View clinical trials related to Cisplatin Adverse Reaction.
Filter by:Evaluation of the Effect of N-acetylcysteine in Preventing Cisplatin-Induced Toxicities in Cancer Patients
Late subclinical cardiovascular disease in testicular cancer survivors exposed to cisplatin-based chemotherapy and bone marrow transplant
Cisplatin is an effective anti-cancer drug for the treatment of many solid tumors in humans. Although the clinical response to cisplatin chemotherapy is encouraging, the nephrotoxicity and ototoxicity of the drug makes it difficult to continue its administration in many cases. Cisplatin nephrotoxicity occurs through several mechanisms, mainly through the transport and accumulation of cisplatin into renal epithelial cells, injury to nuclear and mitochondrial DNA, activation of multiple cell death pathways and initiation of inflammatory response. Accordingly, several experimental strategies were developed to prevent this toxicity. For example, drugs that reduced renal cisplatin accumulation such as organic cation transporter 2 (OCT2) and copper transporter (Ctr1) inhibitors, antioxidants, antiapoptotic and anti-inflammatory agents were investigated. However, many of these drugs interfered with the cytotoxic effects of cisplatin. Statins are agents used for reducing plasma cholesterol through the inhibition of the enzyme 3- hydroxy-3- methylglutaryl coenzyme A (HMG-CoA) reductase. In addition, statins are also proven to have pleiotropic, non-lipid dependent effects. These effects include anti-inflammatory actions and reduction of oxidative stress. Based on animal studies performed, statins have been shown to reduce the nephrotoxic effects of cisplatin in rats. In addition, ongoing clinical trials are aiming to investigate the role of statins in the protection against the ototoxicity of cisplatin as well. Our aim is to assess the protective effect of statins on cisplatin-induced nephrotoxicity and ototoxicity in humans.
Cisplatin is a potent chemotherapeutic agent, however, its nephrotoxicity manifested by acute kidney injury (AKI) often limits applicability. Dipeptidylpeptidase-4 (DPP4) inhibitors are well known to improve glucose intolerance by augmentation of endogenous glucagon like peptide (GLP-1) and glucose-dependent insulinotropic peptide (GIP). DPP4 inhibitor also has the potential anti-apoptotic and renoprotective effect in a mouse model of cisplatin-induced AKI. This is a single-center, randomized, double-blind, parallel-group, placebo-controlled, prospective study to investigate the renoprotective effect of DPP4 inhibitor on cisplatin-induced AKI. A total 182 patients, who are scheduled to treat with cisplatin, will be recruited and randomly assigned to either Gemigliptin or placebo groups. Subjects will take study drugs for 8 days starting from one day before cisplatin treatment. Serum creatinine (Cr) and estimated glomerular filtration rate (eGFR) will be measured at 7 days after cisplatin treatment.