During tumour lysis syndrome (TLS) following chemotherapy, massive cell death releases intracellular contents. The metabolic consequences include hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. The mechanism causing hypocalcemia in TLS specifically is:

• A Phosphate released from lysed cells binds calcium, forming insoluble calcium phosphate deposits ✓
• B Uric acid chelates ionised calcium, reducing free calcium levels
• C Hyperkalaemia inhibits parathyroid hormone release, reducing calcium
• D Hyperuricemia inhibits calcitriol synthesis in the kidney

Explanation

In TLS, massive intracellular phosphate is released from nucleic acids and phospholipids of lysed tumour cells. Hyperphosphatemia causes precipitation of calcium phosphate in tissues (particularly kidneys and blood vessels), directly reducing serum ionised calcium. Hypocalcemia in TLS correlates with the degree of hyperphosphatemia. This can cause tetany, seizures, and arrhythmias. Rasburicase (recombinant urate oxidase) prevents hyperuricemia in TLS. Treatment of TLS includes aggressive IV hydration, allopurinol/rasburicase for uric acid, and correction of electrolytes. The Ca × PO4 product > 70 mg2/dL2 risks acute nephrocalcinosis.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.