Abstract

e21595 Background: Chemotherapy-induced peripheral neuropathy (CIPN) is a complex, dose-limiting toxicity impacting prognosis and quality of life. The optimal approach to identification and assessment remains unclear. This study aims to prospectively characterize the development and trajectory of CIPN using a combination of patient-reported outcomes (PROs) and objective Quantitative Sensory Testing (QST) measures in gynaecological, colorectal and lung cancer patients receiving neurotoxic platinum and/or taxane-based chemotherapy. Methods: Patients (n = 33, mean age 60.8) were evaluated at baseline prior to chemotherapy, during (every 3 weeks) and post-treatment every 3 months up to 1 year. Assessments at each time point included: PRO (EORTC QLQ-CIPN20 questionnaire) and QST measures (thermal and mechanical detection and grooved pegboard test). Statistical modelling using repeated measures analysis by patient was conducted. Results: Significant and parallel changes were observed in PROs and QST measures over time. Total EORTC score (sensory, motor and autonomic) increased in severity from baseline at all time points, peaking at 3 months post-treatment (34.8% increase; p < 0.0001) and persisting at 1 year (17.9% increase; p = 0.01). Every increase by one point in EORTC sensory score over time corresponded with an elevation in QST parameters: warm detection threshold (upper limb; p = 0.02 and lower limb; p = 0.03) and mechanical detection threshold, MDT (upper limb; p = 0.04 and lower limb; p = 0.02). Equally, rising total EORTC and motor score were related to increasing MDT in the upper limb p = 0.02 and p = 0.003 respectively. A delay of one second taken to complete the grooved pegboard test (dominant hand) was linked to a proportional increase in EORTC motor score (p = 0.01). Conclusions: Associations are shown here amongst PROs and QST parameters providing an opportunity to quantify and synthesize objective with subjective measures of neuropathy in CIPN patients. This may have potentially informative implications to underlying mechanisms of CIPN symptom burden, contributing to a more comprehensive clinical picture and allow stratification of patients by phenotype severity. Additional studies are warranted.

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