Lithium and NSAID interaction — MRCPsych Paper A MCQ

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ModeratePsychopharmacologyLithium and NSAID interactionMRCPsych Paper A

A 50-year-old woman has been stable on an unchanged dose of lithium, with a therapeutic plasma lithium concentration and stable renal function. Two weeks after starting regular ibuprofen for osteoarthritis, she develops coarse tremor, vomiting and ataxia. Which mechanism most likely explains this presentation?

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Correct answer: C — Reduced renal clearance of lithium

The correct answer is C. The new coarse tremor, vomiting and ataxia are characteristic of lithium toxicity occurring after regular ibuprofen was introduced. NSAIDs inhibit renal prostaglandin synthesis, which can reduce renal perfusion and decrease lithium elimination, thereby increasing its plasma concentration. Lithium is excreted almost entirely through the kidneys, so reduced renal clearance is clinically important. Reduced intestinal absorption would lower, rather than raise, lithium exposure. Ibuprofen does not produce serotonin toxicity with lithium. CYP3A4 inhibition and hepatic enzyme induction are incorrect because hepatic metabolism is not an important route of lithium elimination. NSAIDs should preferably be avoided in patients taking lithium; if required, lithium concentrations and renal function need additional monitoring.

Reference: Essential Pharma, Lithium Carbonate Essential Pharma 250 mg film-coated tablets, SmPC sections 4.2, 4.5 and 5.2, revised 26 November 2024. https://www.medicines.org.uk/emc/product/10828/smpc