自拟通络活血汤熏洗配合低频脉冲防治奥沙利铂神经毒性临床观察

目的:观察自拟通络活血汤熏洗配合低频脉冲对防治奥沙利铂神经毒性的临床疗效。方法:收集符合标准接受奥沙利铂联合化疗的患者82例,分为对照组和观察组,每组各41例,2组均接受6个疗程的基于奥沙利铂的方案化疗并同时全程口服B族维生素预防OPIN(奥沙利铂导致的末梢神经毒性),观察组在对照组的基础上在每个化疗周期的第1天至第5天予以自拟通络活血汤熏洗及足三里穴位低频脉冲电治疗。2组患者均在辅助化疗开始前及6个疗程的辅助化疗结束后分别对外周神经的传导速度进行检测,具体包括正中神经、腓肠神经及胫神经的感觉神经(SCV)传导速度和运动神经(MCV)传导速度。结果:对照组、观察组外周神经毒性发生率分别是65.85%、36.58%,差异有统计学意义(P<0.05);2组外周毒性出现的时间、毒性分级比较,差异均有有统计学意义(P<0.05);2组组患者经化疗后正中神经、腓总神经、胫神经的传导速度均可见不同程度的减慢,但观察组减慢的程度明显低于对照组(P<0.05)。结论:自拟通络活血汤配合低频脉冲可有效防治奥沙利铂所引起的外周神经毒性。     

甲钴胺对结直肠癌患者XELOX方案引起的外周神经病变的影响

【目的】探讨甲钴胺对结直肠癌患者XELOX方案引起的外周神经病变的影响。【方法】92例结直肠癌恶性肿瘤术后转化疗的患者,采用随机数字表法将其分为观察组(在传统的XELOX方案化疗的基础上给予甲钴胺治疗,46例)和对照组(采用传统的XELOX方案化疗,46例)。两组均以21 d为一个化疗周期,至少进行3个周期。统计并比较两组患者化疗前及化疗3个周期后的神经传导速度,急性神经毒性发生率、慢性毒性发生率以及其他不良反应发生情况。【结果】化疗前后,两组化疗患者的运动神经传导速度比较,差异均无统计学意义(P>0.05)。化疗前两组化疗患者的感觉神经传导速度比较,差异无统计学意义(P>0.05);化疗后,对照组患者的感觉神经传导速度低于化疗前(P<0.05),观察组化疗前后无明显变化(P>0.05)。两组患者急性神经毒性的发生率比较,差异均无统计学意义(P>0.05)。化疗1、2、3周期后,观察组患者的慢性神经毒性发生率低于对照组(P<0.05)。两组患者的恶心、呕吐、骨髓抑制、全身乏力等不良反应发生率比较,差异均无统计学意义(P>0.05)。【结论】甲钴胺可以有效预防化疗药物对结直肠癌患者的感觉神经的影响,也可有效预防化疗药物导致的慢性神经毒性,但对于化疗药物引起的急性神经毒性效果不明显,使用甲钴胺安全性较好。     

黄芪桂枝五物汤加味预防奥沙利铂神经毒性临床观察

目的:观察黄芪桂枝五物汤加味预防奥沙利铂神经毒性的疗效。方法:56例接受FOLFOX4方案化疗的胃肠道肿瘤患者,治疗组33例接受黄芪桂枝五物汤加味预防,对照组23例接受甲钴铵片预防。结论:4周期后治疗组出现感觉神经经毒性6例,对照组11例,差异有统计学意义(P<0.05)。结论:预防性运用黄芪桂枝五物汤加味能降低奥沙利铂神经毒性的发生率。     

益气温阳通络中药联合氨磷汀预防胃肠道肿瘤患者奥沙利铂神经毒性临床观察

目的:探究益气温阳通络中药联合氨磷汀预防胃肠道肿瘤患者奥沙利铂神经毒性的临床效果。方法:选取2015年1月~2017年5月福建省龙岩市第二医院82例胃肠道恶性肿瘤患者,随机数字表法分组,各41例。2组均予以奥沙利铂、亚叶酸钙、氟尿嘧啶联合化疗方案,对照组给予氨磷汀,实验组给予氨磷汀+益气温阳通络中药,共治疗6个周期。观察2组神经毒性发生情况,对比治疗前后感觉神经传导速度(SCV)、神经传导速度(MCV)。结果:(1)治疗后2个周期、4个周期、6个周期实验组周围神经毒性发生率低于对照组(P0.05),治疗后6个周期实验组周围神经毒性在1~3级所占比例低于对照组(P0.05);(2)治疗前后2组腓神经、正中神经的MCV比较,无显著差异(P0.05),治疗后实验组腓神经、正中神经的SCV高于对照组(P0.05)。结论:益气温阳通络法联合氨磷汀可有效预防胃肠道肿瘤患者奥沙利铂神经毒性,发挥周围神经保护作用。     

TXT+FOLFOX4方案联合沙利度胺治疗晚期胃癌的疗效

目的观察TXT+FOLFOX4方案联合沙利度胺一线治疗晚期胃癌的临床疗效及安全性。方法对36例晚期胃癌患者采用TXT+FOLFOX4方案联合沙利度胺进行治疗,2周为1个周期,化疗4个周期后行疗效评价。结果所有病例均可评价,完全缓解(CR)0例,部分缓解(PR)21例(58.3%),稳定(SD)11例(30.5%),进展(PD)4例(11.1%)。患者出现的主要不良反应为粒细胞减少、外周神经毒性、乏力、贫血、粒细胞减少等。结论 TXT+FOLFOX4方案联合沙利度胺治疗晚期胃癌有较好的疗效,是很好的晚期胃癌一线化疗方案之一。     

雷替曲塞联合奥沙利铂与FOLFOX 4方案治疗中晚期原发性肝癌的疗效评价

目的探讨雷替曲塞联合奥沙利铂(RALOX方案)与5-氟尿嘧啶+亚叶酸钙+奥沙利铂(FOLFOX 4方案)对中晚期原发性肝癌(PLC)的疗效及药物毒性反应。方法选取72例中晚期PLC患者,随机分为RALOX组(n=34)与FOLFOX 4组(n=38)。化疗后每6周评价客观疗效,观察客观缓解率(OR)、疾病控制率(DCR)、中位生存期(mOS)、中位无进展生存期(mPFS)、1年存活率(SR)及毒副反应。结果 RALOX组可评价31例,OR为19.4%,DCR为51.6%,mOS为7.2个月,mPFS为3.4个月,1年SR为22.6%;FOLFOX 4方案组可评价29例,OR为13.8%,DCR为48.3%,mOS为6.9个月,mPFS为3.3个月,1年SR为20.7%,2组差异无有统计学意义(P0.05)。RALOX组消化道反应、肝毒性、心脏毒性、外周神经毒性及手足综合征的发生率均低于FOLFOX 4组,肾毒性、骨髓抑制的发生率2组相当。结论 RALOX方案应用于中晚期PLC患者安全有效,疗效不劣于FOLFOX 4方案且副反应较轻。     

针灸对多发性骨髓瘤患者化疗相关周围神经病变的干预效果

目的 探讨针灸对化疗相关周围神经病变(CIPN)的多发性骨髓瘤(MM)患者生活质量及预后的影响。方法 将符合入选标准的54例MM患者随机分为药物组28例和针灸组26例。采用肌电图(EMG)记录神经传导速度(NCV),评估治疗效果。分别记录2组患者治疗前后运动神经传导速度(MNCV)、感觉神经传导速度(SNCV)及癌症治疗功能评价系统/妇科肿瘤组-神经毒性评价工具量表(FACT/GOG-Ntx)评分。结果 2组治疗后的正中神经和腓总神经MNCV与治疗前比较,差异有统计学意义(P<0.05);药物组治疗后腓浅神经SNCV与治疗前比较,差异有统计学意义(P<0.05)。治疗后,针灸组FACT/GOG-Ntx量表评分下降,差异有统计学意义(P<0.01);药物组治疗后FACT/GOG-Ntx量表评分也有所下降,但差异无统计学意义(P>0.05); 2组治疗后FACT/GOG-Ntx量表评分比较,差异无统计学意义(P>0.05)。结论 针灸是多发性骨髓瘤CIPN的有效干预手段之一,可提高患者的生活质量。     

钙镁合剂联合维生素B_6防治奥沙利铂神经毒性的临床观察

目的:观察钙镁合剂联合维生素B6防治奥沙利铂神经毒性的临床疗效.方法:128例接受FOLFOX4方案化疗的胃癌根治术后患者随机分3组,A组单用维生素B6,B组单用钙镁合剂,C组联用钙镁合剂和维生素B6防治神经毒性.神经症状采用奥沙利铂Levi专用感觉神经毒性分级标准评定.结果:化疗4～6个周期后3组不同药物干预下奥沙利铂神经毒性总发生率分别为A组25/41(60.97%).B组23/37(62.16%),C组17/50(34.00%),C组防治奥沙利铂神经毒性总发生率明显低于其他两组(P＜0.012 5).结论:钙镁合剂联合维生素B6能有效降低奥沙利铂神经毒性的发生率.     

结肠癌患者使用乐沙定重要不良反应的观察与护理

乐沙定(奥沙利铂)是结直肠癌主要化疗药物之一,胃肠道反应及骨髓抑制是化疗药物的常见不良反应,但过敏反应及外周神经毒性是乐沙定相对特有的重要不良反应,本文总结我科结肠癌患者使用乐沙定化疗的过敏反应及外周神经毒性的观察与护理经验。化疗前告知患者相关预防措施,不良反应的临床表现及出现不良反应后的应对措施,化疗过程中应密切观察患者症状及体征,化疗后及时了解患者外周神经毒性。早期预防及发现过敏及外周神经毒性,以便及时治疗及护理。     

加味黄芪桂枝五物汤防治奥沙利铂急性周围神经毒性观察

目的:观察用加味黄芪桂枝五物汤防治奥沙利铂急性周围神经毒性的临床疗效。方法:将80例患者随机分成2组,试验组40例,化疗同时联用加味黄芪桂枝五物汤。对照组40例单用化疗。化疗方案均采用FOLFOX方案,急性周围神经毒性评定参考Levi及赵国光等关于奥沙利铂外周神经毒性评分标准。结果:可评定疗效病例试验组40例,发生奥沙利铂化疗后急性周围神经毒性患者1级10例,2级4例,3级2例,4级0例,发生率约为40.0%。对照组40例,发生急性周围神经毒性1级12例,2级13例,3级8例,4级2例,发生率约为87.5%。2组具有显著性差异(P0.02)。而发生3、4级急性周围神经毒性患者,治疗组和对照组有显著差异(P0.01)。结论:运用加味黄芪桂枝五物汤可以有效预防奥沙利铂引起的急性外周神经毒性。     

2型糖尿病周围神经传导速度与病程及尿清蛋白的关系：附66例报告

目的：了解２例糖尿病病程及尿清蛋白（白蛋白）排泄率对周围神经传导速度的影响。方法：测定６６例２型糖尿病患者的周围神经传导速度,并就其与病程及尿蛋白排泄的关系进行分析。结果：在病程不到５年、５￣１０年和超过１０年的患者的右尺神经感觉电生理异常的发生率分别为７５％、８６％和９２％;右腓肠神经感觉电生理异常分别为７３％、７１％和９２％。而运动神经病变早期多不明显,仅在病程超过１０年的患者中,其神经传导速     

Glycemic control and peripheral nerve conduction in children and young adults after 5-6 mo of IDDM. Wisconsin Diabetes Registry.

OBJECTIVE--A cohort of people (n = 86) was examined in the first few months after insulin-dependent diabetes mellitus (IDDM) diagnosis to evaluate the effect of hyperglycemia on nerve conduction velocities and latencies. RESEARCH DESIGN AND METHODS--Unselected cases with IDDM, who were 6-29 yr of age, were identified at diagnosis from a large, geographically defined area of southern Wisconsin. Peripheral nerve conduction was measured on a sample from this cohort. RESULTS--Peroneal nerve conduction velocity was significantly inversely related to glycosylated hemoglobin (P less than 0.05, age and height adjusted). All other nerve conduction velocities and latencies (median motor, median sensory, and sural) showed the same tendency, but the associations were not statistically significant. Twenty-four-hour urine C-peptide and duration of diabetes (3-11 mo) were not consistently related to nerve conduction parameters after controlling for age and height. CONCLUSIONS--These findings suggest that as early as 5-6 mo after diabetes diagnosis, and at a time frequently characterized by partial remission of IDDM, hyperglycemia has a role in the acute slowing of nerve conduction velocity. Other factors such as residual endogenous insulin production do not appear to influence these early changes.     

Effects of the sulphydryl donor N-acetyl-L-cysteine on nerve conduction, perfusion, maturation and regeneration following freeze damage in diabetic rats

Abstract. Peripheral nerve conduction velocity deficits in diabetic rats depend on decreased nerve perfusion, which may be related to increased free radical activity and impaired endogenous protection by the glutathione redox cycle. We studied the effect of treatment with the glutathione precursor N -acetyl-L-cysteine on nerve conduction, blood flow, maturation and regeneration. Two months of diabetes in mature rats caused 20% and 48% deficits in sciatic motor conduction velocity and endoneurial blood flow, respectively, which were largely corrected by N -acetyl-L-cysteine treatment during the second month. In young non-diabetic rats, sciatic motor conduction velocity increased by 31% over 6 weeks. Diabetes halved the conduction velocity maturation rate, however N -acetyl-L-cysteine treatment allowed a normal pattern of development. After 1 month of treated or untreated diabetes, the sciatic nerve was lesioned by a liquid nitrogen-cooled probe. Myelinated fibre regeneration distance, determined electrophysiologically, was reduced by 12.2% with diabetes; this was prevented by N -acetyl-L-cysteine treatment. Thus, the data stress the importance of free radical-mediated changes in the aetiology of experimental diabetic neuropathy.     

Impact of oxaliplatin-induced neuropathy: a patient perspective

Introduction

Dose-limiting neurotoxicity is a major side effect of oxaliplatin treatment, producing initial acute neurotoxicity and chronic neuropathy with increasing exposure. The improvement in survival for patients with early-stage colorectal cancer treated with oxaliplatin has highlighted the need for valid and reliable assessment of peripheral neuropathy.

Objectives

The objective of this paper was to explore neuropathic symptoms in oxaliplatin-treated patients as assessed using different methods.

Methods

Consecutive symptomatic patients reporting peripheral neuropathy after oxaliplatin chemotherapy for colorectal cancer were interviewed using a semi-structured clinical interview. Neurotoxicity was also assessed using the National Cancer Institute Common Toxicity Criteria scale (clinician-rated), patient ‘self-report’ questionnaires (PNQ), nerve conduction and clinical assessment.

Results

Twenty patients were assessed, 12.6?±?2.8?months after treatment cessation (mean cumulative oxaliplatin dose, 789?mg/m²). In 40% of patients, neurotoxicity necessitated early cessation of treatment. Only 10% of patients were designated by clinicians with severe neurotoxicity, whilst, in contrast, patient interviews and self-report questionnaires described significant physical limitations due to neuropathic symptoms in 60% of patients. The majority (85%) of patients had objective evidence of sensory neuropathy with nerve conduction studies. Reports from clinical interviews were strongly correlated with patient self-assessment (Pearson coefficient?=?0.790, p?Conclusion Given the discrepancies in symptom prevalence highlighted by these findings, the monitoring of oxaliplatin-induced neurotoxicity would benefit from more informative clinical assessment, with inclusion of patient-reported outcome measures. Such an approach would be beneficial in a clinical trial setting to monitor the efficacy of interventions and in prospective studies of survivorship to determine the true burden of peripheral neuropathy in oxaliplatin-treated patients.     

Peripheral nerve function is increasingly impaired during puberty in adolescents with type 1 diabetes

OBJECTIVE--To evaluate the impact of puberty on peripheral nerve function in adolescents with type 1 diabetes. RESEARCH DESIGN AND METHODS--Of 138 eligible patients with type 1 diabetes, 100 patients (age >9 years and diabetes duration >2 years) attending an outpatient diabetes clinic and 100 age- and sex-matched healthy control subjects took part in this cross-sectional study. Peripheral motor and sensory nerve conduction tests, cardiovascular reflex tests on the autonomic nervous system, and measurements of vibration-perception threshold (VPT) were performed. RESULTS--Nerve conduction velocity (NCV) in the distal motor and sensory nerves, the motor nerve distal latency, and the sensory nerve action potential (SNAP) amplitude were impaired in the adolescent patients with type 1 diabetes. The deterioration in motor NCV, H-reflex latency, and SNAP amplitude became more conspicuous in late puberty and postpuberty and was related to poor metabolic control. A total of 10 patients had distal diabetic polyneuropathy (DP) neurophysiologically, and these patients had significantly lower heart-rate variation in the deep breathing test than the other patients. Three of the patients with DP had peripheral neurological signs or symptoms. A slight difference in the VPT between the patients and control subjects was observed after puberty. CONCLUSIONS--Increasing subclinical motor nerve impairment can be detected during late puberty and after puberty, and sensory NCV and SNAP amplitude are reduced in adolescents with type 1 diabetes. Poor metabolic control during puberty appears to induce deteriorating peripheral neural function in young patients with type 1 diabetes.     

α-硫辛酸联合甲钴胺治疗糖尿病周围神经病变疗效评估

目的评估α-硫辛酸联合甲钴胺治疗糖尿病周围神经病变的临床疗效.方法选择并发糖尿病周围神经病变的2型糖尿病患者90例,分为甲钴胺组、硫辛酸组、硫辛酸联合甲钴胺组,每组各30例,分别予静脉应用甲钴胺、硫辛酸或硫辛酸联合甲钴胺治疗.3周为1个疗程.观察治疗1周、2周、3周后的神经症状总评分(TSS)的变化,并观察治疗前后神经传导速度的变化.结果治疗3周后三组TSS评分及神经传导速度均较治疗前明显改善,硫辛酸组TSS评分下降较甲钴胺组明显,联合治疗组的TSS评分下降及神经传导速度增加较甲钴胺组及硫辛酸组更显著.结论α-硫辛酸和甲钴胺联合用药能有效地改善糖尿病周围神经病变的的症状及神经传导速度,且明显优于单一用药.     

一氧化氮合酶抑制剂促进大鼠坐骨神经再生的电生理实验研究

目的研究一氧化氮合酶抑制剂（L—NAME）对横断的大鼠坐骨神经再生的促进作用。方法取SD大鼠40只随机平均分成4组。剪断右侧坐骨神经总于，两断端的神经外膜缝合。实验组给以L-NAME，剂量为10mg／kg体重，用生理盐水（SAL）稀释至100μl。对照组给药方式与第一组相同，给以D-NAME。将获得的各组动物实验侧MCV及PR分别与对照侧数据作比率，获得的比值在实验组和对照组间进行t检验。结果实验组明显优于对照组。结论L-NAME对周围神经损伤再生有明显加强作用。     

空气波压力治疗仪在改善老年糖尿病病人周围神经病变中的作用

[目的]探讨空气波压力治疗仪在老年糖尿病病人周围神经病变中的作用。[方法]将80例糖尿病周围神经病变病人随机分为治疗组和对照组,两组各40例,两组采用常规降糖并给予凯时、弥可保治疗。治疗组在此基础上加用空气波压力治疗仪治疗。观察治疗前后感觉减退、麻木、疼痛及肌电图神经传导速度改善情况。[结果]在肢端麻木、感觉减退、疼痛的改善及肌电图传导速度上,治疗组优于对照组（P〈0．05）。[结论]空气波压力治疗仪能明显改善糖尿病周围神经病病人肢体麻木、感觉减退症状,减轻疼痛及改善神经传导速度,提高病人生活质量。     

Preventing paclitaxel-induced peripheral neuropathy: a phase II trial of vitamin E supplementation

A randomized, controlled trial was performed to assess the efficacy and safety of vitamin E supplementation for prophylaxis against paclitaxel-induced peripheral neuropathy (PIPN). Thirty-two patients undergoing six courses of paclitaxel-based chemotherapy were randomly assigned to receive either chemotherapy with vitamin E (300 mg twice a day, Group I) or chemotherapy without vitamin E supplementation (Group II). A detailed neurological examination and electrophysiological study was performed during and 3 months after chemotherapy. The severity of PIPN was summarized by means of a modified Peripheral Neuropathy (PNP) score. The incidence of neurotoxicity differed significantly between groups, occurring in 3/16 (18.7%) patients assigned to the vitamin E supplementation group and in 10/16 (62.5%) controls (P=0.03). The relative risk (RR) of developing PIPN was significantly higher in controls than in vitamin E group patients (RR=0.3, 95% confidence interval (CI)=0.1-0.9). Mean PNP scores were 2.25+/-5.1 (range 0-15) for patients in Group I and 11+/-11.63 (range 0-32) for those in Group II (P=0.01). Vitamin E supplementation was well tolerated and showed an excellent safety profile. This study shows that vitamin E effectively and safely protects patients with cancer from the occurrence of paclitaxel-induced peripheral nerve damage. A double-blind, placebo-controlled trial is needed to confirm these results.