Regenerative Medicine Institute at CÚRAM SFI Research Centre, School of Medicine, National University of Ireland Galway (NUIG), Galway, Ireland
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Department of Clinical Biochemistry, SUHCG, GUH, Galway, Ireland
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Lambe Institute for Translational Research, School of Medicine, NUIG, Galway, Ireland
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Regenerative Medicine Institute at CÚRAM SFI Research Centre, School of Medicine, National University of Ireland Galway (NUIG), Galway, Ireland
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Newcastle upon Tyne NHS Hospitals Foundation Trust, Newcastle upon Tyne, UK
NIHR Newcastle Biomedical Research Centre, Newcastle upon Tyne, UK
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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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Centre for Cardiovascular Science, Queen’s Medical Research Unit, University 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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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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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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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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-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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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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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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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
The University of Warwick, Coventry, UK
Royal Devon and Exeter NHS Foundation Trust, Exeter, 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