Endocrine Abstracts

Introduction

Lithium remains a first-line treatment for several mental disorders.Hypercalcaemia has been associated with long-term lithium treatment, yet it is often unrecognized. The manifestations of hypercalcaemia can develop insidiously and mimic psychiatric disturbances.

Cases

Case Report 1 – A 53-year-old Caucasian gentlemen referred by his GP following routine bloods with an adjusted calcium of 3.46 mmol/l (2.2–2.6), PTH of 8.7 pmol/l (1.6–6.9), and a lithium level of 0.56 mmol/l (0.4–1). The patient was asymptomatic and clinically well. With a background of depression and right-sided hydrocele, this patient was on the following medications: lithium, atorvastatin, folic acid, mirtazapine, olanzapine and venlafaxine. An ultrasound of the parathyroid showed a small hypoechoic ovoid lesion adjacent to the inferior pole of the right lobe of the thyroid measuring 7 mm × 4 mm, suspicious for a small parathyroid adenoma. He was treated with IV fluids and given IV pamidronate prior to discharge. Additionally, his lithium dose was reduced and sodium valproate was initiated. Case Report 2 – A 73-year old Caucasian gentlemen was admitted with confusion and acute kidney injury on a background of Chronic Kidney Disease. Prior to admission, he described being generally unwell for the last two months, with poor oral intake and appeared significantly unkempt. His past medical history was notable for primary hyperparathyroidism secondary to a parathyroid adenoma, type 2 diabetes mellitus with retinopathy, severe depression with previous psychotic symptoms and hypertension. He was taking lithium, sitagliptin, venlafaxine, aspirin, and gliclazide. Blood tests results revealed an elevated calcium at 3.25 mmol/l (2.20–2.60), a raised PTH of 71.1 pmol/l (1.3–6.8) and a lithium level of 1.16 mmol/l (0.4–1). This patient’s lithium was stopped, and he was treated with IV fluids and pamidronate. His AKI resolved and his discharge calcium was 3.11 mmol/l.

Discussion

While primary hyperparathyroidism usually arises from parathyroid adenomas, in patients on lithium, drug-induced hypercalcaemia should be considered and ruled out. Lithium is thought to cause hyperparathyroidism by altering the set points of extracellular calcium-sensing receptor (CaSR). This promotes excess parathyroid release. Thus, consistently elevated PTH levels may lead to hypercalcaemia.

Conclusion

Lithium-induced hypercalcaemia is likely more common than reported. Many patients are asymptomatic, with diagnosis only becoming apparent on routine blood tests. These cases and previously reported cases highlight that either reduction of lithium dosing or cessation of lithium can be effective management strategies. Regular measurement of serum calcium, PTH, as well as thyroid function test upon commencing lithium treatment is advisable.