CHEMOTHERAPY INDUCED PERIPHERAL NEUROPATHY IN CANCER PATIENTS RECEIVING MICROTUBULE AGENTS & PLATINUM COMPOUNDS

Background: Chemotherapy-induced peripheral neuropathy (CIPN) is one of the most common dose-limiting toxicities associated with anticancer therapy, particularly in patients receiving microtubule-targeting agents (paclitaxel, docetaxel, vincristine, and vinblastine) and platinum compounds (cisplatin, carboplatin, and oxaliplatin). CIPN adversely affects sensory, motor, and autonomic nerve function, leading to symptoms such as numbness, tingling, burning pain, impaired proprioception, muscle weakness, and reduced quality of life. These complications frequently necessitate dose reduction, treatment delays, or discontinuation of chemotherapy, potentially compromising therapeutic outcomes. Objective: To review the incidence, risk factors, pathophysiological mechanisms, clinical manifestations, assessment methods, prevention strategies, and management of chemotherapy-induced peripheral neuropathy in cancer patients receiving microtubule agents and platinum-based chemotherapy. Methods: A comprehensive review of published literature was conducted using electronic databases including PubMed, Scopus, Web of Science, and Google Scholar. Peer-reviewed articles, clinical practice guidelines, systematic reviews, meta-analyses, and randomized controlled trials published in English were evaluated. Studies focusing on the epidemiology, mechanisms, diagnosis, prevention, and treatment of CIPN associated with microtubule agents and platinum compounds were included. Results: The incidence of CIPN varies according to the chemotherapeutic agent, cumulative dose, treatment duration, and patient-related factors such as age, diabetes mellitus, nutritional deficiencies, and pre-existing neuropathy. Platinum compounds primarily induce neuronal damage through DNA adduct formation, oxidative stress, mitochondrial dysfunction, and dorsal root ganglion injury, whereas microtubule agents disrupt axonal transport by destabilizing or excessively stabilizing microtubules, resulting in distal axonal degeneration. Current evidence supports duloxetine as the pharmacological agent with the strongest evidence for the treatment of painful CIPN, while preventive strategies remain limited. Emerging interventions, including neuroprotective agents, exercise-based rehabilitation, cryotherapy, compression therapy, and neuromodulation techniques, have demonstrated variable efficacy and require further investigation. Conclusion: Chemotherapy-induced peripheral neuropathy remains a significant clinical challenge in oncology, particularly among patients receiving microtubule-targeting agents and platinum compounds. Early identification of high-risk patients, routine neurological assessment, patient education, individualized chemotherapy planning, and multidisciplinary supportive care are essential to minimize the burden of CIPN. Continued research into predictive biomarkers, neuroprotective therapies, and evidence-based management strategies is needed to improve patient outcomes, preserve quality of life, and optimize cancer treatment.