A nurse is providing education to a client who has been prescribed allopurinol to treat gout. Which of the following side effects should the nurse inform the client to expect when starting this medication?

Allopurinol reduces serum uric acid levels by inhibiting xanthine oxidase, the enzyme responsible for converting hypoxanthine and xanthine into uric acid. Although this ultimately lowers the risk of long-term gout attacks, initiating allopurinol therapy can actually trigger acute gout flares in the first weeks to months of treatment. This paradoxical effect occurs because rapid changes in uric acid levels — even decreases — can destabilize existing urate crystal deposits in joints, causing crystals to shed into the synovial space and provoke an inflammatory response. For this reason, clinicians typically co-prescribe a low-dose anti-inflammatory agent such as colchicine or a non-steroidal anti-inflammatory drug during the initiation phase to suppress these flares. Nurses must educate patients that experiencing an acute gout attack early in therapy does not mean the medication is ineffective or harmful and that they should not discontinue allopurinol without consulting their provider. Hypertension is not a recognized side effect of allopurinol. Tachycardia is likewise not associated with this drug. Hyperglycemia is not a pharmacological effect of allopurinol, which has no meaningful impact on glucose metabolism. The most clinically important patient teaching point unique to allopurinol initiation is the expected risk of early acute gout flares.