Endocrine Abstracts

We report a 61-year-old female with a history of bronchiectasis, primary Sjogren’s syndrome and osteoporosis. She had taken oral glucocorticoids initiated by the rheumatologists for 10 years, which were stopped 2 years ago. She was referred to the Endocrine Clinic with a short history of polyuria and polydipsia. Biochemistry confirmed new hypercalcaemia and an acute kidney injury: corrected calcium 3.14 mmol/l, phosphate 1.13 mmol/l and 25-hydroxyvitamin D 66.4 nmol/l. At the time of referral, she was taking Adcal D3 1 tablet twice daily. After being encouraged to consume 2.5 l of fluid daily, her corrected calcium improved 2.66 mmol/l, phosphate 0.79 mmol/l, creatinine 128 umol/l and PTH low-end of normal reference range 2.2 pmol/l. Simultaneously, she was being seen by the respiratory physicians due to increased breathlessness, cough and fatigue. CT chest demonstrated a new increase in mediastinal lymph nodes and the development of parenchymal changes suggestive of sarcoidosis. Serum ACE was raised at 79 IU/L. She is currently awaiting an endobronchial ultrasound to facilitate a histological diagnosis of pulmonary sarcoidosis. Non-parathyroid hormone-mediated hypercalcaemia is a prevalent complication of sarcoidosis in 10–20% of patients, meaning it should be considered in all patients presenting with hypercalcaemia with no apparent cause. It is due to uncontrolled synthesis of 1,25-dihydroxyvitamin D3 by macrophages and leads to increased intestinal absorption and increased bone resorption of calcium. Treatment of hypercalcaemia in sarcoidosis depends on the degree of hypercalcaemia and its persistence. General advice includes avoiding excessive sunlight, avoiding foods which are rich in vitamin D and consuming 2.5 l of fluid daily. For those patients who experience calcium levels >3 mmol/l or severe symptoms, oral glucocorticoids can be used, which inhibits enzymatic conversion of cholecalciferol to calcitriol via 1-alpha hydroxylase in macrophages. Furthermore, patients with sarcoidosis who receive vitamin D supplements are at increased risk of developing hypercalcaemia and therefore renal impairment.