514P - Role of glutamine for preventing oxaliplatin induced peripheral neuropathy (GELUPO): results of randomized open-label phase II trial

Date 08 October 2016
Event ESMO 2016 Congress
Session Poster Display
Topics Complications/Toxicities of Treatment
Colon and Rectal Cancer
Translational Research
Basic Principles in the Management and Treatment (of cancer)
Therapy
Presenter Ozan Yazici
Citation Annals of Oncology (2016) 27 (6): 149-206. 10.1093/annonc/mdw370
Authors O. Yazici1, A.P. Titiz2, N. Ozdemir1, S. Aksoy3, M.A. Sendur4, B. Arlı2, N. Zengin1
  • 1Medical Oncology, Ankara Numune Education and Research Hospital, 06100 - Ankara/TR
  • 2Neurology, Ankara Numune Education and Research Hospital, 06100 - Ankara/TR
  • 3Department Of Medical Oncology, Hacettepe University Faculty of Medicine, 06100 - Ankara/TR
  • 4Department Of Medical Oncology, Yıldırım Beyazıt University, Faculty of Medicine, 06800 - Ankara/TR

Abstract

Background

Aimed to evaluate role of oral glutamine replacement for preventing neuropathy in patients with colorectal cancer receiving oxaliplatin.

Methods

The patients planned to receive modified FOLFOX6 were blindly 1:1 randomized to glutamine and control group. In both groups, prior to first mFOLFOX6 regimen and after 8 cycles of therapy detailed neurological examination and EMG was performed.Assuming a neuropathy rate was > 30 % and 10 % in control and glutamine and it was estimated a total of 80 patients needed to be randomized to achieve 80% statistical power with a p level of 0.05 and a 10% drop-out rate. The patients with neuropathy in basal EMG, diabetes, history of neuropathy were excluded. In glutamine group all of the patients received 3x10 gr/day glutamine given before and during chemotherapy until the control EMG. The secondary end point of study was quality of life evaluated by EORTC-QLQ C3O.

Results

In between December 2013 and September 2015, eighty eligible patients were randomized glutamine (n = 40) and control (n = 40) group. In glutamine and control group basal and control EMG was performed in 87.5% (n = 35) and %80 (n = 32) of the patients, respectively. In between glutamine and control group after 8 cycles of therapy motor axonal and demyelinating neuropathy was detected in 8.5 % (n = 3) vs 18.7 % (n = 6) and 14.2 % (n = 5) vs 15.6 %(n = 5) of the patients and difference was not significant. In between glutamine and control group sensory axonal and demyelinating neuropathy was determined in 14.2 % (n = 5) vs 15.6 % (n = 5) and 17.1 % (n = 6) vs 18.7 % (n = 6) of patients, respectively (p = 1 and p = 0.8). Following the 8 cycles of therapy in control EMG there was no difference in between upper extremity and lower extremity distal latency, compound muscle action potential, motor nerve conduction velocity, F latency, compound nerve action potential and sensory nerve conduction velocity. The hematological and non-hematological toxicities were similar in between two groups. Basal and control median EORTC-QLQ scores were not different in between two groups (p = 0.46).

Conclusions

In final analysis of the current open label randomized phase II trial, oral glutamine replacement therapy was ineffective to prevent oxaliplatin induced neuropathy.

Clinical trial identification

ClinicalTrials.gov Identifier: NCT02024191

Legal entity responsible for the study

Ankara Numune Education and Research Hospital

Funding

Ankara Numune Education and Research Hospital

Disclosure

All authors have declared no conflicts of interest.