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Lithium Hyperparathyroidism — MRCPsych Paper B MCQ

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HardMood DisordersLithium HyperparathyroidismMRCPsych Paper B

A 45-year-old woman with bipolar I disorder has taken lithium for 12 years. Repeated investigations show an adjusted serum calcium of 2.72 mmol/L with an inappropriately elevated parathyroid hormone concentration. Her eGFR is normal, she is vitamin D replete, and urinary calcium excretion is low-normal. Her serum lithium concentrations have remained within the therapeutic range. Which lithium-related mechanism best explains this biochemical pattern?

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Correct answer: B — Reduced calcium-sensing receptor sensitivity, raising the calcium threshold for PTH suppression

Lithium reduces parathyroid calcium-sensing receptor pathway sensitivity, shifting the calcium–PTH set-point to the right. A higher serum calcium concentration is therefore required to suppress PTH, producing hypercalcaemia with an inappropriately normal or elevated PTH and sometimes relatively low urinary calcium. Chronic exposure may additionally promote parathyroid hyperplasia or reveal adenomatous disease. Increased receptor sensitivity would suppress PTH at lower calcium concentrations. Lithium does not act as a PTH1-receptor agonist. Calcitriol-mediated hypercalcaemia should suppress PTH, while reduced calcitriol synthesis due to renal disease typically causes secondary hyperparathyroidism with low or normal calcium; the normal eGFR and vitamin D status argue against this. UK SmPCs recognise hypercalcaemia and hyperparathyroidism as lithium adverse effects, and NICE recommends calcium monitoring every 6 months.

Reference: Lithium-associated hyperparathyroidism, British Journal of Hospital Medicine, 2020. https://pubmed.ncbi.nlm.nih.gov/33263481/