Tumor lysis syndrome (TLS) is a constellation of metabolic disturbances that may be
observed in patients with malignancies. Clinically significant TLS can occur spontaneously,
but most often is seen 48-72 h after initiation of cancer treatment. The metabolic abnormalities
observed in patients with TLS include hyperkalemia, hyperuricemia, and hyperphosphatemia,
which leads to secondary hypocalcemia. The precise incidence of TLS is not
defined, risk factors being represented by large tumor burden, neoplasms with either high
growth fraction or high sensitivity to chemotherapy, and by pre-existing impairment of renal
function. Neither racial, nor sex predilection exists. The pathogenesis of TLS is related to the
rapid tumor cell turnover or destruction, which may result in release of intracellular ions and
metabolic byproducts into the systemic circulation. Acute renal failure (ARF) may frequently
complicate TLS and is mainly due to renal tubule precipitation of uric acid, calcium
phosphate, or hypoxanthine. Hemodynamic changes reducing glomerular flow due to stillundefined
mediators are also involved in TLS pathophysiology. Pre-existing volume depletion
or renal dysfunction may worsen metabolic derangements and ARF. A good comprehension
of TLS pathophysiology has provided the basis for an effective and rational treatment of this
complication, adversely affecting the outcome of cancer patients.
Article / Publication Details
Published online: 12/3/2004
Cover Date: 2005
Number of Print Pages: 8
Number of Figures: 0
Number of Tables: 0
ISBN: 978-3-8055-7857-8 (Print)
eISBN: 978-3-318-01169-2 (Online)
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