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Chemotherapy-induced peripheral neuropathy in adults: a comprehensive update of the literature

Authors Argyriou A, Kyritsis A, Makatsoris T, Kalofonos H

Received 31 December 2013

Accepted for publication 9 February 2014

Published 19 March 2014 Volume 2014:6 Pages 135—147

DOI https://doi.org/10.2147/CMAR.S44261

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 6


Andreas A Argyriou,1,3 Athanasios P Kyritsis,2 Thomas Makatsoris,3 Haralabos P Kalofonos3

1Department of Neurology, "Saint Andrew's" General Hospital of Patras, Greece; 2Department of Neurology, University Hospital of Ioannina, Greece; 3Department of Medicine-Division of Oncology, University of Patras Medical School, Rion-Patras, Greece

Abstract: Commonly used chemotherapeutic agents in oncology/hematology practice, causing toxic peripheral neuropathy, include taxanes, platinum compounds, vinca alkaloids, proteasome inhibitors, and antiangiogenic/immunomodulatory agents. This review paper intends to put together and discuss the spectrum of chemotherapy-induced peripheral neuropathy (CIPN) characteristics so as to highlight areas of future research to pursue on the topic. Current knowledge shows that the pathogenesis of CIPN still remains elusive, mostly because there are several sites of involvement in the peripheral nervous system. In any case, it is acknowledged that the dorsal root ganglia of the primary sensory neurons are the most common neural targets of CIPN. Both the incidence and severity of CIPN are clinically under- and misreported, and it has been demonstrated that scoring CIPN with common toxicity scales is associated with significant inter-observer variability. Only a proportion of chemotherapy-treated patients develop treatment-emergent and persistent CIPN, and to date it has been impossible to predict high- and low-risk subjects even within groups who receive the same drug regimen. This issue has recently been investigated in the context of pharmacogenetic analyses, but these studies have not implemented a proper methodological approach and their results are inconsistent and not really clinically relevant. As such, a stringent approach has to be implemented to validate that information. Another open issue is that, at present, there is insufficient evidence to support the use of any of the already tested chemoprotective agents to prevent or limit CIPN. The results of comprehensive interventions, including clinical, neurophysiological, and pharmacogenetic approaches, are expected to produce a consistent advantage for both doctors and patients and thus allow the registration and analysis of reliable data on the true characteristics of CIPN, eventually leading to potential preventive and therapeutic interventions.

Keywords: neurotoxicity, incidence, diagnosis, treatment

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