ECE2016 Eposter Presentations Calcium and Vitamin D metabolism (61 abstracts)
Severe hungry bone syndrome after incidental parathyroidectomy in hypophosphatemic rickets
Luís Cardoso 1 , Isabel Paiva 1 , Dírcea Rodrigues 1, , Daniela Guelho 1, , Nuno Vicente 1 , Margarida Balsa 3 , Diana Martins 1 , Diana Oliveira 1 , Adriana Lages 1 , Mara Ventura 1 & Francisco Carrilho 1
1Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal; 2Faculty of Medicine, University of Coimbra, Coimbra, Portugal; 3Department of Endocrinology, Centro Hospitalar do Baixo Vouga, Aveiro, Portugal.
Introduction: Hypophostemic rickets is characterized by phosphate renal loss associated with a primary defect of osteoblasts and metabolism of vitamin D. Marked bone turnover caused by high levels of parathyroid hormone attribute to these patients an elevated risk for hungry bone syndrome after parathyroidectomy.
Case report: A 34-years old woman with a past history of Lynch syndrome and hypophostemic rickets associated with hyperparathyroidism and brown tumours. She had multinodular goitre and 10 years ago she underwent left hemithyroidectomy, isthmectomy, and subtotal right hemithyroidectomy, without immediate complications, but hypothyroidism subsequently developed. Her current daily medications are: 88 mcg of levothyroxine, 120 mg of cinacalcet, 4500 mg of phosphorus and 1 mcg of calcitriol. Goitre relapsed and nodule cytological assessment revealed a follicular tumour. Again, she underwent thyroid surgery and two parathyroids were incidentally removed (one of them was histological suggestive of parathyroid adenoma). She developed hypoparathyroidism and severe hypocalcaemia after surgery. The lowest total calcemia identified was 5.5 mg/dl (8.8–10.6), magnesemia 1.1 mg/dl (1.9–2.5), and phosphatemia 3.5 mg/dl (2.5–4.5). Urinary calcium and phosphate levels, under intravenous calcium infusion, were 108 mg/24 h (<250) and 1032 mg/24 h (400–1300), respectively. Even though she was being treated with intravenous and oral calcium, magnesium and calcitriol, hypocalcaemia remained refractory. Additionally, she developed frequent phlebitis and 20–60 mg of teriparatide was added. Normocalcaemia was achieved after 4 months of intravenous calcium gluconate (total elemental calcium of 150 g), oral calcium carbonate (total elemental calcium of 1.5 kg).
Conclusion: Hungry bone syndrome, associated with hypophosphatemic rickets, is a rare complication of parathyroidectomy, particularly in the setting of tertiary hyperparathyroidism. The treatment of hungry bone syndrome should be directed to the reestablishment of calcium deficit and restauration of bone turnover, which may take several months. The absence of guidelines and the different pharmacokinetics of calcium formulations pose a particular challenge in the management of these patients.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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