2型糖尿病患者高血压与糖尿病性神经病变的关系

目的 探讨2型糖尿病患者高血压与糖尿病性神经病变的关系。方法 利用心自主神经功能检测系统和神经电生理检测仪对107例（高血压组52例,非高血压组55例）2型糖尿病患者的心自主神经功能和肢体的末梢神经传导速度、皮肤痛温觉、振动沉进行测定,以判断心自主神经病变和末梢神经病变。结果 两组间末梢神经功能和心自主神经功能各指标除心的是距频谱分析的高频值外差异均无显著性（P＜0.05）。Logistic回归分析显示高血压与心自主神经病变显著相关（P＜0.01）,而与末梢神经病变无显著相关。结论 2型糖尿病患者高血压是心自主神经病变发病的危险因素,而与末梢神经病变无明显关系。     

糖尿病性心自主神经病变与心源性猝死

糖尿病性心自主神经病变是糖尿病严重的慢性并发症之一 ,与糖尿病患者心源性猝死的关系密切。流行病学由于糖尿病性心自主神经病变起病隐匿 ,且长时间无临床症状 ,加之目前尚无明确统一的诊断标准 ,因此对其自然病程和确切的人群发病率尚不清楚。为了便于资料对比分析、交流和统一各家对糖尿病性神经病变的诊断认识 ,临床上采用在ＳａｎＡｎ ｔｏｎｉｏ会议[1] 上推荐的Ｅｗｉｎｇ和Ｃｌａｒｋｅ[2 ] 非创伤性且重复性良好的方法用于糖尿病性心自主神经病变的诊断 ,使糖尿病性心自主神经病变的诊断趋于规范化和标准化。利用此方法可观察到在…     

2型糖尿病外周感觉神经病变和心自主神经病变关系的研究

目的探讨T2DM外周感觉神经病变和心自主神经病变之间的关系。方法选取T2DM患者148例,采集临床资料,测定FPG、HbA1c及LDL-C等生化指标;进行定量感觉神经检查(以色列TSA-II定量感觉神经测定仪),结合临床症状评价糖尿病外周感觉神经病变;进行心血管反射试验检查,结合临床症状评价糖尿病心自主神经病变。结果外周感觉神经病变的患病率为28%,心自主神经病变的患病率为10%;无外周感觉神经病变的患者中心自主神经病变的患病率为6%,存在外周感觉神经病变的患者中心自主神经病变的患病率为21%;与对照组相比,外周感觉神经病变组和心自主神经病变组的病程较长,FPG、HbA1c及LDL-C水平较高,差异有统计学意义(P<0.05)。结论糖尿病心自主神经病变可发生于无外周感觉神经病变的患者;病程、FPG、HbA1c及LDL-C可能为糖尿病外周感觉神经病变和心自主神经病变的危险因素。     

糖尿病性心脏自主神经病变及其诊断与临床对策

糖尿病是一种严重危害人类健康的慢性代谢性疾病。2008年的流行病学调查显示，中国20岁以上成年人糖尿病患病率为9．67％，我国糖尿病患者高达9240万。糖尿病及其急、慢性并发症给人类健康和社会发展带来了沉重的负担。糖尿病神经病变（DPN）为糖尿病重要的慢性并发症之一，最常见的神经病变为慢性感觉运动性神经病变和自主神经病变。     

高血糖——糖尿病周围神经病变的发病基础

糖尿病周围神经病变(diabetic peripheral neuropathy,DPN)是糖尿病常见的慢性并发症之一,可以出现在1型和2型糖尿病病程中,其表现有多种形式,一般末梢神经首先受累,对称性多发性神经病变及自主神经病变较常见,而且常呈慢性进行性发展。对高血糖与糖尿病周围神经病变发病机制关     

糖尿病神经病变的六大祸首

糖尿病神经病变是糖尿病的并发症之一。2001年我国调查发现，61．8％的2型糖尿病患者并发神经病变，并且1型和2型糖尿病患者发生神经病变的几率是一样的。研究发现在糖尿病前期就可出现神经损伤。神经病变包括外周神经病变和自主神经病变。外周神经病变的主要表现是四肢疼痛、麻木、感觉丧失等，     

导致2型糖尿病心血管自主神经病变的主要危险因素及其对病情评估的价值

目的分析2型糖尿病中影响心血管自主神经病变（CAN）的危险因素,探讨这些因素对CAN的危害程度,并建立回归模型。方法325例2型糖尿病患者根据心血管自主神经功能试验结果分为：正常组、早期病变组、确诊组和严重组。对所有患者询问病史、体格检查、生化检查及ECG、神经传导速度、眼底镜检查、颈动脉和下肢动脉Doppler检查。结果64．0％的病人存在自主神经病变,30．2％确诊为CAN;相关指标随自主神经病变程度加重而恶化;等级回归显示,年龄、平均糖化血红蛋白、高血压、周围神经病变、视网膜病变、静息心动过速和周围神经病变病程是显著影响因素（P〈0．05）;根据这些因素,建立数学模型,可推算患者自主神经病变的病情。结论除年龄和血压外,其他自主神经病变的影响因素都与血糖有关,进一步证实控制血糖是预防糖尿病并发症的首要因素。     

如意珍宝丸治疗糖尿病末梢神经炎54例疗效观察

糖尿病末梢神经炎是一种以节段性脱髓鞘为主的多发性神经病变，是糖尿病神经病变最常见的慢性并发症之一，也是糖尿病患者主要的致残因素之一。由于本病起病隐匿，进程缓慢，给治疗造成了一定的困难。自2009年2月至今，笔者使用如意珍宝丸治疗糖尿病末梢神经炎54例，取得满意效果。现报告如下。     

关注糖尿病神经病变,提高患者生活质量

<正>糖尿病神经病变严重影响生活质量糖尿病神经病变(DN)是糖尿病最常见的慢性并发症之一,其发生早,甚至在糖尿病前期就可以出现;患病率高,对健康影响巨大。糖尿病神经病变的发生与多种危险因素相关。周围神经病变所引起的麻木、感觉异常、疼痛等会让患者彻夜难眠,严重者导致溃疡、足部结构及功能改变,甚至截肢。而各种自主神经病变也     

糖尿病心脏自主神经病变的诊治

糖尿病周围神经病变是糖尿病患者较早出现也是最常见的慢性并发症,其中糖尿病自主神经病变可累及心血管、胃肠道和泌尿生殖系统等组织器官.糖尿病心脏自主神经病变（DCAN）可导致心率控制和血管血液动力学异常,显著增加糖尿病患者心律失常和猝死的风险[1],是2型糖尿病患者最严重的慢性并发症之一.但由于起病隐匿,早期无明显临床症状,常被忽视.近年来,随着人们对DCAN认识的提高,客观的检测手段使早期发现心脏自主神经功能异常成为可能,从而达到早期干预甚至逆转DCAN的目的.     

Autonomic neuropathy in non-insulin dependent (type II) diabetes mellitus. Possible influence of obesity

To assess the prevalence of autonomic neuropathy (AN) in non-insulin dependent diabetes mellitus (NIDDM) and its relationships with other diabetic complications, duration of diabetes, and obesity, we evaluated 51 NIDDM patients (age 41-59 years, mean 49 years, duration of diabetes 0-15 years, mean 6.9 years). AN tests included a deep breathing test (E/I ratio) and an orthostatic tilt table test (acceleration and brake (25 of 51, 49%) and the most frequent disturbance was an impaired E/I ratio (18 of 25; 72%). There were no obvious correlations between AN indices and the duration of diabetes, symptoms of AN, peripheral neuropathy or retinopathy. However, an influence of obesity on AN was suggested. Patients with AN showed a significantly higher BMI than patients without AN (31.0 +/- 0.9 vs. 27.5 +/- 0.8; P less than 0.01).     

Peripheral neuropathy does not invariably coexist with autonomic neuropathy in diabetes mellitus

Background: Peripheral somatic and autonomic neuropathies are the most common types of diabetic polyneuropathy. Although duration and degree of hyperglycemia are considered to be risk factors for both autonomic and peripheral neuropathy, recent studies have raised the question of a different development and natural history of these neuropathies in diabetes. In addition, a few studies have investigated the relationship between chronic painful and autonomic neuropathy. The aim of this study was to investigate to what extent autonomic and peripheral neuropathy coexist, as well as whether painful neuropathy is more common in diabetic patients with autonomic neuropathy. Methods: Subjects with type 1 (n=52; mean age 31.7 years) and type 2 diabetes (n=53; mean age 54.5 years) were studied. Evaluation of peripheral neuropathy was based on clinical symptoms (neuropathic symptom score), signs (neuropathy disability score), and quantitative sensory testing (vibration perception threshold). Assessment of autonomic neuropathy was based on the battery of standardized cardiovascular autonomic function tests. Results: Prevalence rates of pure autonomic and of pure peripheral neuropathy in patients with type 1diabetes were 28.8 and 13.5%, respectively. The respective rates in patients with type 2 diabetes were 20.7% (P=0.33 vs. type 1 diabetes) and 20.7% (P=0.32). Peripheral and autonomic neuropathy coexisted in 28.8% of type 1 and in 45.3% of type 2 diabetic subjects (P=0.08). Prevalence rates of chronic painful neuropathy in subjects with type 1 diabetes, with and without autonomic neuropathy, were 16.6 and 22.7%, respectively (P=0.85) and in type 2 diabetic subjects 20 and 22.2%, respectively (P=0.58). Multivariate analysis after adjustment for age, sex, blood pressure, duration of diabetes, HBA(1c), and presence of retinopathy or microalbuminuria showed that neither the indices of peripheral nerve function (neuropathic symptom score, neuropathy disability score, vibration perception threshold) nor the presence of peripheral neuropathy or chronic painful neuropathy are associated with the presence of autonomic neuropathy in individuals with either type 1 or type 2 diabetes. Conclusions: Peripheral and autonomic neuropathies do not invariably coexist in diabetes. In addition, chronic painful neuropathy may be present irrespective of the presence of autonomic neuropathy.     

Prevalence of diabetic autonomic neuropathy measured by simple bedside tests

Summary To investigate the prevalence of diabetic autonomic neuropathy, five simple bedside tests, beat-to-beat variation during quiet respiration, beatto-beat variation during forced respiration, heart rate and blood pressure response to standing, heart rate response to exercise, and heart rate response to Valsalva's manoeuvre were applied to 75 male insulindependent diabetics, mean age 40 years, (range 30–49 years). The subjects were subdivided into three groups according to duration of diabetes, which was between 0 and 40 years. Twenty-eight healthy age-matched male controls were also studied. The prevalence of diabetic autonomic neuropathy in the whole diabetic population indicated by abnormal response in beat-to-beat variation during forced respiration was 27%. Diabetic autonomic neuropathy increased in frequency with duration of disease. Patients with nephropathy or proliferative retinopathy had a significantly higher prevalence of diabetic autonomic neuropathy as indicated by abnormal beat-to-beat variation during forced respirations (p<0.01) than patients without these complications.     

Autoantibodies to nervous tissue structures are associated with autonomic neuropathy in Type 1 (insulin-dependent) diabetes mellitus

Summary There is evidence that the immune system may play a role in the pathogenesis of autonomic neuropathy in Type 1 (insulin-dependent) diabetes mellitus. In the present study, we investigated the presence of autoantibodies to sympathetic and parasympathetic nervous structures and their correlation with other conventional autoantibodies in well-characterised diabetic populations, with or without diabetic neuropathy, and normal subjects. An indirect immunofluorescent complement-fixation technique was used, with monkey adrenal gland, rabbit cervical ganglia and vagus nerve as substrates. Of the patients with symptomatic autonomic neuropathy 33% were positive for at least one autoantibody (20% anti-sympathetic ganglia, 10% anti-vagus nerve and 13% anti-adrenal medulla). The frequency of having one or more antibodies to nervous tissues and the prevalence of anti-cervical ganglia antibodies were significantly higher in the neuropathic patients than in the diabetic control subjects with disease of similar duration and in the normal subjects (p<0.05). Of the patients without complications with diabetes of shorter duration 33% were also positive for at least one autoantibody (13% anti-ganglia, 13% anti-vagus nerve and 13% anti-adrenal medulla). No correlation was found with other tissue autoantibodies, including islet cell antibodies. Our data indicate that nervous tissue autoantibodies are associated with symptomatic autonomic neuropathy. Anti-sympathetic ganglia and anti-vagus nerve antibodies seem to be more disease-specific. Patients with diabetes of shorter duration who were positive for these autoantibodies may represent pre-neuropathic patients.     

Platelet activation in diabetic cardiovascular autonomic neuropathy.

AIMS: Platelet activation is known to be associated with arrhythmic effects in myocardial ischaemia. The present study attempts to clarify whether diabetic cardiovascular autonomic neuropathy (CAN) is associated with intravascular platelet activation. METHODS: Platelet activation was assessed by flow cytometry analysis in 30 patients with Type 1 diabetes mellitus screened for diabetic complications. Fifteen patients showed evidence of CAN as assessed by a battery of standard cardiovascular autonomic reflex tests. Fifteen patients without CAN were then selected as a matched control group. Platelet activation was assessed by flow cytometric detection of activation-dependent platelet membrane antigens (P-selectin (CD62), thrombospondin, lysosomal GP53 (CD63) and ligand-induced binding site-1 of GPIIb/IIIa (LIBS-1)). RESULTS: Significantly more activated platelets were detected in the patients with CAN showing 20.9% (coefficient of variation (CV) 44%) CD63+ (vs. 17.2% (CV 19%) in controls, P < or = 0.05), 6.4% (CV 87%) CD62+ (vs. 4.1% (CV 37%), P < or = 0.05), and 6.7% (CV 55%) thrombospondin+ (vs. 4.6% (CV 39%), P < or = 0.01) platelets, respectively. LIBS-1 on platelets was not significantly different between patients with and without CAN. No correlation was found between glucose metabolism and platelet activation. CONCLUSIONS: Cardiovascular autonomic neuropathy is associated with platelet activation in Type 1 diabetes mellitus. The high platelet activation may reflect an increased prothrombotic state in diabetic cardiovascular autonomic dysfunction.     

Helicobacter pylori prevalence in diabetic patients and its relationship with dyspepsia and autonomic neuropathy

AIMS: We evaluated the prevalence of Helicobacter pylori (HP) in Type 2 diabetic patients and its relationship with dyspeptic symptoms and complications of diabetes. MATERIALS AND METHODS: Seventy-eight Type 2 diabetic patients (54 females, 24 males, mean age: 51.9 +/- 10.6 yr) and 71 non-diabetic control subjects were involved in the study. Patients were questioned for dyspeptic symptoms. Cardiovascular autonomic neuropathy, nephropathy and retinopathy were investigated in diabetic patients. Upper gastrointestinal tract endoscopy was performed for all patients and gastric biopsies were obtained and searched for HP. RESULTS: Helicobacter pylori prevalence was significantly higher in diabetic patients than in control subjects (75.6 vs 46%, p < 0.05). No differences were found between women and men with regard to HP infection status in diabetic patients. There was no relation between HP and diabetic complications, nephropathy and retinopathy. Helicobacter pylori prevalence was significantly higher in diabetic patients with cardiovascular autonomic neuropathy than in diabetic patients without cardiovascular autonomic neuropathy (90.6 vs 44.0%, p < 0.02). Forty-seven subjects with diabetes had symptoms of dyspepsia (60.3%) and the prevalence of HP was higher in these patients (p < 0.002). CONCLUSION: There is a high prevalence of HP infection in diabetic patients and it is correlated with dyspeptic symptoms. Diabetic subjects complicated with cardiovascular autonomic neuropathy and dyspepsia are at high risk of HP infection and should be carefully investigated and considered for eradication therapy.     

Autonomic nerve function in adolescents with Type 1 diabetes mellitus: relationship to microalbuminuria.

AIMS: Thirty adolescent patients with Type 1 diabetes mellitus and microalbuminuria were studied for evidence of early autonomic neuropathy. METHODS: Using tests involving cardiovascular and pupillary reflexes, the adolescents were compared with a normoalbuminuric group of patients with diabetes, who were matched for age, sex, puberty and duration of diabetes. RESULTS: There was an increased prevalence of autonomic nerve dysfunction in the patients with microalbuminuria. These patients had higher resting heart rates (86 beats/min in the microalbuminuric group vs. 77 beats/min in normoalbuminuric controls, P = 0.002), and impaired pupillary dilatation in darkness (pupillary diameter % 56.5% vs. 62.5%, P = 0.003). Patients with microalbuminuria also had poorer long term glycaemic control (mean HbA1C 8.7% vs. 7.8%, P = 0.002) and higher blood pressures (systolic 125 vs. 116 mmHg, P = 0.001; diastolic 69 vs. 62 mmHg, P = 0.0001; mean arterial pressure 90 vs. 83 mmHg, P = 0.002) than those with normal urinary albumin excretion. CONCLUSIONS: Microalbuminuria and autonomic nerve dysfunction co-exist in patients with Type 1 DM. Longitudinal studies will determine whether these findings have implications for the identification of patients at higher risk of progression of early renal complications.     

Shoulder capsulitis in type I and II diabetic patients: association with diabetic complications and related diseases.

OBJECTIVE: To examine the association between shoulder capsulitis and chronic diabetic complications and diseases closely related to diabetes. METHODS: A cross sectional study in 291 type I [mean (SD) age 33.2 (9.9) years] and 134 type II [61.1 (12.4) years] diabetic patients. The presence of shoulder capsulitis, Dupuytren disease, and limited joint mobility was sought. The patients were assessed for background and proliferative retinopathy, nephropathy, autonomic neuropathy, and peripheral symmetrical somatic polyneuropathy. Diseases closely related to diabetes (hypertension, history of myocardial infarction, coronary heart disease, and peripheral vascular disease) were also recorded. RESULTS: Prevalence of shoulder capsulitis was 10.3% in type I and 22.4% in type II diabetic subjects. Shoulder capsulitis was associated with the age in types I (P < 0.01) and II (P < 0.05) diabetic patients, and with the duration of diabetes in type I patients (P < 0.01). Odds ratios for autonomic neuropathy in type I and type II diabetic subjects with shoulder capsulitis were 4.1 (95% confidence interval, 1.6 to 10.9) and 2.7 (95% CI, 1.1 to 7.0), respectively, after controlling for age and duration of diabetes. Odds ratio for history of myocardial infarction in type I diabetic subjects with shoulder capsulitis was 13.7 (95% CI, 1.3 to 139.5) after controlling for age, duration of diabetes, hypertension, and smoking habits. Other associations between shoulder capsulitis and diabetic complications, related diseases, and other hand abnormalities were fully explained by age and the duration of diabetes. CONCLUSIONS: Shoulder capsulitis is common in type I and type II diabetic patients. It is associated with age in type I and II diabetic patients and with the duration of diabetes in type I patients. It is associated with autonomic neuropathy in type I and II diabetic patients and with history of myocardial infarction in type I diabetic patients, independently of time related variables.     

Impairment of cerebral autoregulation in diabetic patients with cardiovascular autonomic neuropathy and orthostatic hypotension.

AIMS: Impaired cerebrovascular reactivity and autoregulation has been previously reported in patients with diabetes mellitus. However, the contribution of cardiovascular diabetic autonomic neuropathy and orthostatic hypotension to the pathogenesis of such disturbances is not known. The purpose of this study was to evaluate cerebral blood flow velocity in response to standing in patients with diabetes and cardiovascular autonomic neuropathy with or without orthostatic hypotension. METHODS: We studied 27 patients with diabetes--eight had cardiovascular autonomic neuropathy and orthostatic hypotension (age 46.4 +/- 13.5 years, diabetes duration 25.0 +/- 11.0 years), seven had autonomic neuropathy without hypotension (age 47.3 +/- 12.7 years, diabetes duration 26.4 +/- 12.1 years), and 12 had no evidence of autonomic neuropathy (age 44.1 +/- 13.8 years, diabetes duration 17.1 +/- 10.2 years)-and 12 control subjects (age 42.6 +/- 9.7 years). Flow velocity was recorded in the right middle cerebral artery using transcranial Doppler sonography in the supine position and after active standing. RESULTS: Cerebral flow velocity in the supine position was not different between the groups studied. Active standing resulted in a significant drop of mean and diastolic flow velocities in autonomic neuropathy patients with orthostatic hypotension, while there were no such changes in the other groups. The relative changes in mean flow velocity 1 min after standing up were -22.7 +/- 16.25% in patients with neuropathy and orthostatic hypotension, +0.02 +/- 9.8% in those with neuropathy without hypotension, -2.8 +/- 14.05% in patients without neuropathy, and -9.2 +/- 15.1% in controls. CONCLUSIONS: Patients with diabetes and cardiovascular autonomic neuropathy with orthostatic hypotension show instability in cerebral blood flow upon active standing, which suggests impaired cerebral autoregulation.