Tumor lysis syndrome pathophysiology: Difference between revisions
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==Overview== | ==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== | ==Pathogenesis== | ||
Revision as of 15:13, 24 September 2015
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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.
- 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]