Poster Presentation NSW State Cancer Conference 2023

Investigating Clinical Profiles Associated with Recovery of Chemotherapy-Induced Peripheral Neuropathy (#291)

Tiffany Li 1 , Hannah C Timmins 1 , Fawaz M Mahfouz 1 , Terry Trinh 2 , Lisa Horvath 3 , Michelle Harrison 3 , Peter Grimison 3 , Michael L Friedlander 4 , Tracy King 5 , Matthew C Kiernan 1 , David Goldstein 2 , Susanna B Park 1
  1. Brain and Mind Centre, University of Sydney, Sydney
  2. Prince of Wales Clinical School, UNSW, Kensington
  3. Chris O’Brien Lifehouse, Camperdown
  4. Prince of Wales Hospital, Randwick
  5. Institute of Haematology, Royal Prince Alfred Hospital, Camperdown

Background

Chemotherapy-induced peripheral neurotoxicity (CIPN) is a common adverse effect of numerous anti-cancer treatments with symptoms often persisting for years post treatment completion and negatively affecting cancer survivors’ quality of life. However, there is considerable variability in CIPN recovery and little is known about clinical profiles of patients who are more likely to experience CIPN symptom improvement. This longitudinal study aimed to identify clinical phenotypes associated with improvement in CIPN.

Method

Patients commencing neurotoxic treatments (taxane, platinum, vinca-alkaloid, bortezomib, thalidomide) were assessed longitudinally. Data from two timepoints were compared for this analysis, end-of-treatment and 6-12 months post treatment. CIPN was graded by the National Cancer Institute (NCI) sensory neuropathy scale by trained researchers after comprehensive evaluation. Improvement in CIPN was defined as reduction by at least one NCI grade. Odds ratios (OR) were computed using logistic regression with results presented as mean±SD.

Results

270 patients (54.9±12.5 years, 68.1% female) were included in the study, with 207 (76.7%) patients experiencing CIPN by end-of-treatment. At second follow-up (6.9±2.6 months post treatment), 101(48.8%) experienced CIPN improvement. Each year of older age was associated with a 3.8% decrease in the odds of CIPN improvement (P<0.005), while there was no significant association with other clinical factors (gender, body mass index, diabetic status, baseline neuropathy, all P>0.05). There was no difference in CIPN improvement between patients receiving taxane compared to platinum therapy (P>0.05), or between patients receiving paclitaxel alone versus paclitaxel with carboplatin (P>0.05). Subgroup analysis in taxane-treated patients with CIPN by end-of-treatment (n=130) suggested older age was associated with decrease in CIPN improvement (P<0.001), but not gender, BMI, diabetic status, baseline PN or paclitaxel dose (all P>0.05).

Discussion

This series of longitudinal analyses demonstrated CIPN as a long-term toxicity with only 49% of patients experiencing symptom improvement at 6-12 months post treatment. Older age was identified as a clinical risk factor for CIPN persistence. However, mechanisms underlying CIPN improvement are complex, and clinical variables alone may not be sufficient to ascertain a patient’s long-term CIPN outcome. It is likely that other parameters, such as genetic risk factors also play a significant role in CIPN symptom reversibility.