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  • Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, often accompanied by azotemia and oliguric acute renal failure.
  • Caused by the rapid release of the intracellular contents of tumor cells into the systemic circulation.
  • Most commonly seen following treatment of hematologic malignancies of high cellular burden and chemosensitivity, such as lymphomas and leukemias.

First described in 1929, tumor lysis syndrome (TLS) defines a well-established constellation of potentially fatal metabolic derangements that can occur most commonly following chemotherapy for certain hematologic malignancies such as acute lymphoblastic leukemia or high-grade non-Hodgkin's lymphoma (NHL) (Table 13–1). Less commonly, TLS complicates the treatment of other hematologic malignancies such as chronic lymphocytic leukemia, acute myeloid leukemia, plasma cell disorders including multiple myeloma or isolated plasmacytomas, Hodgkin's lymphoma, and low- or intermediate-grade NHL. Finally, TLS has been reported anecdotally in the setting of solid tumors such as testicular cancer, breast cancer, and lung cancer. Although usually seen after the administration of cytoreductive chemotherapy, TLS can occur spontaneously prior to initiation of any treatment and also may be seen following other therapies such as radiation, corticosteroids, interferon-α, rituximab, and tamoxifen.

Table 13–1. Characteristic Laboratory Abnormalities Encountered in Tumor Lysis Syndrome and Their Clinical Consequences.

This oncologic emergency is characterized by the acute onset of hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia, often associated with acute renal failure (ARF). TLS results from the rapid release of the intracellular contents of tumor cells (ie, uric acid, phosphate, potassium) into the systemic circulation that overwhelms physiologic metabolic pathways that maintain homeostasis. Not all patients with cancer develop TLS, and the incidence varies depending on the patient population studied ...

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