Which electrolyte imbalances are associated with Tumor Lysis Syndrome (TLS)?

The association of hyperuricemia, hyperphosphatemia, hypocalcemia, and hyperkalemia with Tumor Lysis Syndrome (TLS) is well established in clinical practice. TLS occurs when rapid cell breakdown leads to the release of intracellular contents into the bloodstream, particularly following the treatment of certain cancers, such as leukemias and lymphomas.

Hyperuricemia arises due to the breakdown of nucleic acids into uric acid. As tumor cells lyse, they release purines, which are then metabolized to uric acid. This accumulation can lead to further complications, including acute kidney injury due to the precipitation of uric acid in the renal tubules.

Hyperphosphatemia results from the release of phosphate from lysed tumor cells, leading to elevated serum phosphate levels. This imbalance can subsequently lead to hypocalcemia because high phosphate levels can cause calcium to precipitate, decreasing serum calcium levels.

Hypocalcemia, as mentioned, is associated with this cascade of events, particularly due to the binding of calcium to the elevated phosphate in the bloodstream.

Hyperkalemia also occurs because potassium is predominantly an intracellular ion, and its release into the bloodstream follows cell lysis. Elevated potassium levels can have significant cardiac implications, making