12125 Background: Poorly controlled diabetes is a predictor of chemotherapy induced peripheral neuropathy (CIPN), and hyperglycemia (HG) may mediate CIPN risk. The association between CIPN and HG is not well studied. Our objective was to evaluate the association between HG and CIPN development. Methods: The CONTRoL trial was a phase IIB randomized adaptive sequential selection trial that evaluated cryotherapy vs. compression vs. placebo to prevent CIPN in patients with Stage I-III breast cancer during taxane therapy. Patients completed the Functional Assessment of Cancer Therapy Neurotoxicity (FACT-NTX) survey at baseline, week-12, and week-24. CIPN development was defined as ≥ 5-point increase in FACT-NTX from baseline. We included patients who completed FACT-NTX at baseline and week-12. HG (any glucose ≥ 140 mmol/L) was assessed via chart review of random glucose laboratory results collected from time of taxane initiation through week-24. Patients were divided into two groups based on CIPN development (yes/no). For each group we calculated the proportion of patients with HG, and mean glucose at baseline, week-12 and week-24 with values obtained +/-7 days of specified timeframe; 95% confidence intervals were constructed. Results: Sixty-three patients participated in the CONTRoL study and 59 patients were included in this analysis. All 59 patients had ≥1 recorded glucose value during the 24-week period (n= 410 total values), with a median of 6 values (range 1-12) per patient. When comparing patients who did and did not develop CIPN, 29.4% vs. 20.0% were Black (p=0.72), 41.2% vs. 52.0% were Hispanic/Latino (p=0.69), 17.6% vs. 8.0% had diabetes (p=0.49) and 64.7% vs. 48.0% received docetaxel (p=0.31). There were higher rates of HG, 47.1% vs. 36.0%, in patients who developed CIPN vs. those who did not (p=0.56). Mean glucose was higher in patients who developed CIPN compared to those who did not at all timepoints (Table). Conclusions: In this secondary analysis, we found that almost half of patients with CIPN had HG compared to about a third of patients without CIPN, and that patients with CIPN had higher mean glucose at all timepoints compared to patients without CIPN. Due to the small sample size, differences were not statistically significant, but notable trends were observed. Further research is needed to confirm this finding and evaluate the impact of glucose lowering interventions on preventing the development of CIPN. Clinical trial information: NCT03873272 . [Table: see text]
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