Endocrine Abstracts (2019) 65 P93 | DOI: 10.1530/endoabs.65.P93

Lithium induced hypercalcaemia - local review of presentation, management and surgical outcomes

Mahshad Mousavi1, Uzma Tahreem1, Praveena Deekonda1 & Jana Bujanova2


1General Internal Medicine Department, Southampton University Hospital, Southampton, UK; 2Endocrinology Department, Southampton University Hospital, Southampton, UK


Lithium induced hypercalcaemia can occur in 4.3–6.3% patients. Lithium interacts with CaSR in parathyroid gland and can ‘unmask’ parathyroid adenoma or cause parathyroid gland hyperplasia. It can cause tubular damage leading to tubular concentration defect or nephrogenic DI. Parathyroid hyperplasia in patients with LAH is much more prevalent than in PHPT.

Methods: The aim of this project was to review presentation and management in patients with diagnosis of ‘Lithium induced hypercalcaemia’ and ‘Lithium associated hyperparathyroidism’ presenting to secondary care during 2008–2018. Data was collected on cCa, PTH, presentation, presence of polyuria/DI, localisation investigations type of management lithium discontinuation/continuation and surgical outcomes.

Methods: The aim of this project was to review presentation and management in patients with diagnosis of ‘Lithium induced hypercalcaemia’ and ‘Lithium associated hyperparathyroidism’ presenting to secondary care during 2008–2018. Data was collected on cCa, PTH, presentation, presence of polyuria/DI, localisation investigations, type of management, lithium discontinuation/continuation and surgical outcomes.

Results: 30 patients were identified and divided into two groups. Group 1 (4/30)-those presenting with severe hypercalcaemia, but normal PTH. All presented acutely with severe AKI, lithium toxicity. Mean cCa – 3.01 mmol/l. All normalised with fluids, lithium omission, pamidronate. Group 2 (26/30) – those presenting with lithium associated hyperparathyroidism (LAH). 11/26 (42%) presented acutely, 9/26 (34%) had polyuria or confirmed DI. Mean cCa – 2.9 mmol/l, mean PTH-19 mU/l. 20/26 of patients with LAH were treated conservatively. 12/20 were able to discontinue lithium. cCa normalised in 7/12. 5/12 had ongoing hypercalcaemia. 2/5 started cinacalcet with cCa normalisation. 8 patients continued lithium and 3/6 fulfil criteria for cinacalcet. 4 out of 6 patients referred for surgery underwent surgery. 2/4 had explorative and 2/4 targeted parathyroidectomy. All had single adenoma.

Discussion: Lithium induced renal concentration defect and DI can contribute to significant hypercalcaemia during acute illness even in those without LAH. Lithium discontinuation resolved hypercalcaemia in 58% of conservatively managed patients with LAH. Cinacalcet seems to be an effective therapy in patients with LAH, but higher doses seem to be required. Contrary to literature, all patients who underwent surgery had single adenoma rather than hyperplasia.

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