Background: Chemotherapy for various stages of gastroesophageal cancer (GEC) is often neurotoxic. Chemotherapy-induced peripheral neuropathy (CIPN) impairs health-related quality of life (HRQoL). This study investigates the incidence and severity of CIPN and its association with HRQoL in patients with GEC. Patients and Methods: Patients who received chemoradiotherapy or chemotherapy for GEC were identified from the Netherlands Cancer Registry. Patient-reported data (measured using the EORTC QLQ-CIPN20 and EORTC QLQ-C30) were collected through the Prospective Observational Cohort Study of Esophageal-Gastric Cancer Patients (POCOP) at baseline and at 3, 6, 9, 12, 18, and 24 months after treatment initiation. Linear mixed effects models were constructed to assess CIPN and the correlation between CIPN and HRQoL was analyzed using Spearman’s correlation. Results: A total of 2,135 patients were included (chemoradiotherapy: 1,593; chemotherapy with curative intent: 295; palliative chemotherapy: 247). In all 3 treatment groups, CIPN significantly increased during treatment (adjusted mean score of CIPN at 6 months: chemoradiotherapy, 8.3 [baseline: 5.5]; chemotherapy with curative intent, 16.0 [baseline: 5.6]; palliative therapy, 25.4 [baseline: 10.7]). For chemoradiotherapy, the adjusted mean score continued to increase after treatment (24 months: 11.2). For chemotherapy with curative intent and palliative therapy, the adjusted mean score of CIPN decreased after treatment but did not return to baseline values. CIPN was negatively correlated with HRQoL in all treatment groups, although significance and strength of the correlation differed over time. Conclusions: Because of the poor prognosis of GEC, it is essential to consider side effects of (neurotoxic) treatment. The high prevalence and association with HRQoL indicate the need for early recognition of CIPN.
Submitted June 20, 2023; final revision received January 25, 2024; accepted for publication January 29, 2024. Published online July 8, 2024.
Author contributions: Concept and design: van Velzen, van Kleef, Slingerland, van de Poll-Franse, van Laarhoven. Acquisition, analysis, or interpretation of data: van Velzen, Pape, van Laarhoven. Statistical analysis: van Velzen, Pape. Drafting of the manuscript: van Velzen, Pape, van Laarhoven. Critical revision for important intellectual content: Pape, Sprangers, van Kleef, Mostert, Beerepoot, Slingerland, Gootjes, Hoekstra, van de Poll-Franse, Haj Mohammad, van Laarhoven.
Disclosures: Dr. Sprangers has disclosed serving as an advisor for Bristol Myers Squibb and Lilly. Dr. Mostert has disclosed serving as a consultant for Amgen, AstraZeneca, Bristol Myers Squibb, Lilly, and Servier; and receiving grant/research support from Sanofi, Pfizer, and Bristol Myers Squibb. Dr. Haj Mohammad has disclosed receiving grant/research support from Servier; and serving as a consultant for Merck & Co., Inc., Bristol Myers Squibb, Lilly, and AstraZeneca. Dr. van Laarhoven has disclosed receiving grant/research support from Bayer, Bristol Myers Squibb, Celgene, Janssen Pharmaceuticals, Incyte, Lilly, MSD, Nordic Pharma, Philips, Roche, and Servier; serving on the speakers’ bureau for Astellas, Daiichi Sankyo, and Novartis; and serving as a consultant for Bristol Myers Squibb, Daiichi Sankyo, Dragonfly, Lilly, MSD, Nordic Pharma, and Servier. The remaining authors have disclosed that they have not received any financial consideration from any person or organization to support the preparation, analysis, results, or discussion of this article.
Supplementary material: Supplementary material associated with this article is available online at https://doi.org/10.6004/jnccn.2024.7014. The supplementary material has been supplied by the author(s) and appears in its originally submitted form. It has not been edited or vetted by JNCCN. All contents and opinions are solely those of the author. Any comments or questions related to the supplementary materials should be directed to the corresponding author.