allopurinol

Brand: Zyloprim, Lopurin

Prototype Drug
Drug Class: xanthine oxidase inhibitor
Drug Family: uric acid agent
Subclass: urate-lowering agent
Organ Systems: endocrinemusculoskeletal

Mechanism of Action

Inhibits xanthine oxidase, the enzyme that catalyzes the final two steps of uric acid synthesis (hypoxanthine→xanthine→urate). Allopurinol and its active metabolite oxypurinol both inhibit XO, reducing uric acid production and lowering serum and urinary urate levels.

xanthine oxidase (XO)

Indications

  • gout (prevention of attacks — urate-lowering therapy)
  • uric acid nephrolithiasis
  • tumor lysis syndrome (prophylaxis)
  • hyperuricemia (secondary causes)

Contraindications

  • hypersensitivity to allopurinol
  • do not use in HLA-B*5801 positive patients (high risk for SJS/TEN — common in Han Chinese, Korean, Thai populations)

Adverse Effects

Common

  • rash (especially maculopapular — drug should be discontinued at any rash)
  • nausea
  • diarrhea
  • headache

Serious

  • Stevens-Johnson syndrome / TEN (rare but potentially fatal; strongly associated with HLA-B*5801)
  • DRESS syndrome (drug reaction with eosinophilia and systemic symptoms)
  • allopurinol hypersensitivity syndrome (AHS)

Pharmacokinetics (ADME)

Absorption oral bioavailability ~80%
Distribution low protein binding (~1%); widely distributed
Metabolism metabolized to oxypurinol (active) by xanthine oxidase
Excretion renal (70% as oxypurinol)
Half-life 1–3 hours (allopurinol); 12–30 hours (oxypurinol)
Onset days to weeks
Peak 1.5 hours
Duration continuous
Protein Binding ~1%
Vd 1.6 L/kg

Drug Interactions

Drug / Agent Mechanism Severity
azathioprine or 6-mercaptopurine xanthine oxidase inhibition dramatically increases 6-MP/azathioprine levels; fatal myelosuppression; dose must be reduced 75% major
ampicillin, amoxicillin increased incidence of allopurinol-associated rash moderate
warfarin allopurinol inhibits hepatic metabolism; increases anticoagulant effect major

Nursing Considerations

  1. Discontinue immediately at the first sign of rash — even a macular rash may be the first sign of SJS/DRESS; do not restart after discontinuation for rash.
  2. HLA-B*5801 genetic testing is recommended in patients of Han Chinese, Korean, Thai, or Vietnamese ancestry before initiating allopurinol.
  3. Do not initiate during acute gout attack; begin after attack resolves; initiation can precipitate an acute gout flare — provide colchicine or NSAID prophylaxis for 3–6 months.
  4. Reduce dose in renal impairment as oxypurinol accumulates; dose adjustment based on CrCl.

Clinical Pearls

  • The azathioprine-allopurinol interaction is one of the most dangerous in clinical practice: allopurinol blocks xanthine oxidase, the primary elimination pathway for azathioprine's active metabolites, causing up to 10-fold accumulation and potentially fatal myelosuppression.
  • The HLA-B*5801 allele is found in 6–8% of Han Chinese patients and is associated with an approximately 100-fold increased risk of allopurinol-induced SJS/TEN; pharmacogenomic testing before prescribing is now recommended in relevant populations.

Safety Profile

Pregnancy use-with-caution
Lactation avoid
Renal Adjustment Required
Hepatic Adjustment Not required
TDM Not required