, Saolta University Health Care Group (SUHCG), Galway University Hospitals (GUH), Galway, Ireland
Lambe Institute for Translational Research, School of Medicine, NUIG, Galway, Ireland

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John E Gillan Department of Histopathology, SUHCG, GUH, Galway, Ireland

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John J Morrison Department of Obstetrics and Gynaecology, SUHCG, GUH, Galway, Ireland

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Timothy O’Brien Centre for Endocrinology, Diabetes and Metabolism, Saolta University Health Care Group (SUHCG), Galway University Hospitals (GUH), Galway, Ireland
Regenerative Medicine Institute at CÚRAM SFI Research Centre, School of Medicine, National University of Ireland Galway (NUIG), Galway, Ireland

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John A Sayer Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK
Newcastle upon Tyne NHS Hospitals Foundation Trust, Newcastle upon Tyne, UK
NIHR Newcastle Biomedical Research Centre, Newcastle upon Tyne, UK

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Marcia Bell Centre for Endocrinology, Diabetes and Metabolism, Saolta University Health Care Group (SUHCG), Galway University Hospitals (GUH), Galway, Ireland

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Paula M O’Shea Department of Clinical Biochemistry, SUHCG, GUH, Galway, Ireland

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-of-function mutations in CYP24A1 inhibit the breakdown of 25(OH)D 3 , 25(OH)D 2 , 1,25(OH) 2 D 3 and 1,25(OH) 2 D 2 leading to an accumulation of active vitamin D metabolites and consequent hypercalcaemia ( 8 ), nephrocalcinosis and nephrolithiasis ( 9 ). Therefore

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Laura J Reid Edinburgh Centre for Endocrinology and Diabetes, Royal Infirmary of Edinburgh, Edinburgh, UK

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Bala Muthukrishnan Edinburgh Centre for Endocrinology and Diabetes, Royal Infirmary of Edinburgh, Edinburgh, UK

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Dilip Patel Department of Radiology, Royal Infirmary of Edinburgh, Edinburgh, UK

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Mike S Crane Department of Clinical Biochemistry, Royal Infirmary of Edinburgh, Edinburgh, UK

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Murat Akyol Department of Surgery, Royal Infirmary of Edinburgh, Edinburgh, UK

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Andrew Thomson Department of Pathology, Royal Infirmary of Edinburgh, Edinburgh, UK

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Jonathan R Seckl Edinburgh Centre for Endocrinology and Diabetes, Royal Infirmary of Edinburgh, Edinburgh, UK
Centre for Cardiovascular Science, Queen’s Medical Research Unit, University of Edinburgh, Edinburgh, UK

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Fraser W Gibb Edinburgh Centre for Endocrinology and Diabetes, Royal Infirmary of Edinburgh, Edinburgh, UK

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routine biochemical testing and is, in this milder form, often described as asymptomatic, in distinction from more severe PHPT associated with classical bone, renal and neuropsychiatric manifestations. Many patients with relatively modest hypercalcaemia

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Jennifer Walsh The Mellanby Centre for Bone Research, The Medical School, The University of Sheffield, Sheffield, UK

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Neil Gittoes Centre for Endocrinology, Diabetes and Metabolism, University Hospitals Birmingham & University of Birmingham, Birmingham Health Partners, Birmingham, UK

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Peter Selby Department of Medicine, Manchester Royal Infirmary, Manchester, UK

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the Society for Endocrinology Clinical Committee The Society for Endocrinology, 22 Apex Court, Woodlands, Bradley Stoke, Bristol, UK

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hypercalcaemia <3.0 mmol/L: often asymptomatic and does not usually require urgent correction 3.0–3.5 mmol/L: may be well tolerated if it has risen slowly, but may be symptomatic and prompt treatment is usually indicated >3.5 mmol/L: requires urgent

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Daniel Bell Department of Pharmacy, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK

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Julia Hale Department of Endocrinology, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK

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Cara Go Department of Endocrinology, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK

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Ben G Challis Department of Endocrinology, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK

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Tilak Das Department of Radiology, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK

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Brian Fish Department of Head and Neck Surgery, Cambridge University NHS Foundation Trust, Cambridge, UK

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Ruth T Casey Department of Endocrinology, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK
Department of Medical Genetics, Cambridge University, Cambridge, UK

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) from one or more parathyroid glands resulting in hypercalcaemia. Chronic hypercalcaemia is often asymptomatic but can lead to classical renal and skeletal complications, as well as neurocognitive and cardiovascular effects ( 2 ). The only curative

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A Chinoy Royal Manchester Children’s Hospital, Manchester, UK

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M Skae Royal Manchester Children’s Hospital, Manchester, UK

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A Babiker King Abdullah Specialized Children’s Hospital, Riyadh, Saudi Arabia

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D Kendall Royal Preston Hospital, Preston, UK

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M Z Mughal Royal Manchester Children’s Hospital, Manchester, UK

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R Padidela Royal Manchester Children’s Hospital, Manchester, UK

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daily. During a two-week period of frequent cCa monitoring, his cCa was stable between 2.0 and 2.2 mmol/L. After one month, his investigations revealed hypercalcaemia (cCa 2.74 mmol/L) and hypercalciuria (Ur Ca:Cr ratio 1.40 mmol/mmol). Although this

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Marie Freel Queen Elizabeth University Hospital, Glasgow, UK

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-specialist clinicians and delay the appropriate treatment of this common and potentially life-threatening condition. Acute hypocalcaemia ( 5 ) and hypercalcaemia ( 6 ): disorders of calcium regulation are the second most common electrolyte disorder requiring endocrine

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Jeremy Turner Norfolk and Norwich University Hospital, Colney Lane, Norwich, UK

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Neil Gittoes Centre for Endocrinology, Diabetes and Metabolism, University Hospitals Birmingham & University of Birmingham, Birmingham Health Partners, Birmingham, UK

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Peter Selby Department of Medicine, Manchester Royal Infirmary, Manchester, UK

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the Society for Endocrinology Clinical Committee The Society for Endocrinology, 22 Apex Court, Woodlands, Bradley Stoke, Bristol, UK

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be approximately 0.25–0.5 micrograms per day 1-alpha hydroxylated vitamin D metabolites are potent causes of hypercalcaemia. Frequent blood tests are required in stabilisation phase of treatment alfacalcidol can be administered (at equivalent

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Anna Eremkina Endocrinology Research Center, Russian Federation, Moscow, Russia

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Julia Krupinova Endocrinology Research Center, Russian Federation, Moscow, Russia

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Ekaterina Dobreva Endocrinology Research Center, Russian Federation, Moscow, Russia

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Anna Gorbacheva Endocrinology Research Center, Russian Federation, Moscow, Russia

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Ekaterina Bibik Endocrinology Research Center, Russian Federation, Moscow, Russia

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Margarita Samsonova Faculty of Fundamental Medicine, ederal State Budget Educational Institution of Higher Education M.V. Lomonosov Moscow State University, Moscow, Russia

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Alina Ajnetdinova Endocrinology Research Center, Russian Federation, Moscow, Russia

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Natalya Mokrysheva Endocrinology Research Center, Russian Federation, Moscow, Russia

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hypercalcaemia in PHPT or HC ( 4 , 12 , 14 ). However, therapy with bisphosphonates has some limitations and side effects including fever, which may exacerbate dehydration, bone pain during and post infusion, osteonecrosis of the jaw, uveitis, orbital

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Shu-Meng Hu Department of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

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Yang-Juan Bai Department of Laboratory Medicine/Research Centre of Clinical Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China

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Ya-Mei Li Department of Laboratory Medicine/Research Centre of Clinical Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China

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Ye Tao Department of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

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Xian-Ding Wang Department of Urology/Institute of Urology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

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Tao Lin Department of Urology/Institute of Urology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

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Lan-Lan Wang Department of Laboratory Medicine/Research Centre of Clinical Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China

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Yun-Ying Shi Department of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

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defined as tertiary hyperparathyroidism (THPT), which is characterized by hypercalcaemia and hypophosphatemia ( 2 ). According to previous studies, THPT still existed in 15–50% of the kidney transplant recipients (KTRs) ( 3 , 4 ) and was reported to be

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Sharon A Huish University Hospitals of Coventry and Warwickshire NHS Trust, Coventry, UK
The University of Warwick, Coventry, UK
Royal Devon and Exeter NHS Foundation Trust, Exeter, UK

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Carl Jenkinson The University of Birmingham, Birmingham, UK

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Janet A Dunn The University of Warwick, Coventry, UK

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David J Meredith Royal Devon and Exeter NHS Foundation Trust, Exeter, UK

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Rosemary Bland The University of Warwick, Coventry, UK

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Martin Hewison The University of Birmingham, Birmingham, UK

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following active analogue administration is met with a catabolic response (by increased 24-hydroxylase activity) in a bid to minimise the risk of hypercalcaemia. This may, in turn, cause 1,25(OH) 2 D 3 to be metabolised to its less-active 24-hydroxylated

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