Endocrine Abstracts

Parathyroid-adenoma is a rare cause of primary-hyperparathyroidism in children. We report a case where in a 15-year-old girl presented with acute necrotising pancreatitis as its sole manifestation.

This high-school girl presented with 2-month history of nausea, vomiting, upper abdominal pain, and weight-loss. An episode of severe acute abdomen led to her hospitalisation. At admission, she was tachycardic, dehydrated and had tenderness in peri-umbilical area.

Preliminary investigations: normal FBC, ESR, renal and liver function tests, urinalysis, lipid profile (including triglycerides), but serum corrected calcium was 3.95 mmol/l (2.1–2.65). Ultrasonography and then CT scan confirmed acute necrotising pancreatitis. Her serum calcium levels were 2.65 and 2.87 mmol/l on two separate occasions in the last 2 months. Hypercalcaemia was hence felt to be the underlying cause for acute pancreatitis. Subsequent investigations: parathyroid-hormone (PTH) 261 pg/ml (10–65), vitamin D 18.5 ng/ml (30–80), phosphorus 2.3 mg/dl (2.3–4.7), TSH 1.3 μIU/ml (0.7–5.5), prolactin 22 ng/ml (3–24); neck ultrasound showed parathyroid adenoma.

Pancreatitis was managed conservatively. Despite aggressive i.v.-rehydration, calcium level remained high; she was started on salmon calcitonin s.c. injections, initially at 4 mg/kg body-weight 6th-hourly; then increased to 8 mg/kg dose. After 2 days, she also needed i.v. pamidronate 60 mg to reduce hypercalcaemia. When calcium was 2.95 mmol/l, she underwent parathyroid-adenomectomy. Consequently, PTH reduced to 7.8 pg/ml. Histopathology showed well-encapsulated parathyroid-adenoma. Post-operatively, despite pre-operative i.m. injection of vitamin D 600 000 units, she developed hungry-bone syndrome with symptomatic hypocalcaemia 1.87 mmol/l, and hypomagnesaemia 0.8 mg/dl (1.6–2.6); she received i.v. calcium and magnesium for 5 days, and then oral supplements plus 1-α-calcidol, with good response.

Literature mentions association of hypercalcaemia with pancreatitis but is uncommon especially in adolescents. Underlying pathophysiology in hypercalcaemia-induced-pancreatitis is unknown. Suggested mechanisms from animal-studies include hypercalcemia-provoked-pancreatic injury via secretory block, accumulation of secretory proteins, and possibly activation of proteases. Since serum calcium levels can acutely increase in parathyroid-adenoma patients, calcium levels should be closely monitored in such situations.