Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2016) 41 EP188 | DOI: 10.1530/endoabs.41.EP188

ECE2016 Eposter Presentations Calcium and Vitamin D metabolism (61 abstracts)

Use of recombinant parathyroid hormone with significant improvement of debilitating hypocalcaemia and hypomagnesaemia

Eleftheria Panteliou 1 , Ajith James 2 , Anna Hawkins 1 , Stuart Jones 3 , Pandina Kwong 3 , Dinesh Gupta 4 , Yousaf Razzak 4 , Edel Casey 1 & Khash Nikookam 1


1Department of Endocrinology and Diabetes, King George’s Hospital, Barking Havering and Redbridge University Hospitals NHS Trust, Greater London, UK; 2Department of Nephrology, King George’s Hospital, Barking Havering and Redbridge University Hospitals NHS Trust, Greater London, UK; 3Department of Clinical Biochemistry, King George’s Hospital, Barking Havering and Redbridge University Hospitals NHS Trust, Greater London, UK; 4Department of Pharmacology, King George’s Hospital, Barking Havering and Redbridge University Hospitals NHS Trust, Greater London, UK.


Primary hypoparathyroidism is a rare condition. Contrary to other endocrine deficiencies treated with hormone replacement, recombinant parathyroid hormone (PTH) is not currently licensed for its treatment in Europe. Emerging evidence of efficacy and safety of recombinant PTH in treating resistant hypoparathyroidism will hopefully provide a new tool in managing this challenging condition.

This is the case of a 45 year-old woman presenting with gradually worsening paraesthesia and limb weakness. Initial investigations revealed low serum calcium of 1.58 (2.2–2.6 mmol/l), magnesium of 0.4 (0.7–1.05 mmol/l), potassium of 3 (3.5–5 mmol/l) and normal phosphate 1.21 (0.8–1.5 mmol/l), bicarbonate 27 (22–28 mmol/l), liver and renal function. Clinical examination only revealed a positive Chovstek’s sign. Further investigations showed low PTH at 0.6 (1.3–6.8 pmol/l), vitamin D at 14 (25–200 nmol/l) with elevated 24-h urine calcium excretion at 13.1 (2.5–7.5 mmol/24 h), urine magnesium excretion of 3.9 (2.4–6.5 mmol/24 h), normal thyroid function, haematinics and a basal cortisol of 375 nmol/l. She had osteopenia on dual energy X-ray absorptiometry and normal whole body computed-tomography, gastroscopy and coeliac screen. She was initially treated with intravenous calcium and magnesium, subsequently switched to oral supplements. She had recurrent admissions over 10 months with low calcium and magnesium. Recombinant PTH(1–34) (teriparatide) led to normalisation of calcium and no further admissions.

In this case hypoparathyroidism was attributed to severe renal magnesium wasting, related to an acquired mutation or a hereditary disorder clinically emerging in adulthood. In the United Kingdom, the N-terminal active fragment (1–34) of recombinant human PTH (teriparatide) is currently only licensed for the treatment of osteoporosis. In 2015, the full-length PTH (1–84) was approved for the treatment of hypoparathyroidism in the United States. The ‘Efficacy and safety of recombinant human PTH (1–84) in hypoparathyroidism’ (REPLACE) study showed good tolerance and therapeutic effect of PTH (1–84) in hypoparathyroidism. Further studies are required to evaluate the role and efficacy of PTH in the management of patients with resistant and/or persistent hypocalcaemia and hypomagnesaemia.

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