亚临床甲状腺功能减退与糖尿病血管并发症

亚临床甲状腺功能减退(亚临床甲减)是一种隐蔽而持久的内分泌代谢性疾病,其与糖尿病常合并存在。近年来,亚临床甲减作为糖尿病血管并发症的危险因素受到广泛重视。大多数研究认为亚临床甲减可通过影响血脂代谢、破坏凝血纤溶系统以及升高同型半胱氨酸和高敏C反应蛋白等糖尿病血管并发症的危险因素,参与和加重糖尿病血管并发症的发生、发展过程。     

他汀类药物在2型糖尿病综合治疗中的研究进展

2型糖尿病的患病率正在世界范围内逐年增加,同时与之相关的微血管并发症和大血管并发症发生率也显著增加.他汀类药物除了调脂作用以外,还可通过抑制炎症因子、保护血管内皮细胞功能及抗氧化应激等途径延缓糖尿病并发症发生发展,显著减少心血管事件.总体而言,及时启动他汀类药物对2型糖尿病的治疗是有益的,尤其是伴有心血管危险因素的糖尿病患者.     

糖尿病血管病变机制与防治进展

糠尿病的血管病变是糖尿病的主要并发症。其大血管病变性质为动脉粥样硬化（AS），主要累及主动脉、冠状动脉等大血管，而糖尿病的微血管病变是糖尿病特有的慢性血管并发症，主要表现为视网膜、肾等微血管病变。糖尿病血管病变机制与防治研究是近年来研究的热点。     

2型糖尿病并血管病变患者凝血功能指标的检测分析

心血管病变是糖尿病的主要慢性并发症之一。脂代谢异常、血栓形成、炎症、行为和习惯、遗传因素等被视为引起心血管病变的五种风险因子。本文通过对糖尿病患者脂类、止血与血栓形成的实验室常用指标的检测，探讨其在2型糖尿病血管病变发生和发展过程中的作用，以期为糖尿病血管并发症患者的预防、治疗和疗效观察提供参考依据。     

1例糖尿病合并下肢血管病变患者行介入治疗的护理

糖尿病足是糖尿病严重的并发症之一,是下肢血管病变、神经病变和感染共同作用的结果,表现为足部疼痛、足部溃疡及足坏疽等临床症状,最常见的是足部溃疡。如果不积极治疗,可导致糖尿病坏疽,甚至截肢,严重影响患者的生存质量和生存时间。血管介入治疗是目前糖尿病下肢血管病变积极有效的治疗方式。我科对1例2型糖尿病合并严重下肢血管病变的患者采用介入治疗手段,取得了满意的临床效果,现报告如下。     

抗炎治疗—糖尿病新的治疗选择

糖尿病的发病率在全球范围内逐年增加.研究认为,炎症是糖尿病重要的病理生理机制之一.炎症的发生可能会增加胰岛素抵抗和及胰岛β细胞分泌缺陷,两者共同作用导致的糖尿病的发生.炎症也可能增加糖尿病和肥胖患者潜在的心血管疾病发病风险.糖尿病的抗炎治疗可能会更好控制血糖并减少糖尿病大血管及小血管并发症,因此,抗炎治疗可能是针对糖尿病及其并发症治疗的一个新方法,是糖尿病新的治疗目标.     

2型糖尿病并发牙周感染与解偶联蛋白3基因多态性的关系

2型糖尿病（DM2）并发牙周感染是糖尿病并发症之一,可造成牙齿松动、牙槽嵴松动、逆行性根尖周炎等后果,严重影响患者的身心健康。研究表明,氧化应激在血管病变的发生、发展中起重要作用,氧化标志物可以用于临床慢性并发症危险性的预测。大量的动物实验和临床研究表明,解偶联蛋白3（UCP3）基因分布广泛,并且在体内外均具有保护组织器官抗氧化的作用。     

第六版“IDF糖尿病地图”对中国糖尿病足诊治的预警和提示

2013年11月14日,国际糖尿病联盟（IDF）公布第六版＂IDF糖尿病地图＂,数据显示中国2013年糖尿病的患病人数为9840万,居全球首位。糖尿病足重在预防,对糖尿病足危险因素（性别、患病时程、周围神经病变、足部畸形、周围血管病变、吸烟、溃疡和截肢病史、血糖监控不足等）的筛查是重中之重。本文总结了糖尿病足病情评估的注意事项及治疗策略,其中加强以糖尿病足患者足跖压力管理为代表的康复治疗具有重要意义。简要阐述了糖尿病足国际区域医疗信息共享系统和治疗机构的开展情况,对比国内这两方面的发展现状,提出进一步提高我国糖尿病、糖尿病并发症的治疗、管理水平的必要性和紧迫性,并给出有效措施和发展方向指导。     

糖基化终产物与糖尿病血管并发症关系的研究进展

糖尿病是临床上一种常见病和多发病 ,血管并发症是糖尿病的主要致残及致死原因。流行病学调查资料表明 ,糖尿病患者发生动脉粥样硬化及危及生命的心血管并发症的危险性较常人增加 3- 4倍 ,而高血糖状态下蛋白质发生的非酶糖基化对糖尿病血管并发症起了重要作用。大量的资料已证明 ,糖尿病患者体内存在着一种重要的毒性产物———糖基化终产物 (ａｄｖａｎｃｅｄｇｌｙｃｏｓｙｌａｔｉｏｎｅｎｄｐｒｏｄ ｕｃｔｓ,ＡＧＥｓ)。本文对有关ＡＧＥｓ在糖尿病血管病变中致病作用的研究进展综述如下 :一、ＡＧＥｓ的生物化学特性及结构早在 1 91 …     

Nrf2在糖尿病血管并发症中的研究进展

近年来,糖尿病(diabetes mellitus,DM)已成为威胁人类健康的全球性疾病之一。糖尿病相关的代谢异常会逐渐引起微血管及大血管并发症,血管并发症的出现及发病是患病率及病死率增加的主要原因。大量研究表明:糖脂代谢紊乱、血小板的高度激活、内皮功能障碍、炎症、氧化应激等都可能导致糖尿病血管并发症。目前,较为被认可的观点是:糖尿病血管并发症发病的重要环节是高血糖状态下的过度氧化应激[1]。     

糖基化终产物与糖尿病血管并发症

糖尿病时糖基化终产物(advanced glycation end products,AGEs)生成与蓄积不仅加速糖尿病本身的发展,还与糖尿病肾病、视网膜病、神经性疾病和心血管疾病等慢性并发症密切相关。AGEs与糖基化终产物受体(receptor for advanced glycation end products,RAGE)相互作用诱导氧化应激,促进炎症反应,影响凝血系统,在糖尿病及其并发症的病理生理过程中起重要作用。抑制AGEs生成、交联结构及阻断AGEs与RAGE相互作用为寻找治疗糖尿病血管并发症的药物提供了新的途径。     

2型糖尿病患者糖尿病足的相关危险因素分析

目的 探讨2型糖尿病患者糖尿病足的危险因素。方法 对2004年3月至2008年1月深圳市人民医院497例2型糖尿病患者（糖尿病足组56例、非糖尿病足组441例）的临床资料和生化指标进行回顾性分析，包括病人性别、年龄、病程、体重、血压、吸烟史、高血压病史、周围神经病变、视网膜病变、外周血管病变等。然后进行多因素非条件Logistic回归分析。结果 糖尿病足组和非糖尿病足组相比．年龄、平均动脉压、空腹血糖、餐后2h血糖、血胆固醇、血甘油三酯、估测的肾小球滤过率（eGFR）、高血压病史、周围神经病变史、外周血管病、视网膜病变差异有统计学意义（P〈0．05）。结论 周围神经病变、外周血管病变、糖尿病肾病是糖尿病足发生的独立危险因素。     

Prospects for smoking cessation among people with insulin-dependent diabetes

As part of an initiative to develop a smoking cessation resource tailored to the needs of smokers with diabetes, we undertook a survey of 223 people with insulin-dependent diabetes (IDDM) aged 15–40 years, 54 of whom were smokers. Smokers had high levels of awareness that smoking increases the risk of heart and peripheral vascular disease, but were less aware of the risk of microvascular complications. Nearly half of the smokers had other members of the household who were smokers, and 56% indicated they would expect to receive no more than a little encouragement from friends and family members to quit. Concern about weight gain and dietary adherence was a barrier to quitting smoking for approximately one-third of smokers. Seventy percent of smokers recalled advice to quit smoking from a general practitioner, but this most often had involved minimal advice to quit. There is scope for patient education with respect to microvascular complications exacerbated by smoking, and a need to consider the smoking habits of other household members and enlist their active support for smoking cessation.     

Therapeutic implications of peptide interactions with G‐protein‐coupled receptors in diabetic vasculopathy

The dramatic worldwide increase in the prevalence of diabetes has generated an attempt by the scientific community to identify strategies for its treatment and prevention. Vascular dysfunction is a hallmark of diabetes and frequently leads to the development of atherosclerosis, coronary disease‐derived myocardial infarction, stroke, peripheral arterial disease and diabetic ‘triopathy’ (retinopathy, nephropathy and neuropathy). These vascular complications, developing in an increasingly younger cohort of patients with diabetes, contribute to morbidity and mortality. Despite the development of new anti‐diabetic or anti‐hyperglycaemic drugs, vascular complications remain to be a problem. This warrants a need for new therapeutic strategies to tackle diabetic vasculopathy. There is a growing body of evidence showing that peptide‐binding G‐protein‐coupled receptors (peptide‐binding GPCRs) play an important role in the pathophysiology of vascular dysfunction during diabetes. Thus, in this review, we discuss some of the peptide‐binding GPCRs involved in the regulation of vascular function that have potential to be a therapeutic target in the treatment of diabetic vasculopathy.     

Intra-aortic balloon pump: indications and complications.

Results obtained with intra-aortic balloon pumps (IABPs) at Harbor-UCLA Medical Center from 1990 to 1995 were reviewed to analyze the indications for its use as well as the incidence and types of vascular complications that occurred. Of 86 patients (53 men and 33 women) in whom pumps were used, 66 underwent coronary bypass, 14 underwent valve replacement, and 6 underwent both coronary bypass/valve replacement. Thirteen (15%) deaths occurred (8 coronary bypass patients, 4 valve replacement patients, and 1 coronary bypass/valve replacement patient). The indications for IABP were broadly classified as prophylactic or inability to wean. Prophylactic IABP placement preoperatively occurred in 35 (41%) patients for profound ventricular dysfunction (27 patients), compelling coronary anatomy including critical left main disease (7 patients), and unstable angina (1 patient). Inability to wean occurred in 51 (59%) patients. Three patients (3.5%) developed major vascular complications resulting in limb ischemia. All three underwent thrombectomies, fasciotomies, and above-knee amputations; two patients subsequently died. Vascular reconstruction was performed in two patients as a direct result of their vascular process. All three vascular complications occurred in women. Besides gender, there was no difference between IABP patients with or without vascular complications in terms of age or presence of diabetes, hypertension, smoking history, obesity, or known peripheral vascular disease. These results indicate that IABPs are effective both prophylactically and intraoperatively in patients who would not otherwise survive cardiac surgery.     

Qualitative and quantitative studies of autoantibodies to phospholipids in diabetes mellitus.

Diabetes mellitus is associated with vascular and neurological complications. We have investigated the presence of antibodies to phospholipids and to phospholipid binding plasma proteins in blood samples collected from 68 clinically and biochemically characterized type I and type II diabetic patients and from 252 healthy blood donor controls. Each sample was analysed for antibodies to three phospholipids (cardiolipin, phosphatidylserine and phosphatidylethanolamine), the antibody isotypes (IgA, IgG and IgM), and whether antibody activity was plasma protein-dependent. Patients were considered to have anti-phospholipid antibodies when one or more of these 18 tests was found above predetermined control values. The results of these experiments revealed an increased incidence of anti-phospholipid antibodies in diabetic patients compared with control subjects. The incidence of IgA isotype to phosphatidylethanolamine was higher than the incidence of other isotypes to other phospholipids, and their reactivities were independent of phospholipid-associated proteins. In addition, these antibody findings were studied for associations with prothrombin degradation products, activated factor VII and activated protein C, and with the incidence of diabetic complications. The anti-phosphatidylethanolamine antibody association with proliferative retinopathy was significant.     

An update on 'progression promoters' in renal diseases

AIM: This paper reviews progression in renal diseases. METHODS: An English language literature search using Medline (1980 January-2001 July) was done to assess research and review articles on progression in renal diseases. RESULTS: Factors that increase the risk of progression in renal diseases are hypertension, dyslipidaemia, underlying nephropathy, high dietary protein intake and proteinuria. Others are smoking, hyperglycemia, low birth weight, obesity, metabolic syndrome X, genetic factors such as angiotensin converting enzyme 'DD' genotype and chromosome 1q21, and exposure to lead. Hypertension induces arteriolar nephrosclerosis. The mechanisms whereby lipids contribute to vascular and renal injury are incompletely understood. Glomerular hyperperfusion and increased proteinuria may explain the adverse effects of increased protein intake on renal disease progression. Proteinuria contains numerous toxic/inflammatory systems that promote progression. Cigarette smoking has vasoconstrictive, thrombotic and direct toxic effects on the vascular epithelium. Hyperglycemia is strongly implicated in the progression of complications in diabetics. Oligonephropathy in low birth weight has been suggested to increase the risk for systemic and glomerular hypertension in adult life. In obesity, the combination of hyperfiltration, glomerular hypertrophy and glomerular hypertension is a primary initiating event for glomerular injury manifesting as glomerulomegally and focal and segmental glomerulosclerosis and proteinuria. Angiotensin I, with enzyme insertion/deletion polymorphism, especially the "DD" genotype, predisposes to a rapid decline in renal function. Finally, long-term exposure to low levels of environmental lead affects renal function. CONCLUSION: The control of hypertension, dyslipidaemia, proteinuria, obesity, avoidance of low birth weight, smoking and heavy metals such as lead are intervention strategies for preventing progression of renal diseases.     

血管平滑肌细胞表型转变与糖尿病血管病变

血管平滑肌细胞按其形态、功能及细胞标志蛋白的不同可分为收缩型和合成型。血管平滑肌细胞受生化因子、细胞外基质成分、机械性刺激等多种因素的调节,其表型转变的分子机制主要与KLF4/Myo D/SRF轴相关。糖尿病的高血糖、胰岛素抵抗、脂类代谢紊乱、炎症反应可诱导血管平滑肌细胞表型转变,使其迁移、增殖能力增强,从而导致糖尿病血管病变。     

Endothelial dysfunction, atherosclerosis and diabetes

The prevalence of early and accelerated development of atherosclerosis associated with high morbidity and mortality is markedly increased among individuals with diabetes and hypertension. Although the link between diabetes and vascular disease is not fully understood, loss of the modulatory role of the endothelium could be implicated in the pathogenesis of diabetic vascular complications. Diabetes-associated pathophysiologic conditions in the endothelium are modifications of lipoproteins, formation of advanced glycation end-products and circulating lipoprotein immune complexes, alteration of the nitric oxide pathway, and elevated levels of homocysteine. The main goals in restoration of endothelial function are optimal glycemic control, lipid lowering, cessation of smoking, normalization of elevated blood pressure, improvement of the NO-status, antioxidants for scavenging free oxygen radicals, normalization of homocysteine levels, antagonizing the hyperinsulinaemia, and regulation of rheology, respectively haemostasis to physiological levels. There is abundant evidence that some pharmacological agents exert direct beneficial effects on endothelium, suggesting that at least part of their therapeutic action is associated with improvement in endothelial dysfunction. A number of new findings about endothelial dysfunction may have potential clinical relevance.