Tumor lysis syndrome pathophysiology
|
Tumor lysis syndrome Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Tumor lysis syndrome pathophysiology On the Web |
|
American Roentgen Ray Society Images of Tumor lysis syndrome pathophysiology |
|
Risk calculators and risk factors for Tumor lysis syndrome pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohamad Alkateb, MBBCh [2]
Overview
Tumor lysis syndrome (TLS) is a group of metabolic abnormalities resulting from rapid lysis of malignant cells and massive release of cell breakdown products into the blood among patients with hematologic malignancies treated with chemotherapy. The most common tumors associated with this syndrome are poorly differentiated lymphomas, such as Burkitt's lymphoma, and leukemias, such as acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). Usually, the precipitating medication regimen includes combination chemotherapy, but those patients with lymphoma and ALL can be affected with steroid treatment alone.
Pathogenesis
- Tumor lysis syndroms is a group of metabolic complications that can occur after treatment of cancer, usually lymphomas and leukemias, and sometimes even without treatment.
- Massive cells destruction will lead to a rapid release of intracellular anions, cations and metabolic products of proteins and nucleic acids into the bloodstream. As consequences of their high intracellular concentration, potassium, calcium, phosphates and uric acid will be released in the extracellular space. ARF may develop, the most common mechanism being uric acid crystal formation in the renal tubules secondary to hyperuricemia. Another cause may be calcium phosphate deposition related to hyperphosphatemia. While ARF leads to further increase in above describe metabolites, a vicious circle will therefore be initiated.Invalid parameter in
<ref>tag - Pretreatment spontaneous tumor lysis syndrome is associated with acute renal failure due to uric acid nephropathy prior to the institution of chemotherapy and is largely associated with lymphomas and leukemias. The important distinction between this syndrome and the post-chemotherapy syndrome is that spontaneous tumor lysis syndroms is not associated with hyperphosphatemia. One suggestion for the reason of this is that the high cell turnover rate leads to high uric acid levels through nucleoprotein turnover but the tumor reuses the released phosphate for resynthesis of new tumor cells. In post-chemotherapy tumor lysis syndroms, tumor cells are destroyed and no new tumor cells are being synthesized.[1]
Gallery
-
Pathophysiology of the tumor lysis syndrome.
