Incidence and characteristics of peripheral neuropathy during oxaliplatin-based chemotherapy for metastatic colon cancer

Argyriou, Andreas A.; Polychronopoulos, Panagiotis; Iconomou, Gregoris; Koutras, Angelos; Makatsoris, Thomas; Gerolymos, Miltiadis; Gourzis, Philippos; Assimakopoulos, Konstantinos; Kalofonos, Haralabos; Chroni, Elisabeth

doi:10.1080/02841860701355055

Cited by 79 publications

(61 citation statements)

References 28 publications

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“…Besides a clinical presentation that shares typical features of the CIPN induced by cisplatin or carboplatin, most patients treated with oxaliplatin also develop a unique acute and reversible toxicity represented by paresthesias and cramps enhanced by exposure to cold, occurring within a few hours of drug infusion [2]. In the reported studies, chronic oxaliplatin-induced CIPN affects from 18% to about 60% or more of exposed patients, mostly depending on the total dose administered [3].…”

Section: Epidemiologymentioning

confidence: 99%

Chemotherapy-Induced Neuropathy

Cavaletti

Alberti

Frigeni

et al. 2010

Curr Treat Options Neurol

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Chemotherapy-induced peripheral neurotoxicity (CIPN) is one of the most severe and unpredictable side effects of modern anticancer treatment. In recent years, a clear understanding of the importance of an integrated approach to CIPN has become evident, and efforts are increasing to better characterize its features and to identify more accurate methods to report and grade its occurrence. The clinically relevant impact of CIPN on cancer patients has been known for a long time, but knowledge of its pathogenetic aspects is still very limited. This incomplete knowledge is one of the major limitations in identifying targets for evidence-based neuroprotective strategies. Nevertheless, several studies have been devoted to the prevention or at least the effective treatment of symptoms secondary to peripheral nerve damage and to the early identification of patients at high risk of developing severe CIPN. Unfortunately, none of these studies has been successful and the optimal management of CIPN patients is still an unmet clinical need. Therefore, the modification of chemotherapy is currently the only available approach to limit the severity of neuropathy in the vast majority of patients. The indications for treatment modification are not universally accepted and they can differ among the various drugs. Generally, treatment modification should be considered as soon as symptoms and signs impair the daily life activities of the patient, but the possibility of a delayed worsening of CIPN after treatment withdrawal ("coasting") should always be considered, and delay of modification decisions should be avoided.

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Section: Epidemiologymentioning

confidence: 99%

Chemotherapy-Induced Neuropathy

Cavaletti

Alberti

Frigeni

et al. 2010

Curr Treat Options Neurol

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“…Often, the potent use of OXL is significantly limited due to the development of OXL-induced peripheral neuropathy (OXLIPN), which is ranked among its major dose-limiting toxicities. OXL induces 2 clinically distinct forms of neurotoxicity: the neuromyotonia-like acute transient syndrome and the chronic form that in most of the cases is a pure sensory, axonal neuronopathy [1]. However, the mechanisms underlying the acute and chronic OXLIPN have not yet been fully elucidated [2].…”

Section: Introductionmentioning

confidence: 99%

Liability of the Voltage-Gated Sodium Channel Gene <i>SCN2A</i> R19K Polymorphism to Oxaliplatin-Induced Peripheral Neuropathy

Argyriou

Antonacopoulou²,

Scopa³

et al. 2009

Oncology

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Aim: It was the aim of this study to test the hypothesis that the voltage-gated sodium channel gene SCN2A R19K polymorphism confers liability to oxaliplatin-induced peripheral neuropathy (OXLIPN). Methods: Sixty-two patients with advanced colorectal cancer were genotyped, using allele-specific primers and SYBR green in real-time polymerase chain reaction. All patients had received adjuvant oxalipla-tin-based chemotherapy. The severity of OXLIPN was defined by means of the clinical total neuropathy score. Following the discontinuation of treatment, 36/62 patients (58.1%) developed OXLIPN. Grade I neurotoxicity was revealed in 14 (38.9%) patients and grade II neurotoxicity in 22 (61.1%) patients. Results: From patients without OXLIPN (n = 26), 80.8% (n = 21) were homozygous for G, 19.2% (n = 5) were heterozygous (AG) and none was homozygous for A. The corresponding percentages for patients developing any grade of OXLIPN (n = 36) were similar. Likewise, among patients experiencing OXLIPN, insignificant differences in R19K genotypes were revealed between those with grade I versus grade II neurotoxicity. Conclusion: Our study failed to provide evidence to support a causal relationship between the SCN2A R19K polymorphism and OXLIPN.

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“…Rates may be as high as 60-70% with taxanes [7,8] and platins [9][10][11]; two agents frequently used as first and second-line treatment for several common malignancies. CIPN may be transient or permanent and can last for many years.…”

Section: Introductionmentioning

confidence: 99%