Hypercalcaemia in patient with primary hyperparathyroidism and acromegaly

Abstract

Introduction: Hypercalcaemia in acromegaly can be a result of several pathophysiological mechanisms. Multiple endocrine neoplasia type 1 (MEN1) syndrome, mitogenic effect of hyperactivated GH–parathyroid gland axis, i.e. primary hyperparathyroidism and hypercalcaemia mediated by elevated 1,25-dihydroxyvitamin D should be considered.

Case report: We describe a case of acromegaly associated with primary hyperparathyroidism. A 52-year-old female was diagnosed with acromegaly due to GH secreting pituitary microadenoma. Evaluation at diagnosis showed normal levels of hormones other than GH and IGF1, and presence of hypertension and multinodular goiter (volume 80 mm3). Because the patient denied surgery, treatment with cabergoline was administrated and a biochemical control was accomplished. Within 1 year of the diagnosis laboratory data showed hypercalcaemia (serum calcium 1.51 mmol/l (1.10–1.40)) in the setting of elevated parathormone (PTH) levels (158 pg/ml (15–65)) and low levels of vitamin D (5.6 nmol/l (>25)). Bone densitometry detected osteoporosis limited to the right radius (T score value −4.0 S.D.). Analysis of 24-h urine showed normal calcium and phosphate excretion. This findings were consistent with diagnosis of primary hyperparathyroidism. Imaging and radioisotope studies identified enlarged thyroid gland, predominantly the left lobe with consequent tracheal compression, and higher radioisotope uptake in the lower pole of the left thyroid lobe. Surgical excision of left lower parathyroid gland and subtotal thyroidectomy was done. Histopathological examination confirmed hyperplasia of parathyroid and thyroid gland. After surgery, serum calcium normalised, PTH levels significantly reduced to 73.2 pg/ml. Vitamin D remained low (17.8 nmol/l) and TSH levels elevated to 27 mU/l (0.4–4) for which vitamin D and levothyroxine substitution was started. Conclusion: The approach to hypercalcaemia in the course of acromegaly implies evaluation for several potential pathophysiological mechanisms, which in turn dictates the treatment strategy – parathyroidectomy vs biochemical control of acromegaly.