硫辛酸联合甲钴胺治疗糖尿病周围神经病变30例疗效观察

糖尿病周围神经病变（diabetic peripheralneuropathy,DPN）是糖尿病常见的慢性并发症之一。目前,对于DPN的发病机制尚未完全阐明,故无特异性治疗手段。本研究采用硫辛酸联合甲钴胺治疗DPN取得良好疗效。现报告如下。     

几种新型小分子核糖核酸与类风湿性关节炎关系的研究进展

目的:为临床治疗类风湿性关节炎(RA)提供思路和参考。方法:以"小分子核糖核酸""类风湿关节炎""microRNAs""miRNAs"等为关键词,组合查询2006-2013年万方数据库和PubMed数据库中有关小分子核糖核酸(microRNAs或miRNAs)和RA的研究文献,对miRNAs在RA中的研究进展进行综述。结果与结论:共查询到文献130篇,其中有效文献29篇。共有11种miRNAs和RA关系的研究,包括miRNA-221/222、miRNA-323-3p、miRNA-146a、miRNA-155、miRNA-223、miRNA-24、miRNA-26a、miRNA-125a-5p、miRNA-18a、miRNA-34a、miRNA-203等。其在人RA或动物RA模型的滑膜组织或滑膜细胞中均有不同程度的表达;加强对miRNAs与RA关系的研究,对明确RA的发病机制具有重要意义,同时也可为临床提供治疗或诊断的潜在靶点。     

前列腺素E_1脂微球制剂治疗糖尿病周围神经病变的疗效观察

糖尿病周围神经病变(DPN)是糖尿病常见的慢性并发症，因其发病机制不确切，目前缺乏特异性治疗。本文观察了前列腺素E1脂微球制剂(Lipo PGE1，商品名凯时)治疗DPN的疗效。报告如下：     

miRNA-140在骨性关节炎中的研究进展

骨性关节炎(OA)是伴随疼痛和关节运动障碍的一种以关节软骨退变和关节周围形成骨质增生为病理特征的慢性进行性骨关节病。临床治疗往往不能令人满意。在OA治疗新进展中基因网络得到广泛研究,尤其是MicroRNA在OA的发病机制过程中有所表达并具有调控降解和修复等作用。该文通过miRNA结构功能;miRNA-140在OA的发病中调控机制、作用靶点以及miRNA-140在骨生长板的作用机制结合近几年的国内外研究做一综述。     

糖尿病周围神经病变的危险因素分析

糖尿病周围神经病变(DPN)是糖尿病常见的慢性并发症之一,其确切的发病机制尚未完全阐明,临床上也缺少有效的治疗手段.本研究通过对我院收治的252例糖尿病合并周围神经病变的情况进行分析.以期找出影响DPN发病的危险因素,为临床治疗与预防提供参考.     

糖尿病周围神经病变发病机制研究进展

糖尿病周围神经病变（diabetic peripheral neuropathy,DPN）是糖尿病最常见的慢性并发症之一。目前已发现糖代谢异常、脂代谢异常、微血管病变等可以导致DPN的发生。同时,Schwann细胞学说、免疫因素、神经生长因子及维生素缺乏等也被认为是DPN的发病机制。     

糖尿病外周神经病变的诊断和治疗

糖尿病外周神经病变(DPN)是糖尿病主要的慢性并发症之一,较为常见,也是糖尿病足的主要危险因素之一。早期诊断和治疗DPN对于改善糖尿病的预后,提高患者的生活质量,延长生存周期有着非常重大的意义。本文结合国内外DPN指南,介绍其发病机制、筛查、诊断及治疗方法。     

糖尿病周围神经病的研究进展

糖尿病周围神经病（diabetic pefipheral neuropathy,DPN）是糖尿病常见的慢性并发症之一,约50％以上的糖尿病患者合并有多发性神经病。DPN起病隐袭,1型糖尿病周围神经病变主要表现为自主神经障碍和疼痛,2型糖尿病周围神经病变则多表现为远端感觉障碍和元力。病理改变主要表现为周围神经的脱髓鞘和（或）轴索变性。由于DPN临床表现多样、发病机制复杂,且一旦出现症状治疗效果不佳,其早期诊断对病情的控制及进一步治疗具有重要意义。神经电生理检查是检测DPN的重要手段,它客观、敏感,有助于发现亚临床病变,是目前DPN早期诊断的关键。本文就近年对DPN的发病机制及电生理表现方面的研究进展综述如下。1发病机制①血管学说：对糖尿病患者神经活检和动物模型的研究都表明糖尿病时微血管内皮细胞肿胀、增生,以致管壁增厚、管腔狭窄、血管阻力增加,造成神经低灌注和神经内膜缺氧,     

2型糖尿病周围神经病变机制研究进展

糖尿病周围神经病变(DPN)是糖尿病患者常见的慢性并发症。2型糖尿病DPN发病机制尚未完全清楚,是由多种因素综合作用的结果。其中,高糖参与的外周神经损伤机制包括线粒体功能障碍及氧化应激、多元醇通路激活、晚期糖基化终产物、硝基化反应、内质网应激等。血脂紊乱的影响机制包括氧化和糖基化低密度脂蛋白、FFA、脂类介质、氧化型胆固醇等。另外,代谢性炎症、胰岛素抵抗、神经滋养血管病变、神经营养因子、外周神经的解剖学特点均参与其中,组成了复杂而相互关联的发病机制。因此,2型糖尿病DPN需要从多靶点进行综合治疗。该文对相关发病机制进行了系统综述。     

糖尿病周围神经病变的发病机制和临床诊疗进展

糖尿病周围神经病变(DPN)是糖尿病最常见的慢性并发症之一,其发病率高,受累神经广泛,症状持续时间长,严重影响患者的生活质量。近年来,随着糖尿病及其并发症研究的进展,使我们对DPN的发病机制有了更深入的了解,从而推动了临床诊断和治疗的进程。现综述如下。     

MicroRNA-29: a potential therapeutic target for systemic sclerosis

Introduction: Systemic sclerosis (SSc) is a systemic autoimmune disease of unknown cause characterized by microvasculopathy, fibroblast activation, and excessive production of collagen, causing tissue and organ damage. Effective medical treatment for SSc is lacking because the etiology and pathogenesis of SSc are not fully understood. MicroRNAs (miRNAs) are endogenous, regulatory, single-stranded, noncoding RNAs that negatively modulate gene expression by either promoting the degradation of mRNA or down-regulating the protein production by translational repression. Among them, miRNA-29 is recently discovered as a class of miRNAs which is related to fibrotic disease. Numerous evidences have confirmed that miRNA-29 involved in the expression of extracellular matrix (ECM) and regulated organ fibrosis. These findings revealed a potential and appealing role for miRNA-29 as SSc therapeutic targets. Areas covered: This review provides a comprehensive view on the biogenesis and functions of miRNAs. We also discuss the aberrant expression of miRNA-29 in SSc, and summarize current understanding of miRNA-29 involved in the process of fibrosis. Finally, we discuss the therapeutic potential of targeting miRNA-29 in SSc. Expert opinion: Although the exact pathogenesis of SSc still remains to be clarified, Targeting miRNA-29 may serve as a promising therapy strategy.     

AGE-RAGE系统与糖尿病足综合征的发病机制及治疗进展

糖尿病足综合征（DFS）是糖尿病严重慢性并发症之一,其发病机制至今尚未完全阐明。晚期糖基化终末产物（AGEs）的形成参与DFS的发生、发展,AGEs与AGEs受体（RAGE）相互作用,并通过一系列分子机制导致糖尿病神经病变和外周血管病变。因此,抑制AGEs形成或阻断AGEs与其受体相互作用可以延缓糖尿病足的发生、发展。本文就AGEs形成、AGE-RAGE系统在DFS中的作用和DFS的治疗进展等作一综述。     

Clinical value of tapentadol extended-release in painful diabetic peripheral neuropathy

Painful diabetic peripheral neuropathy is difficult to treat, partially because the underlying mechanism of pain is not fully understood. Various treatment guidelines recommend first-line agents, such as α2-δ ligands, serotonin-norepinephrine reuptake inhibitors, and tricyclic antidepressants but combination therapy of alternative agents including opiates is often warranted. Tapentadol extended-release has a novel dual mechanism of action; it is both a mu-opioid receptor agonist and a norephinephrine reuptake inhibitor. It has been in the spotlight since it was FDA-approved specifically for the treatment of painful diabetic peripheral neuropathy in 2012. Previous reviews of tapentadol have focused on chronic pain. The purpose of this review article is to assess the efficacy and safety of tapentadol extended-release in adult populations with painful diabetic peripheral neuropathy and provide guidance for formulary decisions.     

MicroRNA-29: a potential therapeutic target for systemic sclerosis

Introduction: Systemic sclerosis (SSc) is a systemic autoimmune disease of unknown cause characterized by microvasculopathy, fibroblast activation, and excessive production of collagen, causing tissue and organ damage. Effective medical treatment for SSc is lacking because the etiology and pathogenesis of SSc are not fully understood. MicroRNAs (miRNAs) are endogenous, regulatory, single-stranded, noncoding RNAs that negatively modulate gene expression by either promoting the degradation of mRNA or down-regulating the protein production by translational repression. Among them, miRNA-29 is recently discovered as a class of miRNAs which is related to fibrotic disease. Numerous evidences have confirmed that miRNA-29 involved in the expression of extracellular matrix (ECM) and regulated organ fibrosis. These findings revealed a potential and appealing role for miRNA-29 as SSc therapeutic targets.

Areas covered: This review provides a comprehensive view on the biogenesis and functions of miRNAs. We also discuss the aberrant expression of miRNA-29 in SSc, and summarize current understanding of miRNA-29 involved in the process of fibrosis. Finally, we discuss the therapeutic potential of targeting miRNA-29 in SSc.

Expert opinion: Although the exact pathogenesis of SSc still remains to be clarified, Targeting miRNA-29 may serve as a promising therapy strategy.     

糖尿病周围神经病变患者尿代谢组学研究

目的：采用气相色谱-质谱联用技术（GC/MS）技术,分析糖尿病周围神经病变患者尿液中小分子代谢物,为糖尿病周围神经病变的发生机制和早期诊断提供代谢水平上的依据。方法：采用气相色谱-质谱联用技术（GC/MS）检测40例正常人（正常组）、20例单纯糖尿病患者（单纯组）以及40例糖尿病周围神经病变患者（合并组）的尿液样本中小分子代谢物。采用主成分分析法（PCA）和偏最小二乘法判别分析方法（PLS-DA）观察正常组、单纯组以及合并组的代谢谱的变化。结果：正常组和单纯组的代谢谱区分良好,正常组和合并组的代谢谱也能良好的区分。利用Wiley和NIST等数据库筛选和及本实验室建立的标准品代谢物谱库,鉴定了17个与糖尿病周围神经病变密切相关的潜在生物标志物。经过代谢通路分析,糖尿病周围神经病变患者体内存在牛磺酸和亚牛磺酸代谢、甘氨酸、丝氨酸和苏氨酸代谢等代谢异常。结论：糖尿病周围神经病变发生与牛磺酸和亚牛磺酸代谢、甘氨酸,丝氨酸和苏氨酸代谢等代谢异常有关,尿液中鉴定的代谢物有望成为糖尿病周围神经病变诊断的潜在生物标志物。     

Mechanisms and pharmacology of diabetic neuropathy – experimental and clinical studies

Neuropathic pain is the most common chronic complication of diabetes mellitus. The mechanisms involved in the development of diabetic neuropathy include changes in the blood vessels that supply the peripheral nerves; metabolic disorders, such as the enhanced activation of the polyol pathway; myo-inositol depletion; and increased non-enzymatic glycation. Currently, much attention is focused on the changes in the interactions between the nervous system and the immune system that occur in parallel with glial cell activation; these interactions may also be responsible for the development of neuropathic pain accompanying diabetes. Animal models of diabetic peripheral neuropathy have been utilized to better understand the phenomenon of neuropathic pain in individuals with diabetes and to define therapeutic goals. The studies on the effects of antidepressants on diabetic neuropathic pain in streptozotocin (STZ)-induced type 1 diabetes have been conducted. In experimental models of diabetic neuropathy, the most effective antidepressants are tricyclic antidepressants, selective serotonin reuptake inhibitors, and serotonin norepinephrine reuptake inhibitors. Clinical studies of diabetic neuropathy indicate that the first line treatment should be tricyclic antidepressants, which are followed by anticonvulsants and then opioids. In this review, we will discuss the mechanisms of the development of diabetic neuropathy and the most common drugs used in experimental and clinical studies.     

Management of painful diabetic neuropathy

The commonest cause of peripheral neuropathy is diabetes and pain occurs in ～ 30% of diabetic patients with neuropathy. It is extremely distressing for the patient and poses significant difficulties in management, as no treatment to date provides total relief and the side effects of therapy limit dose titration. Understanding the pathogenesis of diabetic neuropathy may lead to the development of new treatments for preventing nerve damage. Furthermore, a better understanding of the mechanisms that modulate pain may lead to more effective relief of painful symptoms. This review provides an update on the assessment and treatment of painful diabetic neuropathy.     

2型糖尿病末梢神经病变影响因素探讨

目的探讨糖尿病末梢神经病变影响因素及与其他慢性并发症的关系。方法选择我院 2型糖尿病住院病人 2 4 5例 ,按是否合并末梢神经病变分为两组 ,观察其年龄、病程、体重指数、空腹血糖 (FBG)、餐后 2小时血糖 (2hPBG)、糖化血红蛋白 (HbA1 c)、甘油三脂、胆固醇及其糖尿病肾病、糖尿病视网膜病变、冠心病的发生率。结果糖尿病末梢神经病变组FBG、2hPBG、HbA1 c较对照组明显增高 (P <0 .0 5或P <0 .0 1 ) ,病程明显延长 (P <0 .0 1 )。其合并糖尿病肾病 ,糖尿病视网膜病变及冠心病的发生率亦高于对照组 (P <0 .0 5或P <0 .0 1 )。结论长期血糖控制不良为糖尿病末梢神经病变的危险因素 ;糖尿病末梢神经病变与其他慢性并发症关系密切     

痛性糖尿病周围神经病变患者的药物治疗方案探讨

目的：介绍痛性糖尿病周围神经病变的治疗药物,为临床个体化治疗方案提供参考。方法：查阅最新研究文献、2010年后全球发布的5种糖尿病周围神经病变诊治指南,对比不同指南的差异,分析药物治疗的作用机制、用法、效果、不良反应等。结果：度洛西丁、普瑞巴林、加巴喷丁和三环类抗抑郁药是痛性糖尿病周围神经病变主要的治疗药物,但仍需依据患者的具体情况如是否伴有睡眠障碍、肥胖、肝肾功能等患者特点选择治疗药物。一线的单药治疗方案不能为患者提供疼痛缓解时,可采用换药、联合用药等二线、三线治疗方案。结论：痛性糖尿病周围神经病变发病机制复杂,在严格控制血糖的前提下,应依据患者特点选择最合适的治疗方案。     

依帕司他的药理作用及临床应用

依帕司他是目前唯一上市的醛糖还原酶特异性抑制剂,通过阻断多元醇通路而发挥作用。依帕司他可减轻糖尿病个体的氧化应激,并抑制蛋白非酶糖化。依帕司他主要用以治疗糖尿病神经病变,不仅对糖尿病周围神经病变有效,而且对自主神经病变也有效。依帕司他对糖尿病大血管病变、糖尿病肾病等也有一定的治疗作用,还能增加糖尿病病人中性粒细胞氧自由基的生成而提高病人抵抗力。依帕司他的不良反应发生率低,是一种对糖尿病慢性并发症(特别是糖尿病神经病变)有效且安全的药物。