Abstract
Tumor lysis syndrome (TLS) is a life-threatening oncological condition that is typically characterized by metabolic derangements that are often labeled as an acute kidney injury. The recent advancement in cancer treatment has led to the mounting rate of TLS in solid tumors that were previously rarely linked to this complication. Given that its prognosis is dismal, it is essential to increase recognition of this condition by describing more sensitive markers. Currently, the management of TLS is mainly supportive due to the lack of specific therapy targeting its specific pathology. This review aims to summarize the most recent literature on the underlying mechanism of TLS and the potential implications for novel TLS therapy.
Highlights
BackgroundTumor lysis syndrome (TLS) is a life-threatening medical condition that can occur spontaneously or as a complication of cancer therapy for rapidly proliferating and chemo-sensitive malignancies such as acute lymphoblastic leukemia or high-grade lymphoma [1,2,3]
Tumor lysis syndrome (TLS) is a life-threatening oncological condition that is typically characterized by metabolic derangements that are often labeled as an acute kidney injury
The recent advancement in cancer treatment has led to the mounting rate of TLS in solid tumors that were previously rarely linked to this complication
Summary
Tumor lysis syndrome (TLS) is a life-threatening medical condition that can occur spontaneously or as a complication of cancer therapy for rapidly proliferating and chemo-sensitive malignancies such as acute lymphoblastic leukemia or high-grade lymphoma [1,2,3]. Studies in mice revealed that disseminated microemboli composed of debris from lysed tumor cells prompted mechanical microobstruction of multiorgan capillary beds, including the kidney tubules, brain, lungs, and elsewhere These processes resulted in widespread tissue ischemia, necrosis, and early death [21,22]. Ito et al reported a patient with TLS following docetaxel and carboplatin treatment for recurrent endometrial cancer This patient developed classic laboratory abnormalities for TLS, AKI, in conjunction with sudden onset chest pain, hypoxia, and respiratory distress 19 hours after initiation of chemotherapy, and the autopsy, thereafter, showed pulmonary tumor embolism [28]
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