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Abstract
Mechanism of Oxaliplatin-Induced Sinusoidal Obstruction Syndrome along with Therapeutic Strategy
Oxaliplatin is a backbone drug of many regimens for colorectal cancer and colorectal liver metastasis. Most frequent adverse effects in patients with oxaliplatin-based chemotherapy include the peripheral neuropathy, liver dysfunction, splenomegaly, and thrombocytopenia. Recently, the author described a thorough review of the literature on oxaliplatin-induced hepatic complications focusing on Sinusoidal Obstruction Syndrome (SOS), Nodular Regenerative Hyperplasia (NRH), and Focal Nodular Hyperplasia (FNH) in patients with colorectal cancer and colorectal liver metastasis and emphasized the Liver Stiffness Measurement (LSM), elasticity as a novel predictor reflecting splenomegaly by elastography. The underlying mechanisms of oxaliplatin-induced SOS include the activation of inflammation-related pathways, the activated cellular hypoxia, the upregulation of genes involved in coagulation such as Plasminogen Activator Inhibitor-1 (PAI-1) and Von Willebrand Factor (VWF), and the upregulation of angiogenesis-related genes. In this article, current knowledge and trends of the underlying mechanism of oxaliplatin-induced SOS have been reviewed. Additionally, the potential therapies for oxaliplatinbased chemotherapy have been also described. The underlying mechanisms of oxaliplatin-induced SOS showed liver fibrosis, platelet aggregation and adhesion, inflammatory damage, and oxidative stress. The evidence provided that oxidative stress plays a significant role in the pathogenesis of oxaliplatin-induced acute liver injury. Regarding the therapeutic strategy for oxaliplatin-induced SOS, bevacizumab, Vascular Endothelial Growth Factor (VEGF) inhibitor may contribute to the protection of the development of oxaliplatin-induced SOS. Based on the evidence, Glutathione (GSH) might be a potential treatment for oxaliplatin-induced SOS.
Published Date: 2024-05-02; Received Date: 2024-04-01