糖尿病亚临床周围神经病变与病程、糖基化血红蛋白的关系

目的:探讨糖尿病亚临床周围神经病变与糖尿病病程及糖基化血红蛋白的关系。方法:选取102例无下肢周围神经病变症状、体征的糖尿病患者,对其进行周围神经传导速度、体感诱发电位检测,诊断糖尿病亚临床周围神经病变,并统计分析其与糖尿病病程及糖基化血红蛋白的关系。结果:102例中有37例患者周围神经传导速度和体感诱发电位检测异常,并与病程、糖基化血红蛋白含量有一定关系(P<0.01和P<0.05)。结论:检测糖尿病患者周围神经传导速度、体感诱发电位可以早期诊断亚临床型周围神经病变,且病程越长、糖基化血红蛋白越高,亚临床型周围神经病变发病率越高。     

2型糖尿病患者周围神经传导速度分析

目的:2型糖尿病患者周围神经病变的神经电生理特点。方法:对200例2型糖尿病患者周围神经进行传导速度检测并分析。结果:神经传导速度(NCV)异常检出率63.3%,其中感觉神经(SCV)异常(检出率73.2%)高于运动神经(MCV)异常(检出率53.3%)(P<0.01);下肢NCV异常(检出率78.6%)高于上肢NCV异常(,检出率48.6%)(P<0.01)。结论:NCV检测有助于糖尿病周围神经病变的早期诊断,值得临床进一步研究。     

72例糖尿病并发周围神经病变的回顾性分析

目的 总结糖尿病并发周围神经病变治疗措施,提高的临床诊疗效率.方法 回顾自2009年2月至2011年8月内分泌科收治的268例糖尿病患者,其中72例糖尿病并发周围神经病变,分析总结治疗糖尿病并发周围神经病变的临床诊疗措施.结果 72例糖尿病并发周围神经病变患者,疗效满意68例,2例疗效一般,2例无效,总治疗有效率97.22%.结论 有效控制血糖,早期防范糖尿病患者周围神经病变是降低糖尿病并发周围神经病变的关键.     

382例糖尿病患者神经传导速度检测分析

糖尿病(DM)引起神经系统损害是糖尿病的常见并发症。糖尿病患者一旦出现症状性周围神经病变,5～10年的病死率明显升高,可达25%～50%。若对糖尿病周围神经病变及早明确诊断并给予有效治     

60例糖尿病患者运动及感觉神经传导速度的分析

６０例糖尿病患者运动及感觉神经传导速度的分析广西区人民医院肌电图室张丽香糖尿病神经病变是糖尿病患者最常见的临床并发症之一，其中以周围神经损害症状最多见（１，２）。我们对６０例临床确诊糖尿病的患者进行神经传导速度（ＮＣＶ）测定，旨在为临床早期发现和诊断...     

早期糖尿病性周围神经病变的临床特点与治疗

目的:探讨早期糖尿病性周围神经病变的临床特点与治疗方法和效果。方法:回顾性分析糖尿病性周围神经病变患者120例的临床资料。结果:糖尿病周围神经病变临床特征包括烧灼、疼痛、感觉异常、过敏等,经过综合治疗后,总有效率90.0%。同时治疗前与治疗后正中神经传导(MCV、SCV)差异有统计学意义(P<0.05)。结论:糖尿病周围神经病变临床特征多样,预后差,综合治疗可明显改善糖尿病周围神经病变的症状,确切疗效,值得临床推广。     

糖尿病性周围神经病变的神经电生理分析

糖尿病性周围神经病变是糖尿病常见的并发症。本文分析 6 8例糖尿病人神经电生理变化 ,以探讨其对糖尿病性周围神经病变的诊断价值。1 资料与方法本文 6 8例糖尿病均经临床确诊 ,其中Ⅰ型 7例 ,Ⅱ型 6 1例。男 43例 ,女 2 5例 ,年龄 2 6～ 72岁 ,平均 48岁。糖尿病病程 6月～ 2 0年 ,平均 6 .8年。临床诊断为糖尿病性周围神经病变者 38例 ,均有不同程度的四肢远端麻木、无力和烧灼感 ;查体 :有手套、袜套样感觉障碍者 2 9例 ,轻度肌萎缩者 8例 ,无周围神经临床症状者 30例。均排除其它原因所致的周围神经损害。神经传导速度测定分别选用正中…     

糖尿病周围神经病变的诊断和治疗新进展

糖尿病周围神经病变是糖尿病最常见的慢性并发症,严重影响患者的生活质量,早期诊断、早期治疗是降低糖尿病周围神经病变病残程度,提高患者生活质量的关键。临床症状和肌电图检查能提高临床的诊断率,其治疗涉及多个层面,包括针对病因和病理生理机制的治疗措施,症状控制的方案,预防和治疗神经病变引起的其他器官系统的并发症等。     

丁咯地尔治疗糖尿病神经病变30例疗效观察

糖尿病周围神经病变是糖尿病患者的一种常见并发症，发病率高达60％-90％，而糖尿病末梢神经病变是糖尿病周围神经病变中最常见者，目前这种并发症尚无特异的治疗措施。我院应用丁咯地尔治疗糖尿病末梢神经病变有确切的疗效。现将结果报告如下。[第一段]     

神经传导速度及H反射测定对2型糖尿病周围神经病变的诊断价值

目的:探讨神经传导速度及H反射测定对2型糖尿病周围神经病变的诊断价值。方法:对477例2型糖尿病患者进行神经传导速度及H反射测定,同时与病程进行相关分析。结果:NCV异常率为61.43%,以下肢腓肠神经损害最为常见;H反射异常率为70.23%,高于NCV异常率;NCV异常率、H反射异常率均与病程呈正相关。结论:NCV和H反射对2型糖尿病周围神经病变具有重要的早期诊断价值,两者可互为补充,提高2型糖尿病周围神经病变的诊断率。     

α-硫辛酸联合神经妥乐平治疗糖尿病周围神经病变的临床观察

目的探讨α-硫辛酸联合神经妥乐平治疗糖尿病周围神经病变临床疗效。方法随机将糖尿病周围神经病变患者160例分为观察组和对照组,并分别给予α-硫辛酸联合神经妥乐平和神经妥乐平治疗,疗程2周,对两组患者治疗前后症状和神经传导速度（NCV）测定进行比较。结果正中神经、腓总神经、胫神经的MCV和SCV均显著高于治疗前（P〈0．05）,且观察组在治疗后MCV和SCV传导速度均好于对照组（P〈0．05）,观察组有效34例,基本有效43例,无效4例,总有效率达96．25％,显著高于对照组66．25％（P〈0．01）。结论α-硫辛酸联合神经妥乐平治疗糖尿病周围神经病变,提高神经传导速度,疗效显著,且无明显不良反应,值得临床推广。     

α-硫辛酸联合甲钴胺注射液治疗糖尿病周围神经病变临床价值分析

目的探讨α-硫辛酸联合甲钴胺注射液治疗糖尿病周围神经病变临床疗效。方法选择我院2007年9月～2009年11月收治的糖尿病周围神经病变患者86例,随机分为观察组和对照组,每组各43例,分别给予α-硫辛酸联合甲钴胺注射液和甲钴胺注射液治疗,疗程为2周,对两组患者治疗前后症状和神经传导速度测定进行比较。结果治疗2周后两组肌电图显示正中神经、腓总神经、胫神经的运动神经传导速度（MCV）和感觉神经传导速度（SCV）均显著高于治疗前（P〈0.05）,且观察组在治疗后MCV和SCV传导速度均好于对照组（P〈0.05）。观察组显效17例,有效24例,无效2例,总有效率达95.3%,显著高于对照组60.5%（P〈0.01）。结论α-硫辛酸联合甲钴胺治疗糖尿病周围神经病变,效果显著,安全可靠,值得临床推广。     

尼莫地平对糖尿病周围神经病变48例治疗效果观察

目的：观察尼莫地平口服对糖尿病周围神经病变的治疗效果。方法：采用尼莫地平口服治疗糖尿病周围神经病变患者48例，观察其治疗前后临床症状及肌电图的改变。结果：用尼莫地平口服治疗6月后临床症状有所改善，肌电图有明显改善（P＜0．05）。结论：尼莫地平对早期糖尿病周围神经病变的治疗是安全、有效的。     

The prevalence of diabetic peripheral neuropathy in an outpatient setting

This study was undertaken to clinically estimate the prevalence of diabetic peripheral neuropathy amongst patients attending an outpatient clinic and to evaluate their risk factors for developing peripheral neuropathy. It was a cross-sectional study of 134 diabetes mellitus patients who attended the Primary Care Clinic, University Hospital, Kuala Lumpur. The patients were interviewed for their demographic data, past and present medical/surgical history, social history, personal habits and symptoms of peripheral neuropathy. Foot examination and clinical neurological tests were conducted and the presence of peripheral neuropathy was assessed. The main outcome measures were the Neuropathy Symptom Score and the Neuropathy Disability Score. The prevalence of diabetic peripheral neuropathy was found to be 50.7%. Peripheral neuropathy was related to the age of the patient and the duration of diabetes but did not seem to be significantly related to diabetic control. To conclude, there was a high prevalence of peripheral neuropathy amongst the diabetics in this study. These patients developed peripheral neuropathy at a younger age and shorter duration of diabetes compared to a similar study that was done in the UK.     

弥可保、凯时和金纳多联合治疗老年糖尿病周围神经病变的临床观察

目的了解弥可保、凯时和金纳多联合治疗在改善糖尿病患者周围神经疼痛及感觉异常方面的作用,为临床治疗糖尿病周围神经病变提供参考。方法以老年Ⅱ型糖尿病患者伴周围神经病变为研究对象,给予弥可保、凯时和金纳多联合治疗,动态观察患者的局部神经疼痛、感觉异常和神经传导速度的改善情况。结果共纳入54例临床诊断为Ⅱ型糖尿病伴周围神经病变的患者。在给予联合治疗4周后,54例患者中分别有24例（44.4%）和25例（46.3%）患者的局部自发痛或（和）感觉异常缓解程度达到了临床显效和有效的标准,而仅5例（9.3%）患者的局部不适无改善。结论弥可保、凯时和金纳多联合治疗对改善老年糖尿病周围神经病变疗效显著。     

四藤一仙汤熏洗预防奥沙利铂所致周围神经毒性的临床观察

目的?观察四藤一仙汤熏洗对奥沙利铂所致周围神经毒性的预防作用。方法?选择需要接受含奥沙利铂方案化疗的结直肠癌患者150例,随机分为2组,每组75例。预防治疗组在接受化疗同时采用四藤一仙汤熏洗手足,每次40?min,每日2次;对照组只接受化疗,2组患者均至少接受2个疗程化疗。化疗结束后1月评估其周围神经毒性发生及分级情况,评价其预防作用。结果?预防治疗组、对照组周围神经毒性发生率分别为18.7%和56.0%,差异显著（P<0.01）;预防治疗组和对照组周围神经毒性分级的平均秩次分别是60.63和90.37,预防治疗组周围神经毒性的分级明显低于对照组,有统计学意义（P<0.05）;在发生2级及以上周围神经毒性的患者中,预防治疗组和对照组患者奥沙利铂累积剂量分别是1?054.76±124.6,823.47±190.67,差异具有统计学意义（P<0.05）;Logisitic回归分析发现,中药熏洗是周围神经毒性发生的保护因素。结论?四藤一仙汤熏洗可以降低奥沙利铂所致周围神经毒性发生率、减轻其发生的严重程度,提高患者耐受奥沙利铂化疗累积量,且是周围神经毒性发生的独立保护因素。      

65例糖尿病周围神经病变患者运动及感觉神经传导速度测定及其诊断价值分析

目的:探究运动及感觉神经传导速度测定在诊断糖尿病周围神经病变(DPN)上的临床价值.方法:将65例DPN患者作为观察组,并选择同期在我院体检的无DPN的糖尿病患者65例作为对照组.对比两组的运动、感觉神经传导速度(MNCV、SNCV),从空腹血糖和病程入手,分析神经传导速度与空腹血糖和病程的相关性,并就其MNCV和SNCV在各神经的异常情况进行比较.结果:观察组在尺神经、正中神经、腓总神经上的MNCV及SNCV水平均明显低于对照组.在尺神经、正中神经和腓总神经MNCV以及SNCV上,空腹血糖在7mmol/L以上的患者与空腹血糖低于7mmol/L的患者相比并未见明显差异,而病程5年以上者与病程5年以下者存在明显差异.同时,观察组患者SNCV在尺神经、正中神经、腓总神经上异常率分别为60.00%、56.92%、69.23%,明显高于MNCV(分别为41.54%、38.46%、50.77%).结论:MNCV及SNCV与DPN患者的病程长短呈现正相关.在诊断DPN上,SNCV的敏感性优于MNCV,二者的测定对其早期诊断具有重要意义.     

Assessing taxane-associated adverse events using the FDA adverse event reporting system database

Background:Taxanes are an essential class of antineoplastic agents used to treat various cancers and are a fundamental cause of hypersensitivity reactions. In addition, other adverse events, such as bone marrow toxicity and peripheral neuropathy, can lead to chemotherapy discontinuation. This study aimed to evaluate the safety of taxanes in the real world.Methods:Taxane-associated adverse events were identified by the Medical Dictionary for Regulatory Activities Preferred Terms and analyzed and compared by mining the US Food and Drug Administration Adverse Event Reporting System pharmacovigilance database from January 2004 to December 2019. Reported adverse events, such as hypersensitivity reaction, bone marrow toxicity, and peripheral neuropathy, were analyzed with the following signal detection algorithms: reporting odds ratio (ROR), proportional reporting ratio (PRR), multi-item gamma Poisson shrinker (MGPS), Bayesian confidence propagation neural network (BCPNN), and logistic regression methods. Adverse outcome events and death outcome rates were compared between different taxane groups using Pearson''s χ² test, whereas significance was determined at P < 0.05 with a 95% confidence interval (CI).Results:A total of 966 reports of hypersensitivity reactions, 1109 reports of bone marrow toxicity, and 1374 reports of peripheral neuropathy were analyzed. Compared with paclitaxel and docetaxel, bone marrow toxicity following the use of nab-paclitaxel had the highest ROR of 6.45 (95% two-sided CI, 6.05–6.88), PRR of 5.66, (χ² = 4342.98), information component of 2.50 (95% one-sided CI = 2.34), and empirical Bayes geometric mean of 5.64 (95% one-sided CI = 5.34). Peripheral neuropathy following the use of nab-paclitaxel showed a higher ROR of 12.78 (95% two-sided CI, 11.55–14.14), PRR of 12.16 (χ² = 4060.88), information component of 3.59 (95% one-sided CI = 3.25), and empirical Bayes geometric mean of 12.07 (95% one-sided CI = 11.09).Conclusions:The results showed that bone marrow toxicity and peripheral neuropathy were the major adverse events induced by taxanes. Nab-paclitaxel exhibited the highest potential for taxane-associated adverse events. Further research in the future is warranted to explain taxane-associated adverse effects in real-world circumstances.     

MBK neuropathy among spray painters.

It has been suggested that the solvent methyl N-butyl ketone (MBK) may cause peripheral neuropathy in humans. An investigation was undertaken after two cases of peripheral neuropathy among spray painters at one work site were reported to the National Institute for Occupational Safety and Health. Twenty-six painters were interviewed and examined. Two were found to have definite peripheral neuropathy and one had a probable case. Although one of these men had been exposed to lead in the past, there are strong reasons to believe that MBK was responsible for his neuropathy. There was nothing to suggest excessive lead absorption in the other two men.     

Peripheral neuropathy: pattern recognition for the pragmatist

Long lists of causes of peripheral neuropathy make peripheral nerve disease a dry and uninspiring subject. A simple scheme based on the answers to just six questions should enable the clinician to recognise characteristic patterns, investigate relevant subgroups appropriately, and identify treatable disorders quickly: which systems are involved? What is the distribution of weakness? What is the nature of the sensory involvement? Is there any evidence of upper motor neuron involvement? What is the temporal evolution? Is there any evidence for a hereditary neuropathy? Standard screening investigations suffice for the common length dependent axonal neuropathies while complex presentations need more detailed investigations targeted to their clinical phenotype.