Tumour lysis syndrome (TLS) is an oncologic emergency caused by rapid release of intracellular contents when large numbers of malignant cells die, producing hyperuricemia, hyperkalemia, hyperphosphatemia, and acute kidney injury. It is most common in bulky, rapidly proliferating hematologic malignancies, and in-hospital mortality is markedly higher when TLS occurs.
Prevention and treatment rest on aggressive hydration, electrolyte management, and urate control. Rasburicase, a recombinant urate oxidase that enzymatically degrades existing uric acid, is used for high-risk patients and established hyperuricemia; allopurinol helps prevent new uric acid formation but does not clear the existing burden. A key contemporary point is that TLS is increasingly triggered by highly effective targeted agents — notably the BCL-2 inhibitor venetoclax (which requires a careful dose ramp-up and TLS prophylaxis) and various tyrosine kinase inhibitors — and by immunotherapy combinations, so vigilance and pre-emptive prophylaxis are essential whenever a rapid, deep response is expected.
Further reading: tumour lysis syndrome primer (Howard et al., Nature Reviews Disease Primers 2024); rasburicase and TLS management reviews.