a raised blood urate (hyperuricaemia) with no symptoms does not mean a patient will inevitably develop gout
risk factors for the development of gout should be looked for e.g. drug-induced causes, increased cell turnover (e.g. lymphoma), reduced excretion
modification of factors such as diet/therapy should be undertaken if need be (1)
regarding thiazides and asymptomatic hyperuricaemia (2)
occurs in up to 30% of hypertensive patients treated with thiazide diuretics
the presence of hyperuricaemia per se does not require withdrawal of the thiazide or treatment
if gout develops however then it is prudent to stop thiazide treatment and initiate alternative therapy for hypertension
if a patient has a history of gout then treatment with thiazides are best not used - if necessary concurrent treatment with allopurinol can allow continued treatment with a thiazide
raised uric acid is associated with other factors such as hypertension, dehydration, hyperlipidaemia
there is also a theoretical risk of hyperuricaemia with low carbohydrate diets, due to higher protein content
drug therapy for asymptomatic hyperuricaemia is not indicated unless there are concerns regarding uric acid stones e.g. in renal failure
"..hyperuricaemia, in the absence of gout, does not require treatment unless it is accompanied by other, extra-arthritic, complications such as uric acid nephropathy or urolithiasis.." (3)
cohort study (n=14,792) found lowering serum urate level to <6 mg/dL using urate-lowering therapy (ULT- mainly allopurinol & febuxostat) was not associated with a higher risk of severe or end-stage kidney disease progression vs those who did not achieve this level with ULT (4).
Reference:
Pulse (2004), 64 (12), 96.
Prescriber (2001), 12 (18), 49-61.
Drug and Therapeutics Bulletin (2004); 42(5):37-40.
Wang Y, Dalbeth N, Terkeltaub R, et al. Target Serum Urate Achievement and Chronic Kidney Disease Progression in Patients With Gout and Kidney Disease. JAMA Intern Med. Published online November 25, 2024.
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