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Chemotherapy-Induced Peripheral Neuropathy: Epidemiology, Pathomechanisms and Treatment
PURPOSE: This review provides an update on the current clinical, epidemiological and pathophysiological evidence alongside the diagnostic, prevention and treatment approach to chemotherapy-induced peripheral neuropathy (CIPN). FINDINGS: The incidence of cancer and long-term survival after treatment...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Healthcare
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8593126/ https://www.ncbi.nlm.nih.gov/pubmed/34655433 http://dx.doi.org/10.1007/s40487-021-00168-y |
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author | Burgess, Jamie Ferdousi, Maryam Gosal, David Boon, Cheng Matsumoto, Kohei Marshall, Anne Mak, Tony Marshall, Andrew Frank, Bernhard Malik, Rayaz A. Alam, Uazman |
author_facet | Burgess, Jamie Ferdousi, Maryam Gosal, David Boon, Cheng Matsumoto, Kohei Marshall, Anne Mak, Tony Marshall, Andrew Frank, Bernhard Malik, Rayaz A. Alam, Uazman |
author_sort | Burgess, Jamie |
collection | PubMed |
description | PURPOSE: This review provides an update on the current clinical, epidemiological and pathophysiological evidence alongside the diagnostic, prevention and treatment approach to chemotherapy-induced peripheral neuropathy (CIPN). FINDINGS: The incidence of cancer and long-term survival after treatment is increasing. CIPN affects sensory, motor and autonomic nerves and is one of the most common adverse events caused by chemotherapeutic agents, which in severe cases leads to dose reduction or treatment cessation, with increased mortality. The primary classes of chemotherapeutic agents associated with CIPN are platinum-based drugs, taxanes, vinca alkaloids, bortezomib and thalidomide. Platinum agents are the most neurotoxic, with oxaliplatin causing the highest prevalence of CIPN. CIPN can progress from acute to chronic, may deteriorate even after treatment cessation (a phenomenon known as coasting) or only partially attenuate. Different chemotherapeutic agents share both similarities and key differences in pathophysiology and clinical presentation. The diagnosis of CIPN relies heavily on identifying symptoms, with limited objective diagnostic approaches targeting the class of affected nerve fibres. Studies have consistently failed to identify at-risk cohorts, and there are no proven strategies or interventions to prevent or limit the development of CIPN. Furthermore, multiple treatments developed to relieve symptoms and to modify the underlying disease in CIPN have failed. IMPLICATIONS: The increasing prevalence of CIPN demands an objective approach to identify at-risk patients in order to prevent or limit progression and effectively alleviate the symptoms associated with CIPN. An evidence base for novel targets and both pharmacological and non-pharmacological treatments is beginning to emerge and has been recognised recently in publications by the American Society of Clinical Oncology and analgesic trial design expert groups such as ACTTION. |
format | Online Article Text |
id | pubmed-8593126 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Healthcare |
record_format | MEDLINE/PubMed |
spelling | pubmed-85931262021-12-02 Chemotherapy-Induced Peripheral Neuropathy: Epidemiology, Pathomechanisms and Treatment Burgess, Jamie Ferdousi, Maryam Gosal, David Boon, Cheng Matsumoto, Kohei Marshall, Anne Mak, Tony Marshall, Andrew Frank, Bernhard Malik, Rayaz A. Alam, Uazman Oncol Ther Review PURPOSE: This review provides an update on the current clinical, epidemiological and pathophysiological evidence alongside the diagnostic, prevention and treatment approach to chemotherapy-induced peripheral neuropathy (CIPN). FINDINGS: The incidence of cancer and long-term survival after treatment is increasing. CIPN affects sensory, motor and autonomic nerves and is one of the most common adverse events caused by chemotherapeutic agents, which in severe cases leads to dose reduction or treatment cessation, with increased mortality. The primary classes of chemotherapeutic agents associated with CIPN are platinum-based drugs, taxanes, vinca alkaloids, bortezomib and thalidomide. Platinum agents are the most neurotoxic, with oxaliplatin causing the highest prevalence of CIPN. CIPN can progress from acute to chronic, may deteriorate even after treatment cessation (a phenomenon known as coasting) or only partially attenuate. Different chemotherapeutic agents share both similarities and key differences in pathophysiology and clinical presentation. The diagnosis of CIPN relies heavily on identifying symptoms, with limited objective diagnostic approaches targeting the class of affected nerve fibres. Studies have consistently failed to identify at-risk cohorts, and there are no proven strategies or interventions to prevent or limit the development of CIPN. Furthermore, multiple treatments developed to relieve symptoms and to modify the underlying disease in CIPN have failed. IMPLICATIONS: The increasing prevalence of CIPN demands an objective approach to identify at-risk patients in order to prevent or limit progression and effectively alleviate the symptoms associated with CIPN. An evidence base for novel targets and both pharmacological and non-pharmacological treatments is beginning to emerge and has been recognised recently in publications by the American Society of Clinical Oncology and analgesic trial design expert groups such as ACTTION. Springer Healthcare 2021-10-16 /pmc/articles/PMC8593126/ /pubmed/34655433 http://dx.doi.org/10.1007/s40487-021-00168-y Text en © The Author(s) 2021 https://creativecommons.org/licenses/by-nc/4.0/Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) . |
spellingShingle | Review Burgess, Jamie Ferdousi, Maryam Gosal, David Boon, Cheng Matsumoto, Kohei Marshall, Anne Mak, Tony Marshall, Andrew Frank, Bernhard Malik, Rayaz A. Alam, Uazman Chemotherapy-Induced Peripheral Neuropathy: Epidemiology, Pathomechanisms and Treatment |
title | Chemotherapy-Induced Peripheral Neuropathy: Epidemiology, Pathomechanisms and Treatment |
title_full | Chemotherapy-Induced Peripheral Neuropathy: Epidemiology, Pathomechanisms and Treatment |
title_fullStr | Chemotherapy-Induced Peripheral Neuropathy: Epidemiology, Pathomechanisms and Treatment |
title_full_unstemmed | Chemotherapy-Induced Peripheral Neuropathy: Epidemiology, Pathomechanisms and Treatment |
title_short | Chemotherapy-Induced Peripheral Neuropathy: Epidemiology, Pathomechanisms and Treatment |
title_sort | chemotherapy-induced peripheral neuropathy: epidemiology, pathomechanisms and treatment |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8593126/ https://www.ncbi.nlm.nih.gov/pubmed/34655433 http://dx.doi.org/10.1007/s40487-021-00168-y |
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