肝源性糖尿病56例临床分析

目的探讨肝源性糖尿病的临床特征及其可能的机制,以提高对该病的诊治水平。方法回顾性分析56例肝源性糖尿病患者,并与原发性2型糖尿病进行对比分析。结果口服葡萄糖耐量试验显示,肝源性糖尿病患者空腹血糖水平（7.1±3.2mmol/l）显著低于原发性2型糖尿病患者（9.2±2.1mmol/l,P〈0.05）,两组其他时段血糖差异无统计学意义;两组胰岛素分泌均呈高峰延迟型,但肝源性糖尿病患者各时段胰岛素和C肽分泌水平均高于原发性2型糖尿病患者（P〈0.05）;Child C级患者平均空腹血糖（8.7±2.8mmol/l,P〈0.05）明显高于Child A级（6.5±1.8mmol/l）和Child B级（6.8±2.0mmol/l）患者。结论肝源性糖尿病以餐后高血糖为特征,胰岛素抵抗可能是其重要的发病机制。     

肝硬化伴肝源性糖尿病临床分析

目的分析肝硬化伴肝源性糖尿病的临床特征。方法回顾性分析45例肝硬化伴肝源性糖尿病患者的临床资料。结果 45例患者中,乙型肝炎肝硬化31例（68.9%）;空腹血糖7.3±2.9mmol/L,餐后2h血糖16.2±4.7mmol/L,空腹血糖水平与Child-Pugh分级呈正相关（Spearman等级相关系数rs=0.48,P〈0.01）;通过饮食控制、口服α葡萄糖苷酶抑制剂或皮下注射胰岛素,大部分患者血糖控制在正常水平或接近正常水平;7例死亡病例均死于肝硬化并发症。结论肝硬化伴肝源性糖尿病患者的糖尿病症状多不典型,以餐后高血糖为特征,血糖水平与肝功能的损害程度密切相关,应用胰岛素治疗效果较好,不良预后主要与肝硬化相关。     

肝源性糖尿病临床特征分析

目的 探讨肝源性糖尿病的临床特征及其可能机制,以提高对该病的认识和诊治水平。方法回顾性分析102例肝源性糖尿病患者,并与原发性2型糖尿病进行对比分析。结果102例肝源性糖尿病患者中17％有口干、多饮、多食、多尿等典型糖尿病症状;空腹血糖为（7.8±2．6）mmol／L,餐后2h血糖（12．7±3．0）mmol／L;口服葡萄糖耐量试验（OGTT）显示,肝源性糖尿病患者的空腹血糖水平显著低于原发性2型糖尿病（P〈0．01）,余各时段血糖两组差异无统计学意义;胰岛素＋C肽释放试验显示,两组胰岛素分泌均呈高峰延迟型,但肝源性糖尿病患者各时段胰岛素及C肽分泌水平均高于原发性2型糖尿病（P〈0．05）。经饮食控制、应用胰岛素或口服降糖药治疗后血糖大多能控制在正常或接近正常水平。102例肝源性糖尿病患者中仅5例伴糖尿病并发症,4例死亡病例死因均为慢性肝病并发症。结论肝源性糖尿病临床症状不典型,以餐后高血糖为特征,应用胰岛素治疗效果较好,短期不良预后主要与原发慢性肝病有关。胰岛素抵抗可能是其重要的发病机制。     

肝源性糖尿病的临床研究

目的分析肝源性糖尿病的临床特征,探讨肝源性糖尿病的临床表现和治疗方法。方法回顾性分析52例肝源性糖尿病患者的临床表现、实验室检查、并发症、治疗和转归,并与原发性2型糖尿病进行OGTT、胰岛素和C肽释放的对比分析。结果 52例肝源性糖尿病患者有乏力、纳差43例（82.7%）、腹胀40例（76.9%）,＂三多一少＂5例（9.6%）、血管及神经病变4例（4.9%）;空腹血糖为7.6±2.4mmol/L,餐后2h血糖为13.2±3.6mmol/L;0GTT检测显示,肝源性糖尿病患者各时段血糖水平显著低于原发性2型糖尿病患者（P〈0.05）;胰岛素和C肽释放试验显示,肝源性糖尿病患者各时段胰岛素和C肽分泌水平均高于原发性2型糖尿病（P〈0.05）。结论肝源性糖尿病患者以餐后高血糖为特征,胰岛素抵抗是其重要的发病机制,应常规检查血糖,及时诊断和控制糖代谢异常,可以有效地改善肝硬化患者的顸后。     

肝源性糖尿病的研究现状

肝源性糖尿病(hepatogenous d iabetes)是继发于慢性肝实质损害的糖尿病,1999年在日本糖尿病会议上将其归类为2型糖尿病的一种〔1〕。严重肝病导致的糖耐量异常,是影响患者预后的一个重要因素,除已明确其发病机制为胰岛素抵抗、胰岛素分泌代谢异常、升糖激素增多、乙丙型肝炎病     

脂联素与肝源性糖尿病

脂联素（adiponectin）是脂肪组织特异分泌的一种血浆激素蛋白，具有胰岛素增敏和拮抗胰岛素抵抗作用。研究证实胰岛素抵抗是肝源性糖尿病发病的主要机制之一。因此，脂联素与肝源性糖尿病的发生机制密切相关。对脂联素予以深入的研究将对胰岛素抵抗和肝源性糖尿病的防治带来积极的影响。现就脂联素与肝源性糖尿病的最新研究进展进行综述。     

肝源性糖尿病的研究进展

肝源性糖尿病是指慢性肝病肝实质损害导致糖耐量减低，部分患者最终发展成糖尿病。多数学者认为约50％～80％慢性肝病患者有糖耐量减退，其中20％～30％最终发展为糖尿病。而正常人群糖尿病发病率仅为0．6％，我国各型肝炎、肝硬化的发病率较高，由慢性肝炎和肝硬化引起的糖耐量减退或糖尿病并不少见，及时诊断和正确治疗异常的糖代谢对于有效治疗各种慢性肝病和改善患者预后均十分重要。     

72例肝源性糖尿病患者临床疗效研究

目的分析和研究肝源性糖尿病的临床特点以及治疗方法与效果。方法选择该院消化内科被确诊为肝源性糖尿病的患者共72例,并对于患者临床资料进行系统性的分析与研究。结果因慢性轻、中、重度肝病而引发的肝源性糖尿病的患者,全部随着肝病的治愈或者好转而得到缓解。通过治疗观察,血糖稳定的患者占55.6%,血糖仍然偏高的患者占22.2%。其中,重肝及肝硬化的患者占12.5%。结论肝源性糖尿病通常是在慢性肝病的基础上诱发的糖尿病,通过积极地治疗原发性肝病,并加胰岛素来控制患者的血糖,能够获得良好的临床治疗效果。     

72例肝源性糖尿病患者临床疗效研究

目的：分析和研究肝源性糖尿病的临床特点以及治疗方法与效果。方法选择该院消化内科被确诊为肝源性糖尿病的患者共72例,并对于患者临床资料进行系统性的分析与研究。结果因慢性轻、中、重度肝病而引发的肝源性糖尿病的患者,全部随着肝病的治愈或者好转而得到缓解。通过治疗观察,血糖稳定的患者占55.6%,血糖仍然偏高的患者占22.2%。其中,重肝及肝硬化的患者占12.5%。结论肝源性糖尿病通常是在慢性肝病的基础上诱发的糖尿病,通过积极地治疗原发性肝病,并加胰岛素来控制患者的血糖,能够获得良好的临床治疗效果。     

血糖管理在肝源性糖尿病的进展研究

肝源性糖尿病(HD)是糖尿病的一种具体类型,是指继发于肝实质损害的糖尿病,这种类型在发病过程中的主要表现包括高血糖、糖耐量水平降低等.随着HD发生率的不断增加,越来越多的医护人员对其越发重视,相关调查研究结果显示,从发病机制来看,其主要是破坏了胰岛腺细胞,包括增强了肝炎病毒的复制、出现胰岛素抵抗等.该文主要就研究关于血...     

不同代谢异常高血压病患者的胰岛素敏感性

目的 评价减少样本数的微小模型(MMMI2)方法是否适用于伴有明显代谢异常的高血压患者。方法 以高胰岛素—正葡萄糖钳夹试验(Clamp)和MMM12方法对伴有明显代谢异常的高血压患者进行胰岛素敏感性检测，观察两种方法的一致性和相关性。应用MMM12方法对l18例高血压患者的胰岛素敏感性指数(SI)进行测定，比较不同代谢异常状态高血压患者的S1和胰岛素抵抗(IR)的伴发情况。结果 Clamp和MMM12的结果具有良好的一致性和相关性(r＝0．70，P＝0．012)。以IR为应变量进行Logistic回归分析，腰臀比(WHR)增加、糖耐量异常(IGT)和甘油三酯(TG)升高最终进入方程，三者对高血压患者IR与否的判别准确率为80．5％，合并三者之中的一项、两项、三项的高血压患者，伴发IR的百分比分别为64．3％、84．1％、100％。无代谢异常高血压组与正常对照组相比，S1无显著差异，随代谢异常的程度加重，S1逐渐减低。体重指数(BMI)增加的高血压组及WHR增加的高血压组，S1均明显减低，但以WHR增加组更为显著。TG在1．1—1．7mmol／l的高血压组与正常对照组相比，S1已有明显减低。结论 1．MMM12方法能够可靠地检测伴代谢异常高血压患者的胰岛素敏感性。2．上身性肥胖、高TG和IGT对高血压患者IR与否均有独立的判别价值。高血压本身与IR的关系并不密切，高血压伴发IR的比例随着的代谢异常的程度加重而增加。3．上身性肥胖较全身性肥胖更易导致IR。4．对高血压患者TG水平的控制应该更加积极。     

不同代谢异常高血压病患者的胰岛素敏感性

目的评价减少样本数的微小模型(MMM12)方法是否适用于伴有明显代谢异常的高血压患者.方法以高胰岛素-正葡萄糖钳夹试验(Clamp)和MMM12方法对伴有明显代谢异常的高血压患者进行胰岛素敏感性检测,观察两种方法的一致性和相关性.应用MMM12方法对118例高血压患者的胰岛素敏感性指数(SI)进行测定,比较不同代谢异常状态高血压患者的SI和胰岛素抵抗(IR)的伴发情况.结果 Clamp和MMM12的结果具有良好的一致性和相关性(r=0.70,P=0.012).以IR为应变量进行Logistic回归分析,腰臀比(WHR)增加、糖耐量异常(IGT)和甘油三酯(TG)升高最终进入方程,三者对高血压患者IR与否的判别准确率为80.5%,合并三者之中的一项、两项、三项的高血压患者,伴发IR的百分比分别为64.3%、84.1%、100%.无代谢异常高血压组与正常对照组相比,SI无显著差异,随代谢异常的程度加重,SI逐渐减低.体重指数(BMI)增加的高血压组及WHR增加的高血压组,SI均明显减低,但以WHR增加组更为显著.TG在1.1～1.7 mmol/l的高血压组与正常对照组相比,SI已有明显减低.结论 1.MMM12方法能够可靠地检测伴代谢异常高血压患者的胰岛素敏感性.2.上身性肥胖、高TG和IGT对高血压患者IR与否均有独立的判别价值.高血压本身与IR的关系并不密切,高血压伴发IR的比例随着的代谢异常的程度加重而增加.3.上身性肥胖较全身性肥胖更易导致IR.4.对高血压患者TG水平的控制应该更加积极.     

Nonlinear Metabolic Effect of Insulin across the Blood Glucose Range in Patients with Type 1 Diabetes Mellitus

Background

For insulin therapy to successfully maintain blood glucose (BG) levels of patients with type 1 diabetes mellitus (T1DM) in normoglycemia, it is necessary to understand if the metabolic effect of insulin across the BG range is linear or not.

Methods

We assess the ability of insulin to lower BG in patients with T1DM in hypoglycemia and hyperglycemia. The net metabolic effect of insulin, defined as the total effect resulting from both reduced endogenous glucose production and increased glucose uptake, was used to define the insulin effectiveness (IE), a measure that indicates the amplitude of glucose lowering that a unit of active insulin can achieve at a given BG level. The IE was assessed in hypoglycemia and hyperglycemia through two separate studies. In the first study, patients were subjected to a hyperinsulinemic euglycemic and hypoglycemic glucose clamp. In the second study, another group of patients were clamped at a hyperglycemic level.

Results

The IE increased by 75% when BG dropped from 90 to 50 mg/dl at a steady rate of 1 mg/dl/min and decreased by 10% when BG was increased from 100 to 200 mg/dl.

Conclusions

The net metabolic effect of insulin is nonlinear across the BG range and is amplified in hypoglycemia and dampened in hyperglycemia. Most importantly, the BG lowering per unit of insulin is accelerated when falling into hypoglycemia. The understanding of the accelerated risk for hypoglycemia with falling glucose levels will help the design of more robust hypoglycemia prevention and detection systems.     

Practical Experience with Continuous Subcutaneous Insulin Infusion Therapy in a Pediatric Diabetes Clinic

Continuous subcutaneous insulin infusion therapy (CSII) is an increasingly popular form of intensive insulin administration in pediatric patients. The use of CSII commenced at our large tertiary referral diabetes clinic as recently as 2002. In the intervening years, demand and enthusiasm from both patients and physicians alike have resulted in a steady ongoing increase in CSII use at our clinic. We currently have >200 active patients using insulin pump therapy. This article reviews our experience with CSII and outlines our current multidisciplinary approach to optimizing glycemic control and outcomes in this patient group.     

糖尿病增加肝硬化患者发生肝性脑病风险的临床研究

目的 观察糖尿病(DM)对肝硬化患者发生肝性脑病(HE)风险的影响.方法 回顾性比较肝硬化合并DM与未合并DM的患者HE发病率及严重程度的差异,分析糖化血红蛋白(GHb)水平与HE发病率及严重程度的关系.结果 在197例肝硬化患者中,DM患病率为21.8%;HE在肝硬化合并DM组的患病率为83.7%,显著高于不合并DM组的37.7%(P<0.05);在DM组中,GHb≥8%亚组中HE患病率为91.3%,显著高于GHb<8%亚组的75.0%(P<0.05);Ⅲ、Ⅳ期HE患者占DM组HE患者的61.1%,显著高于不合并DM组的32.8%(P<0.05);Ⅲ、Ⅳ期HE患者占DM并GHb≥8%亚组HE患者的76.2%,显著高于DM并GHb<8%亚组的40.0%(P<0.05).结论 肝硬化和DM可能存在伴随关系,DM可能增加肝硬化患者发生HE的风险.积极控制血糖可能有助于降低肝硬化患者HE的发病率,提高肝硬化患者的生存率.     

The Metabolic Syndrome-from Insulin Resistance to Obesity and Diabetes

In today's society with the escalating levels of obesity, diabetes, and cardiovascular disease, the metabolic syndrome is receiving considerable attention and is the subject of much controversy. Greater insight into the mechanism(s) behind the syndrome may improve our understanding of how to prevent and best manage this complex condition.     

The Influence of Insulin Antibodies on the Pharmacokinetics of NPH Insulin in Patients with Type 1 Diabetes treated with Human Insulin

The influence of insulin binding antibodies on the pharmacokinetics of NPH insulin was studied in Type 1 diabetic patients on human insulin. Insulin-antibody binding (B_o) was measured during a screening procedure in 155 Type 1 diabetic patients. In 36 patients, B_o was <1.5%, and in 38 patients B_o was >10.0%. Of these, 6 patients, group 1 (B_o < 1.5%) and 8 patients, group 2 (B_o > 10.0%), respectively, subsequently participated in a pharmacokinetic study. Free insulin and the glucose infusion rate were measured using a euglycaemic clamp after subcutaneous injection of NPH insulin (0.4 U kg^?1). The areas under the curve (AUC) of free insulin concentration were smaller for group 2 (p = 0.01) than for group 1 (212.2 ± 22.0 vs 316.8 ± 25.3 mU l^?1 h). The AUCs of the glucose infusion rate were also smaller for group 2 (p < 0.05) than for group 1 (2.50 ± 0.32 vs 3.58 ± 0.36 g kg^?1). A significant negative correlation exists between the AUCs for free insulin concentration and insulin-antibody binding B_o (r=0.76, p = 0.001). The daily insulin dosage was higher in group 2 (p = 0.02) than in group 1 (0.66 ± 0.03 vs 0.53 ± 0.03 U kg^?1). We conclude that insulin antibodies influence the pharmacokinetics of NPH human insulin. The demonstrable influence on the kinetics of free insulin and glucose utilization leads to a slight increase in daily total insulin requirements.     

Effect of Insulin on Airway Responsiveness in Patients with Type 2 Diabetes Mellitus: A Cohort Study

Background. The correlation between low insulin levels and a decreased sensitivity of the muscarinic receptor has been shown on induced-diabetes animal models. We designed a cohort study with the aim of evaluating the effects of insulin therapy on airway responsiveness (AR) in human patients with type 2 diabetes mellitus. Methods. We enrolled 92 patients with type 2 diabetes who had switched from oral anti-diabetic therapy to treatment by insulin subcutaneous injection. Patients were administered the methacholine challenge test (MCT) at time 0 (pre-insulin therapy) and at intervals of 15, 30, 90, 180, and 360 days after insulin treatment. The decline of forced expiratory volume in 1 second (FEV₁)% from baseline (Δ FEV₁) in response to inhaled methacholine (MCH) was determined to assess airway hyper-responsiveness (AHR). Results. A total of 81 patients (18 women and 63 men) completed the study. Their mean age was 58 ± 7 years and the mean duration of disease was 13.5 ± 7.7 years. The mean decrease of FEV₁ at pre-insulin assessment was 2.96 ± 2.6%. Compared with the pre-insulin value, a significant increase of Δ FEV₁ was observed at 15, 30, and 90 days after treatment (6.25%, CI 95% 5.4 to 7.2, p = 0.0005; 7.64%, CI 95% 6.6 to 8.1, p < 0.001; 6.45%, CI 95% 5.5 to 7.3, p = 0.0004, respectively), while after 180 and 360 days AR was similar to pre-insulin values (Δ FEV₁, 3.62%, CI 95% 2.7 to 3.5 and 3.11%, CI 95% 7.9 to 9.3, respectively). Conclusions. The finding of an increased AR in patients with type 2 diabetes during the first 3 months of insulin therapy may underline the importance of monitoring pulmonary function and respiratory symptoms in patients switching from oral anti-diabetic drugs to insulin therapy, especially in the subset of individuals with respiratory disorders.     

Effects of Insulin on Body Composition in Patients with Insulin-dependent and Non-insulin-dependent Diabetes

Insulin is used to control blood glucose but may have an adverse effect on the amount and distribution of fat mass and other cardiovascular risk factors. To test this hypothesis the effect of insulin therapy on blood glucose, body composition, and lipid levels was measured during 6 months in 9 patients with newly diagnosed insulin-dependent (Type 1) diabetes mellitus (IDDM) and 15 patients with non-insulin dependent (Type 2) diabetes (NIDDM) and secondary failure of therapy with oral hypoglycaemic agents. Both groups received similar daily doses of insulin (∼0.6 units kg⁻¹ day⁻¹). Glycaemic control improved during 6 months treatment in both groups, although the reduction in HbA_1c was greater in IDDM (5.2 ± 0.7 %) than in NIDDM (2.0 ± 0.4 %, p < 0.001). All parameters of the lipid profile improved in IDDM but not in NIDDM. Body weight, lean mass, and fat mass, measured by dual energy x-ray absorptiometry, increased at 1 month in IDDM but not in NIDDM. By 6 months, body weight had increased more in IDDM than NIDDM (9.1 ± 1.2 vs 3.77 ± 0.5 kg, p < 0.01). The increase in weight was predominantly lean mass in IDDM (60.4 ± 9.3 %) and fat mass in NIDDM (59.9 ± 8.4 %). The increase in lean mass was greater in IDDM than NIDDM (5.6 ± 1.1 vs 1.4 ± 0.3 kg, p < 0.001). Fat mass increased by similar increments in IDDM and NIDDM (3.4 ± 0.8 vs 2.4 ± 0.5 kg, p = ns) and was predominantly an increase in trunk fat (IDDM: 2.3 ± 0.6 kg, NIDDM: 2.0 ± 0.4 kg, p = ns). The central/peripheral fat mass ratio prior to treatment was lower in IDDM than NIDDM (0.64 ± 0.05 vs 1.09 ± 0.09, p < 0.01) and then increased in IDDM by 0.32 ± 0.15 (p = 0.07) and in NIDDM by 0.22 ± 0.06 (p < 0.001). In conclusion, insulin therapy is associated with weight gain in both IDDM and NIDDM. In the former, weight gain reflects increases in lean mass whereas in NIDDM it reflects an increase in trunk fat mass. It remains to be determined whether this trend to central obesity partly offsets other benefits of insulin therapy in NIDDM.