Endocrine Abstracts

Background: Somatostatin analogues are widely used in neuroendocrine tumours (NETs). While their metabolic and gastrointestinal (GI) side-effects are recognised, its clinical implications in calcium homeostasis are rarely reported. We describe a case of recalcitrant hypocalcaemia precipitated by somatostatin analogue in a patient with post-surgical hypoparathyroidism,

Case presentation: A 65-year-old woman with post-surgical hypoparathyroidism maintained a stable serum calcium concentration with a total daily dose of 2.25 mg alfacalcidol for years. Somatostatin analogue was commenced following the diagnosis of metastatic gastric NET. She developed loose stool and abdominal bloatedness after commencing on Octreotide LAR. Following the fourth monthly dose of Octreotide LAR 30 mg, she was admitted with a serum adjusted calcium of 1.46 mmol/l. She experienced severe symptomatic hypocalcaemia with perioral and extremities paraesthesia, along with carpopedal spasm. She required intravenous calcium infusion. Oral alfacalcidol dose was increased to 3 mg daily and regular calcium supplementation was started. She had two further admissions within two weeks for recurrent recalcitrant hypocalcaemia, with the lowest serum adjusted calcium of 1.55 mmol/l. Her adjusted calcium concentration eventually maintained at 2.00-2.20mmo/l, with a total daily dose of 4 mg alfacalcidol, along with 3g of calcium tablets. Octreotide LAR was discontinued and her diarrhoea and abdominal bloatedness resolved. Four months after cessation of Octreotide LAR, her adjusted calcium increased to 2.40mmol/l, alfacalcidol was gradually titrated down and she eventually returned to 2.25 mg alfacalcidol daily without calcium supplement.

Learning points: Somatostatin analogue therapy could exacerbates hypocalcaemia in patients previously established on active vitamin D analogue and calcium supplement. Pancreatic exocrine insufficiency could be induced by somatostatin analogue within 3 months, resulting in significant reduction in vitamin D absorption. Reduced gastrin and gastric acid secretion would also reduce intestinal calcium absorption, especially for calcium carbonate. Calcium citrate would be preferred in patients with achlorhydria and proton pump inhibitor use.