Premium
Vinca alkaloids, thalidomide and eribulin‐induced peripheral neurotoxicity: From pathogenesis to treatment
Author(s) -
Islam Badrul,
Lustberg Maryam,
Staff Nathan P.,
Kolb Noah,
Alberti Paola,
Argyriou Andreas A.
Publication year - 2019
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1111/jns.12334
Subject(s) - eribulin , medicine , vinca , thalidomide , neurotoxicity , chemotherapy induced peripheral neuropathy , peripheral neuropathy , lenalidomide , bortezomib , pharmacology , neuropathic pain , oncology , adverse effect , breast cancer , cancer , multiple myeloma , toxicity , metastatic breast cancer , endocrinology , diabetes mellitus
Abstract Vinca alkaloids, thalidomide, and eribulin are widely used to treat patients with childhood acute lymphoblastic leukemia (ALL), adults affected by multiple myeloma and locally invasive or metastatic breast cancer, respectively. However, soon after their introduction into clinical practice, chemotherapy‐induced peripheral neurotoxicity (CIPN) emerged as their main non‐hematological and among dose‐limiting adverse events. It is generally perceived that vinca alkaloids and the antiangiogenic agent thalidomide are more neurotoxic, compared to eribulin. The exposure to these chemotherapeutic agents is associated with an axonal, length‐dependent, sensory polyneuropathy of mild to moderate severity, whereas it is considered that the peripheral nerve damage, unless severe, usually resolves soon after treatment discontinuation. Advanced age, high initial and prolonged dosing, coadministration of other neurotoxic chemotherapeutic agents and pre‐existing neuropathy are the common risk factors. Pharmacogenetic biomarkers might be used to define patients at increased susceptibility of CIPN. Currently, there is no established therapy for CIPN prevention or treatment; symptomatic treatment for neuropathic pain and dose reduction or withdrawal in severe cases is considered, at the cost of reduced cancer therapeutic efficacy. This review critically examines the pathogenesis, epidemiology, risk factors (both clinical and pharmacogenetic), clinical phenotype and management of CIPN as a result of exposure to vinca alkaloids, thalidomide and its analogue lenalidomide as also eribulin.