2型糖尿病患者血小板-白细胞聚集体与微血管病变部位及区域数量的关系

目的探讨T2DM患者不同部位及区域数量微血管病变外周血血小板-白细胞聚集体(PLA)水平的改变。方法检测T2DM患者外周血中血小板-中性粒细胞聚集体(PNA)及血小板-单核细胞聚集体(PMA),按照微血管病变部位,比较DR、糖尿病慢性肾脏疾病(CKD)和糖尿病神经病变(DN)患者以及不同损伤区域数量微血管病变患者PNA、PMA水平。结果糖尿病微血管病变患者PNA、PMA水平高于无血管病变患者和健康对照者(P0.01)。DR、CKD及DN患者PNA、PMA水平比较差异无统计学意义。合并3种微血管病变患者PNA、PMA水平高于合并1种微血管病变患者(P0.01),合并2种微血管病变患者PMA水平高于合并1种微血管病变患者(P0.05)。结论糖尿病微血管病变患者PLA水平升高,PLA水平与微血管病变部位无关,与微血管病变损伤区域数量有关,PLA水平与糖尿病微血管病变的广泛性一致。     

2型糖尿病微血管并发症相关因素的有序Logistic回归分析

目的研究2型糖尿病(T2DM)微血管并发症〔主要为糖尿病肾病(DN)、糖尿病视网膜病变(DR)〕的相关因素,为防治提供依据。方法选择T2DM病人190例,根据DN、DR分期分组,比较临床资料的差异,并纳入有序Logistic回归分析微血管病变的危险因素。结果 DR分组中年龄、病程、高血压、TC、HDL、空腹C肽差异有统计学意义(P<0.05),经有序Logistic回归分析后,发现高血压、病程与DR严重程度呈正相关(P<0.05),C肽水平与DR严重程度呈负相关(P<0.05);DN分组中年龄、病程、高血压差异有统计学意义(P<0.05),有序Logistic回归分析示高血压、病程与DN严重程度呈正相关(P<0.05)。结论糖尿病病程、高血压是微血管病变的独立危险因素;空腹C肽是微血管病变的保护因素。     

血浆同型半胱氨酸与2型糖尿病微血管病变的关系

目的了解血浆同型半胱氨酸（Hcy）与2型糖尿病微血管病变间的关系,并分析影响糖尿病患者Hcy代谢的因素。方法将122例糖尿病患者分为无微血管并发症（NDC）组、糖尿病视网膜病变（DR）组和糖尿病肾病（DN）组3组。酶免疫分析法测定血浆Hcy和血浆血栓调节蛋白（sTM）浓度;发光免疫法测定血清叶酸和VitB12水平。结果DR组和DN组的空腹血浆Hcy浓度明显高于NDC组和对照组（P〈0．01）;高Hcy血症的糖尿病患者DR、DN发生率明显高于无高Hcy血症糖尿病患者（P〈0．01）;相关分析表明,糖尿病患者Hcy水平与sTM、肌酐（Scr）水平呈显著正相关（P〈0．01）,与叶酸、VitB12水平呈显著负相关（P〈0．01）。Logistic回归分析显示空腹Hcy、甘油三酯、VitB12、叶酸、sTM与DN的发生有关;Hcy、FPG、Scr、甘油三酯均为DR的独立危险因素。结论血清叶酸、VitB12、Scr以及代谢紊乱程度影响Hcy的浓度;空腹高Hcy血症是糖尿病微血管病变发生、发展的危险因素之一。     

糖尿病微血管并发症与血清E-选择素关系探讨

目的研究2型糖尿病并发微血管病的老年患者血清可溶性E选择素(sE selectin,sE sel)水平的变化。方法应用酶联免疫吸附法(ELISA)测定153例2型糖尿病患者和30例健康对照者血清sE sel水平,并测定BMI、糖化血红蛋白(HbA1c)、空腹血糖、甘油三酯(TG)、胆固醇(TC)、BUN、UAER(尿白蛋白排出率)水平。结果所有糖尿病患者血清sE sel浓度均显著高于正常对照组(P<0.01);2型糖尿病有微血管病变组均高于无微血管病变组(均为P<0.05);sE sel水平与HbA1c呈正相关(r=0.61,P<0.05)。结论血清sE sel参与了老年糖尿病微血管病变的发病过程,是糖尿病视网膜病(DR)、糖尿病肾病(DN)的严重程度监测指标之一。     

血浆同型半胱氨酸浓度与2型糖尿病视网膜病变的关系

目的　观察空腹血浆总同型半胱氨酸 (Hcy)水平与 2型糖尿病视网膜病变发生发展的关系。方法　研究对象为 5 5例 2型糖尿病 (DM)和 19例 (男 12例 ,女 7例 )非DM健康对照者 (CON)。DM组分为两个亚组 :无微血管并发症 (NDC)组 39例 (男 17例 ,女 2 2例 ) ,糖尿病视网膜病变 (DR)组16例 (男 8例 ,女 8例 )。所有患者肾功能和尿白蛋白 /肌酐 (Alb/Cr)均正常。根据眼底荧光造影判断视网膜病变的严重程度。应用高效液相 反相色谱分析和荧光检测的方法测定空腹血浆总Hcy水平。结果　DR组、NDC组和CON组间的血浆总Hcy浓度差异有显著性 (F =2 4 0 5 ,P =0 0 31) ,DR组血浆总Hcy水平 [(14 7± 5 2 8) μmol/L]显著高于NDC组 [(11 3± 4 94) μmol/L]和CON组 [(9 6 5± 2 6 6 )μmol/L]。NDC组与CON组比较差异无显著性。在DR组 ,增殖性视网膜病变 (PDR)亚组总Hcy水平显著高于背景性视网膜病变 (BDR)亚组 (t=2 4 0 5 ,P =0 0 31)。本研究中 ,总Hcy超过 14 97μmol/L即为高同型半胱氨酸血症 ,其中PDR亚组有 4例 ,BDR亚组为 1例。结论　伴视网膜病变的 2型DM患者血浆总Hcy水平高于正常人 ,其中PDR组的血浆总Hcy浓度高于BDR组。空腹血浆同型半胱氨酸水平可能是 2型糖尿病视网膜病变的重要危险因素之一。     

2型糖尿病肾病患者血浆同型半胱氨酸水平的变化

将60例糖尿病患者分为无血管并发症组(NDC)32例和DN组28例,并以30例健康人作为对照组(CON),测定空腹血浆HCY浓度.结果2型糖尿病患者各组HCY浓度高于CON组,DN组又高于NDC组(P＜0.01),HCY浓度与HbA1c、FBG和PBG呈正相关.结论空腹高HCY血症是DN的相关因素.     

住院老年2型糖尿病患者微血管病变的相关因素分析

目的探讨老年2型糖尿病患者微血管病变的构成比及相关因素。方法用回顾性分析的方法研究2003年～2010年于卫生部北京医院住院治疗的年龄≥60岁的2型糖尿病患者876例,分为糖尿病肾病(DN)组和非糖尿病肾病(非DN)组,糖尿病视网膜病变(DR)组和非糖尿病视网膜病变(非DR)组,糖尿病周围神经病变(DPN)组和非糖尿病周围神经病变(非DPN)组,计算DN、DR、DPN构成比,比较患者的临床特点,并探寻老年2型糖尿病患者DR、DN、DPN的相关因素。结果 (1)DN构成比为34.5%,DR构成比为42.4%,DPN构成比为82.3%。(2)DN与非DN两组间体质量指数(BMI)、糖尿病病程、高血压病程、收缩压(SBP)、舒张压(DBP)、空腹血糖(FBS)、糖化血红蛋白(HbA1c)、空腹胰岛素(Fins)、高密度脂蛋白胆固醇(HDL)、甘油三酯(TG)、尿酸(UA)均有显著性差异(P<0.05或P<0.01);DR与非DR两组间仅糖尿病病程、SBP、空腹C肽(FCP)有显著性差异(均P<0.01);DPN与非DPN两组间年龄、糖尿病病程、HbA1c、TC、LDL有显著性差异(P<0.05或P<0.01)。(3)Logistic回归结果显示,DN与SBP、HbA1c、FBS、HDL、UA、糖尿病病程有关(OR值分别为1.022、1.098、1.075、0.501、1.004,1.048,P<0.05或P<0.01);DR与SBP、HbA1c、糖尿病病程有关(OR值分别为1.017、1.102、1.097,P<0.05或P<0.01);DPN与HbA1c、LDL、糖尿病病程、年龄有关(OR值分别为1.226、1.370、1.041、1.058,P<0.05或P<0.01)。结论对于老年2型糖尿病患者,DN、DR、DPN均与糖尿病病程和HbA1c有关,控制血糖对防治微血管病变意义重大,综合控制血糖、血压、血脂、尿酸可以更好的防治糖尿病微血管并发症。     

不同分期老年2型糖尿病肾病患者外周血调节性和辅助性T细胞的表达

目的分析不同分期老年2型糖尿病肾病(DN)患者外周血调节性和辅助性T细胞的表达水平。方法选择老年DN患者38例(早期DN23例和中、晚期DN15例),另择同期老年糖耐量异常(IGT)患者19例,同期健康老年人21例为对照组,入选对象均接受了外周血调节性T细胞(CD4+CD25+Treg和CD4+CD25+Foxp3+Treg)和辅助性T细胞(CD+3、CD+4、CD+8、CD+4/CD+8)检测。结果不同分期的老年DN患者外周血CD4+CD25+Treg和CD4+CD25+Foxp3+Treg水平均明显低于IGT组和对照组,而前两者的外周血CD+4水平和CD+4/CD+8比值均显著高于对照组,CD+8水平显著低于对照组(P<0.05,P<0.01)。中、晚期DN患者的外周血CD4+CD25+Treg和CD4+CD25+Foxp3+Treg水平均明显低于早期DN组,而CD+4水平和CD+4/CD+8比值均显著高于早期DN组(P<0.05,P<0.01)。结论老年DN患者存在明确的外周血调节性T细胞和辅助性T细胞异常表达,并随病情分期升级而进一步失衡。     

血清VEGF及ICAM-1水平与糖尿病视网膜病变患者微血管损伤的关系

目的探讨血清中血管内皮生长因子(VEGF)及细胞间黏附分子(ICAM)-1水平与糖尿病视网膜病变(DR)患者微血管损伤之间的关系。方法未应用抗凝类药物治疗的2型糖尿病(T2DM)患者120例,根据临床及眼底检查确诊将其分为非DR(NDR)组(n=56)、非增生型DR(NPDR)组(n=30)、增生型DR(PDR)组(n=34)。比较各组微血管病变发生率;采用流式细胞仪检测内皮细胞(ECs)、内皮祖细胞(EPCs)计数百分比;采用酶联免疫吸附法(ELISA)检测各组血清中VEGF及ICAM-1水平。结果 PDR组糖尿病肾病(DN)及神经病变的发生率明显高于NDR组和NPDR组(均P<0.05);与未发生微血管病变患者相比,发生微血管病变患者的EPCs水平明显下降,而ECs、VEGF和ICAM-1水平均明显升高(均P<0.05);不管是否发生微血管病变,PDR组的ECs、VEGF和ICAM-1水平均高于NDR组和NPDR组,NPDR组均高于NDR组,PDR组EPCs水平低于NPDR组,NPDR组低于NDR组(均P<0.05);PDR组VEGF、ICAM-1水平与ECs水平呈正相关(r=0.995,0.852,P<0.05),与EPCs水平呈负相关性(r=-0.895,-0.920,P<0.05)。结论 VEGF和ICAM-1在DR患者微血管损伤中高表达,与ECs和EPCs密切相关,提示VEGF和ICAM-1在DR患者微血管损伤形成中与血管内皮功能密切相关。     

醛糖还原酶基因启动子区C-106T多态性与2型糖尿病患者视网膜病变易感性的研究

目的　研究中国北方汉族人 2型糖尿病视网膜病变 (DR)的易感性与醛糖还原酶 (AR)基因启动子区C 10 6T多态性的相关性 ,并探讨此多态性与AR基因 5′端 (AC)n多态性的连锁关系。　方法　 2型糖尿病 (T2DM)患者 116例 ,分为无微血管并发症 (NDC)组和糖尿病视网膜病变 (DR)组 ,提取外周血基因组DNA ,经PCR后用限制性内切酶BfαⅠ 5U进行酶切 ,酶切产物于 3 %琼脂糖凝胶电泳 ,用紫外凝胶成像系统GDS 76 0 0S观察结果。　结果　NDC组和DR组患者均发现 2种等位基因C T ,三种基因型CC、CT和TT ,CC基因型频率在DR组明显高于NDC组 ( 6 4.0 %vs 43.9%,P <0 .0 5 ) ,CT基因型频率在DR组明显低于NDC组 ( 30 %vs 5 4%,P <0 .0 1) ;Z - 2 C单倍型频率在DR组明显高于NDC组 ( 37.0 %vs 3 .0 %,P <0 .0 1) ,Z +2 C和Z +2 T单倍型频率在DR组明显低于NDP组 ( 11.0 %vs 42 .0 %,P <0 .0 1;2 .0 %vs 14.0 %,P <0 .0 5 )。　结论　CC基因型可能增加DR易感性 ,CT基因型可能减低DR易感性 ,且该多态性位点可能与AR基因 5′端 (AC)n多态性之间存在连锁不平衡。     

阿托伐他汀对急性冠脉综合征患者血清高敏C反应蛋白和妊娠相关血浆蛋白-A水平的影响

目的探讨阿托伐他汀干预对急性冠脉综合征(ACS)患者血清高敏C反应蛋白(hs-CRP)和妊娠相关血浆蛋白-A(PAPP-A)水平的影响。方法采用酶联免疫吸附法测定不稳定型心绞痛患者(UAP,n=37)、急性心肌梗死患者(AMI,n=24)、稳定型心绞痛患者(SAP,n=29)和健康体检者(n=32)的hs-CRP和PAPP-A水平。同时将ACS患者(包括UAP和AMI组,n=61)随机分为常规治疗组(n=30)和阿托伐他汀干预组(阿托伐他汀10mg/d,n=31),并于治疗前后分别测定血清hs-CRP和PAPP-A水平。结果(1)hs-CRP和PAPP-A水平在UAP组[(16.7±1.24)mg/L,(63.88±1.82)μg/L]、AMI组[(18.52±1.96)mg/L,(66.41±1.24)μg/L]比SAP组[(4.6±1.16)mg/L,(47.56±0.72)μg/L]、正常对照组[(3.2±0.88)mg/L,(45.17±1.28)μg/L]显著升高(P<0.05)。(2)2周后,阿托伐他汀干预组血清hs-CRP和PAPP-A水平较治疗前明显降低[hs-CRP(18.52±2.37)mg/Lvs.(3.58±1.33)mg/L;PAPP-A(67.83±2.15)μg/Lvs.(45.62±1.58)μg/L,P<0.05],且较常规治疗组治疗2周后亦有显著降低[hs-CRP(3.58±1.33)mg/Lvs.(5.23±1.98)mg/L;PAPP-A(45.62±1.58)μg/Lvs.(51.35±2.15)μg/L,P<0.05]。结论阿托伐他汀干预可以减少急性冠脉综合征患者动脉粥样硬化斑块的炎症反应,具有稳定斑块的作用。     

Serum Sialic Acid and the Long-term Complications of Insulin-dependent Diabetes Mellitus

Elevated serum sialic acid (SSA) predicts cardiovascular disease in the non-diabetic population and is also associated with the presence of microalbuminuria and clinical proteinuria in patients with insulin-dependent diabetes (IDDM). We have studied 121 patients with IDDM of long duration (mean duration 25.2 years) to investigate the relationship of SSA concentrations to the presence of retinopathy, nephropathy, and neuropathy. SSA levels were elevated in patients with retinopathy (0.578 ± 0.161 g l⁻¹, n = 98) when compared with those without retinopathy (0.468 ± 0.145 g l⁻¹, n = 23, p = 0.002). Patients with nephropathy (urinary albumin:creatinine ratio of > 3 mg mmol⁻¹ in all of three early morning specimens of urine) also had raised SSA levels (0.625 ± 0.169 g l⁻¹, n = 30) compared with those without nephropathy (0.533 ± 0.160 g l⁻¹, n = 91, p = 0.006). There was a significant correlation of SSA with urinary albumin:creatinine ratio (correlation coefficient 0.33, p < 0.001). SSA levels were not related to the presence or absence of neuropathy (0.567 ± 0.181 g l⁻¹, n = 28, vs 0.533 ± 0.160 g l⁻¹, n = 93, p = 0.92, respectively). In conclusion, retinopathy and nephropathy but not neuropathy are associated with increased SSA levels in patients with IDDM. The significance of this is not yet clear but it is possible that sialic acid is involved in the pathophysiology of microvascular disease in IDDM.     

Prevalence of left ventricular hypertrophy in Type I diabetic patients with diabetic nephropathy

Summary The increased mortality of patients with diabetic nephropathy is mainly due to cardiovascular disease and end stage renal failure. Left ventricular hypertrophy is an independent risk factor for myocardial ischaemia and sudden death. The aim of our cross-sectional study was to evaluate left ventricular structure and function in Type I (insulin-dependent) diabetic patients with diabetic nephropathy. M-mode and Doppler echocardiography were done on 105 Type I diabetic patients with diabetic nephropathy [61 men, age (means ± SD) 44 ± 9 years, and albuminuria [median(range)] 567(10–8188) mg/24 h, serum creatinine 109 (53–558) μmol/l], and 140 Type I diabetic patients with persistent normoalbuminuria [79 men, 47 ± 10 years, urinary albumin excretion rate 8 (0–30) mg/24 h, and serum creatinine 81 (55–121) μmol/l]. Patients with and without nephropathy were comparable with respect to sex, body mass index, and duration of diabetes. Arterial blood pressure was slightly higher in patients with nephropathy: 140/79 ± 17/9 mm Hg vs 134/78 ± 15/8 mm Hg, p < 0.01, and the majority of proteinuric patients received antihypertensive drugs, 84 vs 17 %, respectively, p < 0.001. Left ventricular mass index was increased in the nephropathic group (means ± SD) 100.6 ± 23.9 g/m² compared with the normoalbuminuric group 91.4 ± 21.9 g/m², p = 0.002. Left ventricular hypertrophy was found more often in patients with nephropathy 23 (14–31)% compared with patients with normoalbuminuria 9 (5–14)%, p < 0.005. Diastolic function, assessed by the ratio between the peak diastolic velocity and the peak atrial systolic velocity (E/A ratio) and isovolumic relaxation time, was reduced in patients with vs without nephropathy: 1.17 ± 0.29 vs 1.34 ± 0.32, and 81.7 ± 16.5 vs 74.6 ± 14.5, p < 0.001 and p = 0.002, respectively. Systolic function was about the same and normal in both groups. Our study suggests that an increase in left ventricular mass index and a decrease in diastolic function occurs early in the course of diabetic nephropathy. [Diabetologia (1999) 42: 76–80] Received: 16 April 1998 and in final revised form: 5 August 1998     

2型糖尿病肾病亚甲基四氢叶酸还原酶基因多态性研究

目的探讨亚甲基四氢叶酸还原酶(methylenetetrahydrofolate     

慢性情绪应激对高脂饮食大鼠炎症反应和主动脉Toll样受体4表达的影响

目的通过观察慢性情绪应激对高脂饮食大鼠脂代谢、炎症反应和主动脉内皮细胞TLR4表达的影响,探讨慢性情绪应激在动脉粥样硬化病变形成中的作用、机制。方法雄性Wistar大鼠40只,随机分为正常对照组(NC)、无应激组(NS)、生理应激组(PS)和情绪应激组(ES),每组各10只,并制作慢性情绪应激模型。于末次应激结束后采集血标本,全自动生化分析仪检测血清TC、TG、HDL-C、LDL-C和hs-CRP,ELISA法测定血清ox-LDL、放免法检测TNF-α水平;HE染色观察大鼠主动脉形态学变化;免疫组化法(S-P)测定主动脉内皮细胞TLR4表达。结果 (1)ES组大鼠较其他3组出现了明显的脂代谢紊乱和炎症反应。与PS组、NS组、NC组比较,ES组TC、LDL-C、ox-LDL水平明显升高[TC:(5.30±0.69)mmol/L比(3.94±0.42)mmol/L、(3.82±0.48)mmol/L、(2.07±0.26)mmol/L;LDL-C:(1.57±0.22)mmol/L比(1.18±0.13)mmol/L、(1.11±0.11)mmol/L、(0.75±0.11)mmol/L;ox-LDL:(65.18±6.51)μg/dl比(45.65±2.70)μg/dl、(38.35±2.27)μg/dl、(14.99±1.46)μg/dl,均为P<0.01];ES组HDL-C[(0.94±0.14)mmol/L]低于NS组[(1.09±0.14)mmol/L,P<0.05],低于NC组[(1.16±0.18)mmol/L,P<0.01];与PS组、NS组、NC组比较,ES组hs-CRP、TNF-α水平升高[hs-CRP:(1.748±0.082)mg/L比(1.485±0.067)mg/L、(1.381±0.067)mg/L、(0.757±0.069)mg/L;TNF-α:(2.447±0.083)μg/L比(2.189±0.099)μg/L、(2.181±0.085)μg/L、(1.772±0.075)μg/L,均为P<0.01];(2)ES组大鼠主动脉出现早期动脉粥样硬化性改变;(3)ES组大鼠主动脉内皮细胞TLR4表达明显上调,其阳性细胞单位面积平均吸光度值(A)高于PS组、NS组和NC组[(0.334±0.010)比(0.250±0.012)、(0.238±0.015)、(0.082±0.008),均为P<0.01]。结论慢性情绪应激可能在动脉粥样硬化形成的早期,部分通过激活TLR4释放炎性细胞因子引起机体的炎症反应,进而导致动脉粥样硬化病变形成。     

Telomere length and progression of diabetic nephropathy in patients with type 1 diabetes

Abstract. Fyhrquist F, Tiitu A, Saijonmaa O, Forsblom C, Groop P‐H, on behalf of the FinnDiane Study Group (Minerva Institute for Medical Research; Helsinki University Central Hospital; and Folkhälsan Institute of Genetics; Helsinki, Finland). Telomere length and progression of diabetic nephropathy in patients with type 1 diabetes. J Intern Med 2010; 267 : 278–286. Objectives. To determine whether short telomere length of blood leucocytes from patients with type 1 diabetes is associated with or predictive of progression of diabetic nephropathy. Design and methods. Two consecutive DNA samples were obtained from 132 patients from the nationwide Finnish Diabetic Nephropathy Study with type 1 diabetes. Control DNA samples were taken from 44 healthy blood donors. Telomere length was measured by Southern blot. Patients were divided into three groups according to their urinary albumin excretion rate (AER): 48 patients with normoalbuminuria (AER < 20 μg min^?1); seven patients with microalbuminuria (AER ≥ 20 μg min^?1 <200 μg min^?1) and 77 patients with macroalbuminuria (AER ≥ 200 μg min^?1). Progression was defined as a change in albuminuria to a higher level. Results. Progression occurred in 21 patients. Progressors had shorter mean telomere length (8.1 ± 0.7 kb, mean ± SD; P = 0.017) and higher percentage of short telomeres (32.0 ± 8%, P = 0.002) than nonprogressors (8.5 ± 0.7 kb and 27 ± 7.2%, respectively). Thus, both shorter telomeres (HR = 0.190, 95%CI 0.065–0.558, P = 0.0025) and higher proportion of short telomeres (HR = 1.115, 1.039–1.195, P =0.0023) were independent predictors of diabetic nephropathy. Telomere length was not associated with the degree of albuminuria and was not different in patients with type 1 diabetes compared with healthy controls. Conclusions. Short telomeres are independent predictors of progression of diabetic nephropathy in patients with type 1 diabetes.     

急性冠状动脉综合征患者血液凝固性加强

目的通过研究急性冠状动脉综合征患者凝血状态的变化,探讨急性冠状动脉综合征患者的发病与血栓前状态的关系,以期对危重冠心病患者及早作出诊断和治疗。方法选择急性冠状动脉综合征患者86例,对照组为稳定型心绞痛患者75例,以酶联免疫吸附法测定两组患者血浆凝血酶原片段1和2、可溶性纤维蛋白单体复合物等凝血分子标志物的含量并进行比较。结果急性冠状动脉综合征患者血浆凝血酶原片段1和2及可溶性纤维蛋白单体复合物较稳定型心绞痛患者均显著升高(1.21±0.23nmolL比0.76±0.20nmolL;85.4±12.4mgL比68.7±13.8mgL,P均<0.001)。急性冠状动脉综合征合并2型糖尿病时血浆凝血酶原片段1和2及可溶性纤维蛋白单体复合物较不伴有2型糖尿病时显著升高(1.28±0.19nmolL比1.16±0.20nmolL;89.8±12.4mgL比82.7±13.7mgL,P均<0.05)。急性冠状动脉综合征合并原发性高血压时血浆凝血酶原片段1和2及可溶性纤维蛋白单体复合物较不伴有原发性高血压时显著升高(1.26±0.24nmolL比1.16±0.20nmolL;90.0±12.8mgL比82.7±13.7mgL,P均<0.05)。结论稳定型心绞痛患者的凝血系统处于稳定状态,而急性冠状动脉综合征患者处于高凝状态,合并2型糖尿病或原发性高血压的急性冠状动脉综合征患者高凝状态更显著,提示高凝状态与急性冠状动脉综合征的发病密切相关。     

糖尿病合并脑梗死患者外周血T淋巴细胞亚群与基质金属蛋白酶9的相关性

目的观察糖尿病合并脑梗死患者外周血T淋巴细胞亚群和基质金属蛋白酶9(matrix metalloproteinases 9,MMP-9)的相关性。方法选择住院治疗的急性脑梗死患者164例,将37例合并糖尿病的脑梗死患者作为合并组,127例无糖尿病的脑梗死患者作为脑梗死组。在发病48h内进行MMP-9、CD4T淋巴细胞、CD8T淋巴细胞和CD4/CD8比值检测,并进行相关性分析。结果与脑梗死组比较,合并组MMP-9水平升高[(8.78±2.85)μg/L vs(5.14±2.13)μg/L,P=0.046],CD8T淋巴细胞升高[(47.00±15.42)%vs(37.25±17.90)%,P=0.005],CD4T淋巴细胞降低[(14.80±6.39)%vs(20.98±12.74)%,P=0.029],CD4/CD8比值降低[(0.33±0.16)vs(0.51±0.25),P=0.015]。合并组和脑梗死组MMP-9与CD8T淋巴细胞呈正相关(r=0.774,P=0.041;r=0.526,P=0.037),与CD4T淋巴细胞呈负相关(r=-0.810,P=0.043;r=-0.633,P=0.036),与CD4/CD8比值呈负相关(r=-0.701,P=0.028;r=-0.616,P=0.045)。结论糖尿病合并脑梗死患者较非糖尿病的脑梗死患者更容易出现T淋巴细胞亚群紊乱,与MMP-9表达异常密切相关。     

Detection of monocyte-derived microparticles in patients with Type II diabetes mellitus

Aims/hypothesis. The role of plasma monocyte-derived microparticles (MDMPs) and platelet-activation markers (platelet-derived microparticle [PDMP], platelet-bound CD62P [plt-CD62P], and platelet-bound CD63 [plt-CD63]) in diabetic vascular complications is not clear. We measured and compared plasma concentrations of MDMPs and the platelet-activation markers to investigate their possible contribution to diabetic vascular complications. Methods. Activated platelets and microparticles (PDMP and MDMP) were analysed by flow cytometry. Concentrations of serum sE-selectin were measured with enzyme-linked immunosorbent assay. Results. The concentration of MDMPs in diabetic patients was higher than in normal subjects. We found no differences in the binding of anti-GPIIb/IIIa and anti-GPIb monoclonal antibodies between groups. There were differences, however, in the concentrations of PDMPs, plt-CD62P, and plt-CD63 between Type II (non-insulin-dependent) diabetes mellitus patients and control subjects (PDMPs: 585 ± 25 vs 263 ± 9, p < 0.01; plt-CD62P: 28.1 % ± 1.4 % vs 9.4 % ± 0.6 %, p < 0.001; plt-CD63: 28.1 % ± 1.4 % vs 8.6 % ± 0.5 %, p < 0.001). Amounts of MDMPs correlated positively with these platelet activation markers, and the relation between PDMP and MDMP was the most significant. The concentration of MDMP in patients who had diabetes complicated with nephropathy, retinopathy, or neuropathy was higher than in those without diabetes-related complications. The increase in MDMP was particularly significant in patients with nephropathy. Concentrations of sE-selectin were higher in Type II diabetes patients than in control subjects, and correlated with MDMP, PDMP, plt-CD62P, and plt-CD63 levels in nephropathy patients. Conclusion/interpretation. In Type II diabetes patients, we detected increased activation of monocytes, which could have been stimulated by activated platelets and PDMPs. Because the activation of monocytes is associated with vascular endothelial damage, high concentrations of MDMPs could indicate vascular complications in diabetes patients, especially those who have diabetes-related nephropathy. [Diabetologia (2002) 45: ▪–▪] Received: 21 May 2001 and in revised form: 13 November 2001     

原发性高血压并发初发糖尿病的相关因素

目的 分析原发性高血压并发初发糖尿病的相关因素。 方法 搜集2013年6月~2016年6月陕西省人民医院心内科收住入院诊断高血压病并发从未使用药物治疗的新诊断2型糖尿病患者468例作为并发糖尿病组。与同期入院诊断单纯原发性高血压患者468例作为对照组（非糖尿病组）比较分析。 结果 并发糖尿病组与非糖尿病组比较,体质量指数〔（28.8±3.9） kg/m2 vs.（25.1±3.2） kg/m2,P<0.05〕、HbA1c〔（9.4±1.6）% vs.（6.0±0.4）%,P<0.05〕、总胆固醇（TC）〔（4.8±1.4） mmol/L vs.（3.2±0.8） mmol/L,P<0.05〕、三酰甘油（TG）〔（2.2±1.3） mmol/L vs.（1.6±0.8） mmol/L,P<0.05〕均具有统计学意义。多因素Logistic分析回归分析显示TC、TG偏高为原发性高血压并发初发糖尿病危险因素,OR值分别为2.349（95%Cl:2.10-3.308）、1.903（95%Cl:1.508-2.267）;以HbA1c为因变量,体质量指数、TC、TG、低密度脂蛋白胆固醇为自变量行重线性回归分析,HbA1c与TC成正相关,回归方程为:HbA1c=1.309＋1.626×TC,P<0.01。 结论 TG、TC水平升高是高血压病并发初发糖尿病患者的危险因素,并且HbA1c与TC呈正相关。