视网膜病变与β2微球蛋白、尿微量白蛋白的关系

对207例Ⅱ型糖尿病患者进行糖化血红蛋白(HbA1c)血、尿β2微球蛋白、尿微量白蛋白(UAER)的测定.记录病程,同时行眼底检查.结果207例Ⅱ型糖尿病患者中伴DR者98例,患病率43.34%.DR组与NDR组病程比较(P＜0.01).HbA1c、血β2微球蛋白比较(P＜0.01),尿β2微蛋白,尿微量白蛋白比较(P＜0.01).结论DR与DN均为糖尿病严重并发症.且DR与DN常同时存在,其病变严重程度呈平行关系.     

视网膜病变与β2微球蛋白、尿微量白蛋白的关系

对207例Ⅱ型糖尿病患进行糖化血红蛋白（HbA1c)血、尿β2微球蛋白、尿微量白蛋白（UAER）的测定。记录病程,同时行眼底检查。结果：207例Ⅱ型糖尿病患中伴DR98例,患病率43.34%。DR组与NDR组病程比较（P＜0.01)。HbA1c、血β2微球蛋白比较（P＜0.01),尿β2微蛋白,尿微量白蛋白比较（P＜0.01)。结论：DR与DN均为糖尿病严重并发症。具DR与DN常同时存在,其病变严重程度呈平行关系。     

1型血管紧张素Ⅱ受体基因与2型糖尿病视网膜病变的关系

目的 探讨1型血管紧张素Ⅱ受(AT1R)基因与2型糖尿病视网膜病变（DR）的关系。方法 用PCR－DdeI酶切法检测52例糖尿病伴视网膜病变患者DR（＋）及68例不伴视网膜病变者DR（－)的基因型。正常对照40例。结果 糖尿病患者与对照组间AT1R等位基因及基因型频率均无显著性差异,DR（＋）组突变基因及基因型频率显著性高于DR（－）组及对照组（P＜0．05）;增殖型DR组C等位基因频率显著性高于单纯性DR组,DR发生危险因素分析病程、果糖胺、收缩压进入方程。结论 AT1R基因参与DR的发生,而与DM无关。AT1R突变基因可能促使DR发生。     

眼底荧光造影术及血管内皮生长因子在糖尿病肾病的早期诊断中的作用

糖尿病并发视网膜病(DR,n=65)和不伴视网膜病(non-DR,n=41)的研究显示,DR组尿白蛋白排泄率(UAER,28·9±15·9μg/min)明显高于non-DR组(6·0±1·8μg/min)(P<0·05)。DR病变越严重,则UAER越高。随着DR和UAER进展,血管内皮生长因子(VEGF)水平逐渐升高。结论:眼底荧光血管造影和VEGF可以预言糖尿病肾病的发生。     

2型糖尿病合并视网膜病变患者血清维生素D水平变化及意义

目的探讨2型糖尿病合并视网膜病变(DR)患者血清维生素D水平变化及意义,为DR的早期防治提供诊断依据。方法选取2012年1月—2019年1月于该院内分泌科住院的2型糖尿病患者219例进行研究,分为T2DM不伴DR(NDR)组73例、T2DM伴非增殖期DR(BDR)组69例和T2DM伴增殖期DR(PDR)组77例。收集所有患者临床资料,ELISA法测定血清25羟维生素D3[25(OH)D3]水平,检测各组空腹血糖(FPG)、糖化血红蛋白(HbA1c)、空腹C肽、血脂,C-反应蛋白(CRP)和肝、肾功能等生化指标。将25(OH)D3与各指标间进行相关性分析,并将25(OH)D3按照国际诊断标准,分为维生素D缺乏组[25(OH)D3<20 ng/mL]及非维生素D缺乏组[25(OH)D3≥20 ng/mL],比较两组间DR的发病率及风险,并进一步对DR的危险因素行Logistic回归分析。结果T2DM各组血清25(OH)D3水平由低到高依次为PDR组相似文献   

糖尿病视网膜病变研究现状

第65届美国糖尿病学会(ADA)年会中糖尿病视网膜病变(DR)研究数十篇,现将主要的研究成果概述如下。1流行病学1.1DR的患病率印度Rema等从Chennai城乡流行病学研究(CURES)中随机抽取872例糖尿病患者进行调查,发现DR总患病率为17.1%,冠心病为17.7%;与不伴DR的患者相比,伴有DR患者的     

2型糖尿病患者下肢动脉病变与视网膜病变临床特点分析

目的探讨2型糖尿病（T2DM）患者下肢动脉病变（PAD）、视网膜病变（DR）的发病情况及临床特点,为针对性防治提供临床依据。方法选择700例T2DM患者,筛选出PAD（PAD组）100例、DR（DR组）170例,比较两组患者BM、I血压、糖化血红蛋白、血糖、血脂、吸烟饮酒等情况。结果 PAD组吸烟人群偏多,且多合并血脂异常、肥胖等,糖尿病病程较DR组偏短。而DR组往往在血糖及血压的控制上相对更差。结论 PAD患者应早期加强血脂、血糖及生活习惯的干预,DR患者应加强血糖及血压控制。     

我国苗族人群1型糖尿病患者与HLA-DR基因频率的相关性研究

目的　研究我国苗族人群 1 型糖尿病(T1DM)患者与 HLA-DR基因频率的相关性。　方法　选择无血缘关系的纯苗族 T1DM患者 45 例,纯汉族 T1DM患者 43 例,纯苗族健康对照(NC)组52例,纯汉族NC组58例。运用序列特异性引物 聚合酶链反应(PCR/SSP)技术测定 HLA-DR1.10基因频率。　结果　(1)苗族及汉族T1DM组患者的 DR2 基因频率分别明显低于苗族及汉族NC组(P<0.05);DR3、DR9 基因频率分别高于 NC组(P<0.05)。(2)苗族 T1DM组及苗族 NC组的DR5 基因频率分别明显高于汉族T1DM组及汉族NC组(P<0.05)。(3)苗族 T1DM组的 DR2基因频率明显低于汉族NC组(P<0.05) ;DR3、DR5、DR9 基因频率分别高于汉族NC组(P<0.05)。(4)苗族及汉族人群中,T1DM组的 DR2 基因频率分别明显低于 NC组,其相对危险度 RR<1,P<0.05; DR3、DR9 基因频率分别高于NC组,其相对危险度RR>1,P<0.05。　结论　苗族T1DM组与汉族T1DM组患者 HLA DR1、DR2、DR3、DR4、DR6、DR7、DR8、DR9、DR10 基因频率差异无统计学意义,苗族T1DM组及苗族 NC组 DR5 基因频率高于汉族 T1DM 组及汉族 NC 组。DR3、DR9 与T1DM呈正相关;DR2 与T1DM呈负相关。     

糖尿病视网膜病变患者血浆网膜素的变化及其相关因素

目的探讨2型糖尿病(T2DM)及T2DM伴视网膜病变(DR)患者血浆网膜素水平变化及其与体重指数(BMI)、腰臀比(WHR)、血糖、血脂、血清空腹胰岛素(FINS)水平、肿瘤坏死因子α(TNF-α)等的关系。方法 62例T2DM,根据有无DR进一步分为伴DR和不伴(NDR)两组。同时选择健康成人28例作为正常对照组。采用酶联免疫法测定了空腹血浆网膜素水平,并分析血浆网膜素与BMI、WHR、血脂、血糖、血浆胰岛素水平及TNF-α等的关系。结果 T2DM病人血浆网膜素水平明显低于正常人(P<0.01),伴有DR组病人又明显低于无DR的病人(P<0.01)。血浆网膜素水平与BMI、WHR、空腹血糖(FPG)、餐后2 h血糖(2 h PG)、TNF-α、糖化血红蛋白(HbA1c)、HOMA-IR、FINS和甘油三酯(TG)呈明显负相关(r=-0.415～-0.241,P<0.01或P<0.05),与高密度脂蛋白胆固醇(HDL-C)呈明显正相关(r=0.424,P<0.01)。HOMA-IR是影响T2DM患者血浆网膜素水平的独立相关因素,HOMA-IR和TNF-α是影响DR患者血浆网膜素水平的独立相关因素。结论血浆网膜素与糖脂代谢紊乱、炎症反应及肥胖引起的胰岛素抵抗有关,并可能在T2DM及DR的发生和发展中具有一定的作用。     

血清可溶性血管细胞粘附分子1和选择素E与2型糖尿病血管病变的关系

为研究可溶性血管细胞粘附分子 1和选择素E在 2型糖尿病患者血管病变中的变化 ,应用酶联免疫吸附法检测 2型糖尿病组 (分为并发大血管病变组、微血管病变组和无微血管病变组 )、糖耐量受损组、空腹血糖受损组和正常对照组的血管细胞粘附分子 1和选择素E水平 ,并测定糖代谢指标和尿微量白蛋白水平。结果发现 ,2型糖尿病组和糖耐量受损组血管细胞粘附分子 1和选择素E水平显著高于对照组 (P <0 .0 1) ;糖尿病伴大血管病变组血管细胞粘附分子 1和选择素E显著高于微血管病变组 ,伴微血管病变组高于无微血管病变组 (P <0 .0 1) ;空腹血糖受损组与对照组差异无显著性 ;在不同种类数量的微血管病变组间 ,血管细胞粘附分子 1和选择素E差异存在显著性 (P <0 .0 5 ) ;血管细胞粘附分子 1和选择素E存在相关性 (γ =0 .4 2 ,P <0 .0 5 ) ;选择素E与糖代血红蛋白存在相关性 (γ =0 .5 9,P <0 .0 1)。以上提示 ,血管细胞粘附分子 1和选择素E可能参与了 2型糖尿病血管病变的发生和发展 ,检测血清血管细胞粘附分子 1和选择素E水平在一定程度上可反映 2型糖尿病血管病变的情况。     

5-HT2A receptor antagonist increases circulating adiponectin in patients with type 2 diabetes.

We compared the levels of plasma adiponectin, platelet activation markers (P-selectin, CD63, PAC-1, annexin V, and platelet-derived microparticles), and endothelial injury markers (soluble E-selectin and soluble vascular cell adhesion molecule-1) in 53 patients with type 2 diabetes mellitus to investigate potential contributions to diabetic vascular complications. In addition, we administered serotonin antagonist (sarpogrelate hydrochloride) to type 2 diabetes patients who had increased soluble E-selectin levels. The concentrations of platelet activation markers and endothelial injury markers in diabetic patients were significantly higher than those in normal subjects. However, levels of adiponectin were lower in type 2 diabetes patients than in control subjects. A total of 32 patients had high-soluble E-selectin levels (soluble E-selectin >or= 62 ng/ml); a subset of patients that also had significant elevation of platelet activation and endothelial injury markers compared with patients without high soluble E-selectin. In addition, both platelet-P-selectin and platelet-derived microparticle levels negatively correlated with the adiponectin level. Patients with high soluble E-selectin exhibited significant improvement of all markers after sarpogrelate hydrochloride treatment. These findings suggest that there is a link between vascular change in type 2 diabetes and activated platelets, endothelial dysfunction, and an adiponectin abnormality.     

血清E-选择素和血清C-反应蛋白在急性冠状动脉综合征患者中的变化及意义

目的:观察血清E选择素、血清C反应蛋白(CRP)水平在急性冠状动脉综合征(ACS)患者中的变化,并探讨其与斑块稳定性的关系。方法:30例ACS患者(ACS组)、24例稳定型心绞痛(SAP)患者(SAP组)及30例冠状动脉造影阴性者(对照组)作为入选对象,均以酶联免疫吸附法(ELISA)检测其E选择素,免疫速率散射测浊法测定其CRP水平。结果:ACS组血清E选择素、CRP水平显著高于SAP组(P<0.01)和对照组(P<0.01)。结论:血清E选择素、CRP可能与ACS发病有关,并反映斑块的不稳定性。     

急性冠脉综合征患者血清E-选择素和白细胞CD11b/CD18表达的研究

目的观察血清E-选择素水平、中性粒细胞及单核细胞CD11b/CD18表达在急性冠脉综合征(ACS)患者中的变化,探讨其与斑块稳定性的关系.方法 30例ACS患者(ACS组)、24例稳定型心绞痛患者(SA组),30例冠状动脉造影阴性者作为对照组.酶联免疫吸附法检测E-选择素,流式细胞仪检测CD11b/CD18的表达.结果血清E-选择素水平、中性粒细胞和单核细胞膜CD11b/CD18的表达ACS组显著高于SA组(P<0.01)和对照组(P<0.01).结论 ACS患者血清E-选择素水平、中性粒细胞和单核细胞膜CD11b/CD18的表达增加与斑块不稳定性有关.     

Circulating adhesion molecules in patients with vibration-induced white finger

We investigated whether a relationship existed between soluble adhesion molecules and vascular damage from vibration-induced white finger. Thirty-five men exposed to vibration and 40 healthy control subjects were examined. Concentrations of soluble E-selectin intercellular adhesion molecules, and vascular cell adhesion molecules in serum were measured with sandwich enzyme-linked adhesion immunosorbent assay. Neither E-selectin nor intercellular adhesion molecule levels are elevated in men exposed to vibration with white finger compared to levels in men exposed to vibration without white finger and control subjects. The serum level of soluble vascular cell adhesion molecules is significantly increased in patients with vibration-induced white finger.     

Serum concentration of E-selectin in patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma

Objectives: High levels of soluble E-selectin have been reported in acute and chronic inflammatory disorders. Moreover, in some types of tumor elevated values have been found while in other types reduced levels have been reported. Our aims were to determine whether soluble E-selectin levels might be useful in monitoring the progression of chronic liver disease, including hepatocellular carcinoma. Methods: Circulating soluble E-selectin was measured by an enzyme-linked immunosorbent assay in the sera of 18 patients with chronic hepatitis, 44 with liver cirrhosis, and 38 with hepatocellular-carcinoma-associated liver cirrhosis. Immunohistochemical localization of E-selectin was also performed on liver tissue specimens of patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. Results: Serum levels of soluble E-selectin were higher in the chronic hepatitis and liver cirrhosis patients than in the hepatocellular carcinoma patients and healthy controls. Levels in the hepatocellular carcinoma patients and controls were not significantly different. In the liver cirrhosis group, divided according to the Child-Pugh classification, soluble E-selectin decreased with disease severity. Similarly, in patients with liver cirrhosis who developed hepatocellular carcinoma, soluble E-selectin decreased as the disease progressed. Immunohistochemical localization showed strong membrane staining on endothelial cells in areas rich in inflammatory cells in severe chronic hepatitis. In some hepatocellular carcinoma tissues a marked E-selectin staining was observed on endothelial cells of tumor-associated small vessels. Conclusions: The results obtained suggest that high serum levels of soluble E-selectin are associated with chronic hepatitis and liver cirrhosis, and that levels decrease in liver cirrhosis patients as the disease progresses. Patients with hepatocellular carcinoma have different types of soluble E-selectin behaviour the significance of which requires further investigation. Received: 27 July 1999 / Accepted: 24 December 1999     

Release of Soluble E-Selectin from Activated Endothelial Cells upon Apoptosis

Circulating soluble E-selectin is increased in diseases associated with endothelial apoptosis such as sepsis and acute respiratory distress syndrome. We investigated the mechanism by which endothelial cell (EC) apoptosis may promote soluble E-selectin release. We found that serum deprivation of EC caused apoptosis, yet it did not induce E-selectin EC surface expression. Tumor necrosis factor-α (TNFα) significantly increased EC E-selectin surface expression. Soluble E-selectin was noted, however, only in the medium of TNFα-activated, apoptotic EC. Preincubation of the EC with the caspase inhibitor z-VAD-fmk significantly attenuated soluble E-selectin levels in the culture medium of TNFα-activated, apoptotic EC, but it had no effect on E-selectin surface expression. These results indicate that TNFα activation, but not apoptosis, is necessary for E-selectin surface expression in EC. Furthermore, E-selectin release from EC requires caspase-3 activation. Thus, increased concentrations of circulating E-selectin in serum may serve as a marker for endothelial apoptosis in certain disease states. E. O. Harrington and J. Newton contributed equally to this work.     

Involvement of E-selectin in recruitment of endothelial progenitor cells and angiogenesis in ischemic muscle

E-selectin plays critical roles in tethering leukocytes to endothelial cells (ECs). We studied the role of E-selectin in endothelial progenitor cell (EPC) homing and vasculogenesis. After ischemia, the expression of E-selectin on ECs peaked 6 to 12 hours and returned to baseline at 24 hours, whereas the level of soluble E-selectin (sE-selectin) in serum increased over 24 hours and remained high at day 7. Mouse bone marrow-derived EPCs expressed not only E-selectin but also its ligand. Homing of circulating EPCs to ischemic limb was significantly impaired in E-selectin knock-out mice, as well as wild-type mice pretreated with blocking antibody against E-selectin, which was rescued by local sE-selectin injection. Mechanism for this is that sE-selectin stimulated not only ECs to express ICAM-1, but also EPCs to secrete interleukin-8 (IL-8), leading to enhanced migration and incorporation to ECs capillary formation. In therapeutic aspect, local treatment with sE-selectin enhanced efficacy of EPC transplantation for vasculogenesis and salvage of ischemic limb. Conversely, when E-selectin was knocked down by E-selectin small interfering RNA, blood flow recovery after EPC transplantation was significantly impaired. But this impaired vasculogenesis was rescued by sE-selectin. In conclusion, these data demonstrate E-selectin is a pivotal molecule for EPCs' homing to ischemic limb and vasculogenesis.     

E-selectin permits communication between PAF receptors and TRPC channels in human neutrophils

The selectin family of molecules (L-, P-, and E-selectin) mediates adhesive interactions between leukocytes and endothelial cells required for recruitment of leukocytes to inflammatory sites. Soluble E-selectin levels are elevated in inflammatory diseases and act to promote neutrophil beta(2)-integrin-mediated adhesion by prolonging Ca(2+) mobilization. Although soluble E-selectin alone was unable to initiate Ca(2+) signaling, it allowed a novel "permissive" store-operative calcium entry (SOCE) following the initial platelet-activating factor (PAF)-induced release of Ca(2+) from inositol 1,4,5-trisphosphate (IP(3))-sensitive stores. This induction of permissive SOCE in response to soluble E-selectin and PAF was shown to act through a G protein-coupled receptor (GPCR) coupled to pertussis toxin-insensitive G(q/11). Furthermore, we demonstrated that permissive SOCE was mediated by canonical transient receptor potential channel (TRPC) due to its sensitivity to specific inhibition by MRS1845 and Gd(3+) and that TRPC6 was the principal TRPC family member expressed by human neutrophils. In terms of mechanism, we demonstrated that soluble E-selectin activated Src family tyrosine kinases, an effect that was upstream of phosphatidylinositol 3'-kinase in a signaling pathway that regulates permissive SOCE following exposure of neutrophils to PAF. In summary, this report provides the first evidence for communication between an inflammatory mediator and adhesion receptors at a molecular level, through selectin receptor ligation allowing permissive SOCE to occur following PAF stimulation of human neutrophils.     

Effects of nasal continuous positive airway pressure on soluble cell adhesion molecules in patients with obstructive sleep apnea syndrome

PURPOSE: Obstructive sleep apnea syndrome is common in middle-aged men and may be associated with an increased risk of cardiovascular disease. We investigated the effect of nasal continuous positive airway pressure (CPAP) treatment on levels of soluble cell adhesion molecules-which have been shown to be associated with the development of atherosclerosis-in these patients. SUBJECTS AND METHODS: We studied 23 patients with obstructive sleep apnea syndrome diagnosed by polysomnography who were treated with nasal CPAP. Serum soluble intercellular adhesion molecule-1, E-selectin, and vascular cell adhesion molecule-1 levels were measured before nasal CPAP was started, and after 3 or 4 days (n = 19), 1 month (n = 23), or 6 months (n = 11) of treatment. RESULTS: After 3 to 4 days of nasal CPAP therapy, the mean (+/- SD) soluble E-selectin level had decreased from 89 +/- 44 ng/mL to 69 +/- 28 ng/mL (P = 0.002). After 1 month, the soluble intercellular adhesion molecule-1 level had decreased from 311 +/- 116 ng/mL to 249 +/- 74 ng/mL (P = 0.02). After 6 months, soluble vascular cell adhesion molecule-1 levels had not changed significantly, while the mean soluble intercellular adhesion molecule-1 level (212 +/- 59 ng/mL) had decreased further (P = 0.02). Before treatment, soluble intercellular adhesion molecule-1 levels and the apnea and hypopnea index were correlated (r = 0.43, P = 0.04). CONCLUSIONS: Obstructive sleep apnea and hypopnea have a significant adverse effect on serum soluble cell adhesion molecule-1 levels that may be reduced by nasal CPAP treatment.     

High serum concentrations of soluble E-selectin correlate with obesity but not fat distribution in patients with type 2 diabetes mellitus

Serum concentrations of soluble adhesion molecules, eg, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin are elevated in patients with type 2 diabetes. However, little is known about the role of obesity or abnormal fat distribution in inducing upregulation of adhesion molecules. To investigate this issue, soluble ICAM-1, VCAM-1, and E-selectin levels were evaluated in 40 obese and 30 nonobese patients with type 2 diabetes. Both groups were matched for age, sex, and glycosylated hemoglobin (HbA(1c)) levels. Computed tomography (CT) was used to measure the abdominal subcutaneous and visceral fat areas. Soluble ICAM-1 and VCAM-1 levels did not differ significantly between obese and nonobese patients. However, serum concentrations of soluble E-selectin were significantly higher in obese than in nonobese patients (90 +/- 7 v 56 +/- 4 ng/mL, P <.01). Soluble E-selectin levels significantly correlated with body mass index, subcutaneous fat area, and visceral fat area (Rho = 0.48, 0.37, and 0.30, respectively). Stepwise multiple regression analysis showed that body mass index (F = 16.7), but not subcutaneous and visceral fat areas (F = 0.29 and 0.01, respectively), significantly and independently correlated with soluble E-selectin levels. Our results suggest that obesity may induce endothelial activation or increased shedding of cell surface E-selectin that leads to subsequent increase in soluble E-selectin levels. The high serum concentrations of E-selectin closely correlated with increased total fat volume, but not with regional fat distribution.