Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2012) 28 P10

SFEBES2012 Poster Presentations Bone (22 abstracts)

The use of teriparatide to treat hypoparathyroidism following thyroidectomy; a case report

Akila De Silva 1 , Sarah-Jane De Silva 2 & Karim Meeran 1

1Endocrinology, Imperial Healthcare NHS Trust, London, United Kingdom; 2School of Medicine, University of Leicester, Leicester, United Kingdom.

A 27 year old lady with Graves’ thyrotoxicosis (fT4 50.3 pmol/L, fT3 25.0 pmol/L, TSH<0.05 mU/L) failed to respond adequately to carbimazole (40 mg BD) or propylthiouracil (250 mg QDS). Three months later, following 10 days of potassium iodide to render her biochemically euthyroid, she underwent a total thyroidectomy. Pre-operative bone profile revealed Ca(c) 2.34 mmol/L (NR 2.15–2.60 mmol/L), phosphate 1.36 mmol/L (NR 0.8–1.4 mmol/L), PTH 3.4 pmol/L (NR 1.1–6.8 pmol/L), 25-OH Vit D 27 nmol/L (NR 70–150 nmol/L). Following a significant early post-operative bleed, she became severely hypocalcaemic (Ca(c) 1.73 mmol/L with tetany and widespread T wave inversion on ECG), requiring acute treatment with intravenous calcium. She was then commenced on regular oral calcium and 1α(OH)Vit D3. Three weeks later, her PTH level was 1.0 pmol/L despite hypocalcaemia, indicating post-operative hypoparathyroidism. Over the subsequent 9 months, she required high doses of calcium (up to 8 g daily) and 1α(OH)Vit D3 (2.5 mcg daily) but remained hypocalcaemic (Ca(c) 1.81–2.12 mmol/L) and became hyperphosphataemic (up to 1.81 mmol/L). Her parathyroid function failed to recover (PTH 1.1 mmol/L). Treatment with teriparatide (recombinant human PTH1-34) was commenced (20 mcg/day by subcutaneous injection). Within 2 weeks, her Ca(c) improved to 2.28 mmol/L and phosphate normalised to 1.31 mmol/L. Over the past year, she has been able to reduce her calcium treatment to 2 g daily and reduce 1α(OH)Vit D3 to 0.5 mcg daily, without compromising her serum calcium. She continues on teriparatide. Discussion Conventional treatment for hypoparathyroidism uses calcium replacement with 1α(OH)Vit D3, but risks hyperphosphataemia. Furthermore, increased renal tubular calcium loss (due to the lack of PTH) risks nephrolithiasis when striving to maintain serum calcium. As illustrated by this case, recombinant PTH1-34 represents an effective and more physiological treatment for hypoparathyroidism.

Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.

Article tools

My recent searches

No recent searches.