Within hours of starting induction chemotherapy for T-cell acute lymphoblastic leukaemia, a 19-year-old man develops cardiac arrhythmia. Labs show potassium 6.8 mEq/L, phosphate 8.5 mg/dL, calcium 5.9 mg/dL, and uric acid 18 mg/dL. Which enzyme deficiency explains why allopurinol alone would be inadequate for the hyperuricaemia in this setting?

• A Allopurinol requires xanthine oxidase, which is absent in tumour cells
• B Tumour cell uricase makes xanthine oxidase inhibitors ineffective
• C Allopurinol inhibits new urate formation but does not degrade existing urate ✓
• D Allopurinol is inactivated by elevated phosphate levels

Explanation

Tumour lysis syndrome causes hyperkalaemia, hyperphosphataemia, hypocalcaemia and hyperuricaemia after rapid breakdown of chemosensitive tumour burden. Allopurinol blocks xanthine oxidase and prevents new uric acid formation, but it cannot clear the large urate pool already present, so rasburicase (recombinant urate oxidase) is preferred in established severe cases. Humans naturally lack uricase, which is exactly why urate accumulates.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.