Management of oxaliplatin-induced peripheral neuropathy

Figures & data

Table 1 Grading of oxaliplatin-induced neurotoxicity

Scale	National Cancer Institute Neurosensory	Oxaliplatin Scale Sanofi Specific Scale
Grade 1	Mild paresthesia, loss of deep tendon reflexes	Paresthesia, dysesthesia of short duration
Grade 2	Moderate paresthesia, mild or moderate objective sensory loss	Paresthesia, dysesthesia persisting between cycles
Grade 3	Paresthesia interfering with function, severe objective sensory loss	Paresthesia, dysesthesia causing functional impairment
Grade 4	Permanent sensory loss that impairs function

Table 2 Comparison of neurotoxicity profiles of cisplatin and oxaliplatin

		Oxaliplatin
	Cisplatin	Acute neuropathy	Chronic neuropathy
Incidence	45%	85%–95%	In trials 3% in 16%
DLT	Yes	No	Yes
Symptoms	Paresthesia, sensory ataxia	Paresthesia, dyesthesia	Paresthesiaa, dysethesia, sens. Ataxia
Location	Extremities	Extremities, perioral	Extremities
Trigger	None	Cold exposure	None
Motor symptoms	None	Rare muscle spasms	None
Onset	Delayed	Acute	Delayed
Recovery	Slow, incomplete	Rapid, complete	Less slow, more complete
Schedule dependence	None	Yes	Probably none
Other	Ototoxicity	Laryngospasm	none

Abbreviations: DLT, dose-limiting toxicities.

Figure 1 Postulated mechanism underlying the pathogenesis of neurotoxicity caused by oxaliplatin. Na⁺ channelopathy: the theory that an oxalate affects the sodium channels has been entertained by other researchers as well. Oxalate is released intracellularly from oxaliplatin by bicarbonate ions. Oxalate and BAPTA, another calcium chelator, have produced effects on inward sodium currents in invertebrate models similar to those seen with oxaliplatin.

Abbreviations: BAPTA, 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid; DACH, 1,2-diaminocyclohexane.