Endocrine Abstracts

Introduction: Hypocalcaemia is a rare presentation of thyrotoxicosis. We describe a patient with severe life-threatening hypocalcaemia and suggest pathogenic mechanisms.

Case report: A 66-year old lady with long-standing insulin-treated type 2 diabetes presented acutely with generalised weakness and a collapse at home. Prior to admission, she had been treated for an infected neuro-ischaemic plantar ulcer with broad-spectrum antibiotics. She had developed nausea and diarrhoea during the week before admission. She had chronic kidney disease (stage 4) with an eGFR of 25 ml/min. In the past she had undergone partial thyroidectomy for nodular goitre. There was also a history of hypertension and IHD. On examination, T 34.1°C, Trousseau sign +ve, Chvostek +ve, BP 90/60. Investigations: Hb 10.2 g/dl, WCC 11.6×10⁹/l, urea 39.6 mmol/l, creatinine 260 μmol/l, eGFR 15 ml/min, CK 720 rising to 3406 U/l after 2 days, calcium 0.85 mmol/l, corrected calcium 0.99 mmol/l, albumin 33 g/l, phosphate 2.78 mmol/l, alkaline phosphatase 141 U/l, parathyroid hormone 61.3 pmol/l (NR 1.5–7.5), Vitamin D 24 nmol/l, FT₄ 43.8 pmol/l, TSH<0.05 mU/l. She received intravenous saline, intravenous calcium 2 g/d for 72 h, oral Vitamin D and calcium supplements, and carbimazole 20 mg daily. By the time of discharge her renal function had returned to pre-morbid levels and she was eucalcaemic on oral Vitamin D with planned radio–iodine therapy for her toxic remnant goitre.

Discussion: The cause of this lady’s profound hypocalcaemia is likely to be multi-factorial. We postulate that impaired phosphate excretion as a result of her worsening renal function combined with a high phosphate load from rhabdomyolysis secondary to her fall and to thyrotoxic myopathy, led to hyperphosphataemia. This in turn, resulted in hypocalcaemia by precipitating calcium and inhibiting parathyroid hormone-mediated bone resorption. Clinicians need to be aware of hyperthyroidism as a rare but treatable cause of severe hypocalcaemia.