Thus far, there are conflicting results on the causal role of K+ channels in the pathogenesis of acute oxaliplatin‐induced peripheral neurotoxicity (OXAIPN). As such, we tested the hypothesis that the voltage‐gated K+ channel KCNN3 repeat polymorphism confers liability to acute OXAIPN. DNA from 151 oxaliplatin‐treated patients for colorectal cancer was extracted and genotyped. The incidence of acute OXIPN was measured by the OXA‐neuropathy questionnaire, while the severity of acute OXAIPN was scored basing on the number of symptoms reported by the patients at each clinical assessment. The increased number of acute symptoms was considered as being suggestive of an increased severity of acute OXAIPN. A total of 130/151 (86.1%) patients developed any grade of acute OXAIPN. Grade I acute neurotoxicity was revealed in 43 (28.5%) patients; grade II in 34 (22.5%); and grade III in 53 (53.1%) patients. Genotyping revealed alleles carrying 11 to 20 CAG repeats. The majority of patients were heterozygous (131; 89.4%). The most common numbers of CAG repeats were 15 (n = 46), 16 (n = 53), and 17 (n = 95). Patients carrying alleles with either 15 to 17 CAG repeats (P = .601) did not experience a higher incidence of grade III (treatment‐emergent) acute OXAIPN. Likewise, no increased incidence of acute treatment‐emergent OXAIPN was noted in heterozygous patients carrying either two short alleles (<19 CAG repeats) or one short and one long (≥19 CAG repeats) allele (P = .701). Our results do not support a causal relationship between the KCNN3CAG repeat polymorphism and acute OXΑIPN.

中文翻译：

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电压门控钾通道KCNN3重复多态性对急性奥沙利铂诱导的周围神经毒性的责任。

迄今为止，在急性奥沙利铂诱导的周围神经毒性（OXAIPN）的发病机理中，K +通道的因果作用存在矛盾的结果。因此，我们测试了电压门控K +通道KCNN3的假设重复多态性赋予急性OXAIPN责任。从151名奥沙利铂治疗的大肠癌患者中提取DNA并进行基因分型。急性OXIPN的发生率通过OXA神经病学问卷进行测量，而急性OXAIPN的严重程度则根据患者在每次临床评估中报告的症状数量进行评分。急性症状数量的增加被认为提示急性OXAIPN的严重程度增加。共有130/151（86.1％）患者出现了任何等级的急性OXAIPN。在43名（28.5％）患者中发现了I级急性神经毒性；二级34（22.5％）；53例（53.1％）患者为III级。基因分型显示等位基因携带11至20个CAG重复序列。大多数患者是杂合的（131； 89.4％）。最常见的CAG重复次数为15（n = 46），16（n = 53）和17（n = 95）。携带等位基因具有15至17个CAG重复序列的患者（P = .601）的III级（紧急治疗）急性OXAIPN发生率没有更高。同样，在携带两个短等位基因（<19 CAG重复）或一个短而一个长（≥19 CAG重复）等位基因的杂合患者中，没有发现急性治疗新兴的OXAIPN发生率增加（P = .701）。我们的结果不支持KCNN3 CAG重复多态性与急性OXAIPN之间的因果关系。