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Secondary Hyperuricaemia — SCE Rheumatology MCQ

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ModerateCrystal ArthropathySecondary HyperuricaemiaSCE Rheumatology

A 55-year-old man has recurrent crystal-proven gout. His serum urate is 680 micromol/L. He has polycythaemia vera treated with hydroxycarbamide. His eGFR is 85 mL/min/1.73 m² and he takes no diuretic. Which explanation best identifies relevant secondary contributors to his hyperuricaemia?

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Correct answer: B — Increased purine turnover in polycythaemia vera; hydroxycarbamide-associated serum urate elevation

Polycythaemia vera is a myeloproliferative neoplasm with increased haematopoietic cell turnover. Increased nucleic-acid breakdown increases purine metabolism and urate production, providing a recognised cause of secondary hyperuricaemia. Hydroxycarbamide is also relevant: its UK SmPC specifically warns of increased serum uric acid, gout and uric acid nephropathy. The adverse effect should be described as an association rather than attributed categorically to treatment-induced cell lysis. Normal renal function and absence of a diuretic make renal underexcretion less compelling here, although they do not exclude gout generally. Polycythaemia vera is not protective, and hydroxycarbamide does not inhibit xanthine oxidase or reliably lower serum urate.

Reference: NICE, Chronic kidney disease assessment and management (NG203 evidence: increased purine turnover in myeloproliferative disorders), 2021, https://www.nice.org.uk/guidance/ng203/evidence/full-guideline-2014-early-identification-and-management-of-ckd-in-adults-in-primary-and-secondary-care-pdf-9206080238; eMC, Hydroxycarbamide medac 500 mg capsule SmPC, sections 4.4 and 4.8, revised 2025, https://www.medicines.org.uk/emc/product/254/smpc