同型半胱氨酸与糖尿病微血管病变的相关性研究

本研究纳入糖尿病患120例及健康志愿者40例。分为无微血管病变组(NDC)、糖尿病视网膜病变组(DR)和糖尿病肾病组(DN)。结果各组HCY含量高于NC组,(P 0. 05),FA和Vit B12含量低于NC组,(P 0. 05);微血管病变与HCY含量具有相关性(r=0. 765,P 0. 05),与FA(r=-0. 489,P 0. 05)和Vit B12(r=-0. 891,P 0. 05)含量呈负相关性。结论 HHCY是引发糖尿病微血管病变的有害因素。     

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。     

2型糖尿病患者糖皮质激素变化的临床研究

目的　探讨 2型糖尿病患者糖皮质激素分泌变化的规律及其临床意义。方法　测定 2 2名健康人 (对照组 )和 6 3例 2型糖尿病患者 (其中 39例 2型糖尿病无微血管病变、2 4例 2型糖尿病并微血管病变 )的血皮质醇 (F) ( 8Am、4Pm )、2 4h尿游离皮质醇 (UFC)及血糖 (FBG、2hPG)、HbA1c、TC和TG。结果　 2型糖尿病组的血F( 8Am、4Pm)及 2 4hUFC与对照组比较 ,差异有显著性 (P <0 .0 5 )。糖尿病有微血管病变组的 2 4hUFC的排量高于无微血管病变组 (P <0 .0 5 )。糖尿病组 2 4hUFC与HbA1c呈正相关 (r =0 .2 76 ,P <0 .0 5 ) ,与病程呈正相关 (r =0 .72 4,P <0 .0 1) ,与 2 4h尿微量白蛋白 (UAP)呈正相关 (r =0 .486 ,P <0 .0 1) ,与TG呈正相关 (r= 0 .42 1,P <0 .0 1)。结论　 2型糖尿病患者糖皮质激素水平增高 ,加重了糖代谢和脂代谢紊乱 ,使糖尿病患者的病情恶化 ,最终促使糖尿病并发症的发生。     

2型糖尿病微血管病变的影响因素

目的　探讨 2型糖尿病 (DiabetesMellitus,DM)患者微血管病变发生、发展的危险因素。方法　 6 2例 2型DM患者分为微血管病变组和单纯DM组 ,对两组DM的病程、高血压 (Hypertension ,HT)患病率、体重指数 (BMI)、空腹血糖 (FastingPlasmaGlucose,FPG)、餐后 2小时血糖 (2hoursPlasmaGlucose,2hPG)、糖化血红蛋白 (HbAlc)、总胆固醇 (TC)、甘油三酯 (TG)、高密度脂蛋白 (HDL)、低密度脂蛋白 (LDL)水平进行比较分析。结果　 2型DM微血管病变组FPG、2hPG、HbAlc水平明显高于单纯DM组 (P <0 0 5 ,P <0 0 1,P <0 0 1)。前者糖尿病病程、高血压患病率均大于后者 (P <0 0 5 ,P <0 0 1)。TC、TG、HDL、LDL、BMI两组未见明显差异。结论　高血糖是影响 2型DM微血管病变发生、发展的主要危险因素 ,伴高血压者和病程的延长 ,DM微血管病变也相应增加。预防 2型糖尿病患者微血管病变的关键是早期控制血糖和血压 ,尤其是要尽快控制餐后血糖。     

2型糖尿病与CD_(62)p、CD_(63)表达关系的临床研究

目的　 观察 2型糖尿病 (DM)患者全血血小板α -颗粒膜糖蛋白 (CD62 p)、血小板溶酶体膜糖蛋白 (CD63 )水平及其临床价值。 方法　采用流式细胞仪测定 116例 2型糖尿病患者 (其中大血管病变 4 5例 ,微血管病变 39例 ,无血管病变 32例 )和 32名健康人全血CD62 p、CD63 水平。 结果 　 2型糖尿病大血管病变组、微血管病变组、无血管病变组CD62 p、CD63 平均水平分别为 39.38%和 2 0 .4 7% ,2 8.31%和 14 .75% ,12 .13%和 9.57% ,显著高于对照组的 3.36 %和 2 .6 8% (均P <0 .0 1) ,大血管病变组和微血管病变组CD62 p和CD63 平均水平均高于无血管病变组 ,有显著性差异 (均P <0 .0 1) ;CD62 p与CD63 、TG、病程呈正相关关系 (均P <0 .0 1)。 结论　CD62 p、CD63 可作为 2型糖尿病患者监测病情变化及早期诊断血管并发症的重要指标。     

糖化血红蛋白检测对糖尿病微血管病变评估的价值分析

目的探讨糖化血红蛋白检测对糖尿病微血管病变评估的应用价值。方法选取2013年6月—2014年6月在该院进行治疗的糖尿病患者100例(微血管病变患者50例,无微血管病变患者50例)作为研究对象,对其进行糖化血红蛋白、空腹血糖值的检测,与50例健康者(对照组)进行比较,分析其糖化血红蛋白检测对糖尿病微血管病变评估的应用价值。结果观察组患者的糖化血红蛋白、空腹血糖值明显高于对照组,组间对比差异有统计学意义(P0.05)。将其观察组分为糖尿病微血管病变组与糖尿病无微血管病变组,糖尿病微血管病变组的糖化血红蛋白、空腹血糖值明显高于糖尿病无微血管病变组,组间差异有统计学意义(P0.05)。结论临床诊断中,对糖尿病患者的糖化血红蛋白检测,能及早判断患者微血管病变情况,为其后期的治疗提供可靠的依据,这种方法值得大力推广使用。     

生长激素在糖尿病及微血管病变中的变化及意义

目的观察生长激素在糖尿病及微血管病变中的变化,探讨其临床意义。方法测定18例健康对照者、30例2型糖尿病无微血管病变者和37例2型糖尿病无微血管病变者的血清GH及胰岛素(Ins)、血糖(BS)、HbA1c、TG、LDL、HDL、Lp(a)的水平。结果糖尿病无微血管病变组,空腹生长激素(FGH)明显高于正常对照组(P＜0.01)及糖尿病无微血管病变组(P＜0.01)。糖尿病无微血管病变组的FGH与正常对照组的FGH相比未见明显差异(P＞0.05),餐后2h的生长激素(PGH)在三组之间均无明显差异(P＞0.05)。FGH与HbA1c、空腹血糖(FBG)呈正相关(r=0.546,P＜0.01;r=0.437,P＜0.01),与UAER呈正相关(r=0.486,P＜0.01);与LDL、Lp(a)呈正相关(r=0.379,P＜0.05;r=0.430,P＜0.01);FGH与病程无相关(r=0.22,P＞0.05),与FINS无相关(r=-0.029,P＞0.05)。结论GH水平的增高,加重糖代谢和脂代谢紊乱,参与糖尿病微血管病变的发生。     

2型糖尿病微血管病变与血清抵抗素水平关系的研究

目的　探讨抵抗素与 2型糖尿病 (T2DM )及其微血管病变的相互联系。方法　随机采集临床确诊的T2DM患者 58例为试验组 ,分为不伴微血管病变 (NDC)组及伴微血管病变 (DMAP)组 ;对照组为 40例健康志愿者。记录所有的临床资料和生化资料。采集空腹静脉血 ,采用酶联免疫法进行检测血清抵抗素水平。结果　 (1 )T2DM有微血管病变者血清抵抗素水平与对照组比较具有统计学意义 (P <0 0 1 ) ,T2DM组有微血管病变者血清抵抗素水平高与无微血管病变者 (P <0 0 5)。 (2 )采用相关分析在DMAP组血清抵抗素水平与FPG、HbA1c呈正相关 (P <0 0 1 ) ,与血浆TG、Homa IR、FINS水平呈正相关 (P <0 0 5)。结论　 (1 )血清抵抗素水平与T2DM微血管病变存在一定的联系 ,抵抗素可能在T2DM及其微血管病变的发病中起一定作用。     

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型糖尿病微血管病变患者的胰岛素分泌功能分析

目的 探讨2型糖尿病微血管病变患者的胰岛分泌功能情况及相关因素。方法 应用馒头餐－胰岛素释放试验对115例2型糖尿病患者,其中有微血管并发症56例,无微血管并发症59例,以及正常对照组25例进行血糖、胰岛素测定,计算血糖、胰岛素曲线面积、胰岛素敏感性指数、胰岛素分泌指数,并进行了比较。结果 糖尿病两组各时相血糖值及血糖面积均非常显著高于正常对照组;糖尿病有微血管病变组各时相血糖值及血糖面积高于无微血管病变组（P均＜0．001）。糖尿病有微血管病变且各时相胰岛素值及胰岛素面积均显著低于无微血管病变组（P均＜0．01）,糖尿病有微血管病变组胰岛素分泌指数显著低于无微血管病变组（P＜0．001）。多元Logistic逐步回归分析显示,微血管变与糖尿病病程呈显著正相关,与胰岛素分泌指数呈显著负相关。结论 2型糖尿病微血管病变患者存在严重的持续性高血糖。糖尿病病程的延长,严重的胰岛分泌功能障碍为2型糖尿病微血管病变的主要危险因素。     

老年男性2型糖尿病合并骨质疏松症患者骨代谢生化指标分析

目的探讨老年男性2型糖尿病（T2DM）合并骨质疏松症（OP）患者血清骨形成与骨吸收生化指标随年龄变化及与OP的关系。方法根据是否合并OP,将185例老年男性T2DM患者分为OP组103例,非OP组82例。采用双能X线法检测骨密度,分别检测2组血清骨形成生化指标包括骨碱性磷酸酶（BAP）、骨钙素（OC）、Ⅰ型胶原氨基端前肽（PINP）,血清骨吸收生化指标Ⅰ型胶原C端肽（CTX）、空腹血糖（FPG）、空腹胰岛素（FINS）、糖化血红蛋白（HbA1c）、糖化血清白蛋白（GA）的浓度,并进行比较。结果 OP组的BMI及FINS、骨形成指标（BAP、OC、PINP）浓度低于非OP组,FPG、HbA1c、GA浓度及病程高于非OP组（P〈0.05）,骨吸收指标（CTX）浓度高于非OP组（P〉0.05）。OP组骨形成生化指标浓度低于骨量减少组（P〈0.05）,骨吸收指标浓度高于骨量减少组（P〉0.05）。OP组骨形成生化指标浓度与年龄呈负相关（P〈0.05）。结论老年男性T2DM合并OP的发生与骨形成能力不足有关,在治疗T2DM的同时,应重视早期预防和治疗OP。     

Serum osteocalcin levels in diabetes mellitus: analysis of the type of diabetes and microvascular complications

Summary Recent studies indicate that serum levels of osteocalcin, a 49-aminoacid bone matrix protein, are a biochemical marker of bone formation. In order to study bone metabolism in diabetes mellitus, in 28 patients with Type 1 (insulin-dependent) diabetes mellitus, in 38 patients with Type 2 (non-insulin-dependent) diabetes mellitus and two control groups, matched for Type 1 and Type 2 diabetic patients, respectively, serum levels of osteocalcin, parathyroid hormone and 25 hydroxy vitamin D were measured by radioimmunoassay. Whereas in Type 1 diabetic patients and control subjects serum levels of osteocalcin and 25 hydroxy vitamin D were not statistically different, serum osteocalcin and 25 hydroxy vitamin D levels were significantly decreased in Type 2 diabetic patients when compared with corresponding control subjects (p<0.03 and p<0.001, respectively). Independent of the type of diabetes, serum parathyroid hormone levels were comparable in diabetic patients and matched control subjects. Serum osteocalcin levels were significantly lower in Type 1 diabetic patients with retinopathy and/or proteinuria than in Type 1 diabetic patients without microangiopathy (p<0.05). Whereas serum parathyroid hormone levels in Type 2 diabetic patients with retinopathy and/or proteinuria were significantly increased (p<0.02), 25 hydroxy vitamin D levels were decreased (p<0.02) when compared with Type 2 diabetic patients without microangiopathy. Our data give evidence of a vitamin D deficiency and a decreased bone formation in patients with Type 2 diabetes mellitus. In Type 1 diabetes mellitus bone formation as reflected by serum osteocalcin levels is influenced by the presence or absence of microangiopathic complications.     

Bone mineral density and risk factors of osteoporosis in children

Background: Osteoporosis (OP) is a worldwide problem that could affect children. Aim of the work: to evaluate bone mineral density (BMD) and assess risk factors of OP in children. Patients and methods: This study was carried out on 960 children (410 male and 550 female). All children were subjected to full medical, nutritional history, clinical examination; laboratory investigations, dorsolumbar plain x-ray and dual energy X-ray absorptiometry (DEXA) scan. Results: The children were 57.3% females and 42.7% males (F: M 1.3:1) with a mean age of 9.3 ± 2.7 years. The frequency of low BMD was 28.3% (n = 272), while 11.2% (n = 107) were osteoporotic. OP was idiopathic in 4.7% and secondary in 95.3%. In OP children there was history of vertebral fracture in 91, 2 long bone fractures in 13 and 3 long bone fractures in 3 following low impact traumas. The risk factors of OP were unhealthy nutrition (89.7%), anemia (87.9%), underweight (81.3%), bronchial asthma (68.2%), diabetes mellitus (58.9%), epilepsy (12.2%), delayed puberty (8.4%), chronic kidney disease (4.3%), rheumatic diseases (4.3%) and hypothyroidism (1.9%). There was a significant difference between those with and without OP as regards serum calcium, phosphorous, alkaline phosphatase (p < 0.001) and most common risk factors of OP among studied children (p ≤ 0.05). Conclusions: Osteoporosis is frequent in children and unhealthy nutrition is the most common risk factor. OP is frequent among chronic disease as anemia, diabetes mellitus, bronchial asthma and epilepsy. Raising awareness among rheumatologists, pediatricians and family medicine physicians about this alarming condition is warranted to early detect and treat cases.     

老年2型糖尿病发生骨质疏松的临床多因素分析

目的 探讨老年2型糖尿病(T2DM)患者发生骨质疏松的影响因素. 方法 根据患者的骨密度值将患者分为骨量正常(NOP)组、低骨量(LBMD)组、骨质疏松(OP)组,对比3组在年龄、糖尿病病程、体质量指数(BMI)、胱抑素C(Cys C)、经皮氧分压检查(TcPO2)、糖化血红蛋白(HbA1c)、尿C肽(U-CP)等指标之间的差异,并进行相关性分析. 结果 (1)与NOP组相比,LBMD及OP组年龄、病程显著性升高,U-CP显著性下降;(2)OP组BMI、Cys C显著低于NOP组;(3)OP组年龄显著高于LBMD组,而BMI显著低于LBMD组(P＜0.05或P＜0.01).老年T2DM患者的BMD与年龄、病程呈负相关,与BMI、U-CP呈正相关.逐步多元回归分析显示U-CP是BMD的正性预测因子. 结论 老年T2DM患者并发骨质疏松与多因素有关,包括高龄、低体质量、病程长、胰岛功能差等.     

绝经后2型糖尿病患者骨质疏松影响因素及骨转换特点

目的 探讨绝经后2型糖尿病(T2DM)人群骨质疏松影响因素及骨转换特点及其防治策略.方法 150例绝经后T2DM住院患者测定骨密度(BMD)后分为骨量正常(NP)、骨量减低(DP)和骨质疏松(OP)组.登记年龄(Age),绝经年限(LOP),糖尿病病程(YSM),计算体重指数(BMI),测定空腹血糖(FPG)、餐后2 h血糖(PPG),空腹胰岛素(FIns)、餐后2 h胰岛素(2 h Ins),血Ⅰ型胶原C端肽(CTX-Ⅰ)、抗酒石酸酸性磷酸酶5b(TRACP5b)、骨特异性碱性磷酸酶(BALP)、雌激素(E2).结果 ①绝经后T2DM人群OP发病率54%;②绝经后T2DM并发OP患者与骨量减少和骨量正常组比较绝经年限、糖尿病病程及血糖水平明显增高,胰岛素和E2水平明显降低(P<0.05);③OP组患者与骨量减少和骨量正常组比较CTX-Ⅰ、TRACP5b、BALP等骨转换指标明显升高(P<0.05);④CTX-Ⅰ与腰椎2～4、股骨颈BMD呈明显负相关(P<0.05),与大转子、粗隆间BMD无明显相关性;TRACP5b、BALP与腰椎2～4、股骨颈、大转子、粗隆间BMD呈明显负相关(P<0.05).结论 LOP、血糖、YSM、FIns和E2水平可影响绝经后T2DM患者骨量;该人群骨重建特点为高转换型,骨吸收标记物TRACP5b可作为早期预测绝经后T2DM骨量减少及OP的敏感指标.     

老年男性2型糖尿病患者下肢血管病变与骨质疏松的关系

目的探讨老年男性2型糖尿病患者下肢血管病变与骨质疏松的关系。方法老年男性2型糖尿病患者148例,采用双能X线吸收法测定腰椎骨和股骨区的骨密度,同时用超声探测双下肢动脉内膜中膜厚度及粥样斑块等情况。结果无血管病变组33例,轻中度血管病变组65例,重度血管病变组50例,三组间骨密度值依次降低(P<0.05或0.01);多元Logistic回归分析显示,仅年龄、体质指数、下肢血管病变积分为决定骨质疏松的独立危险因素(OR值分别为1.50、0.52及1.87)。结论老年男性2型糖尿病下肢血管病变患者骨密度减低,骨质疏松风险增加。     

Bone, sweet bone--osteoporotic fractures in diabetes mellitus

Diabetes mellitus adversely affects the skeleton and is associated with an increased risk of osteoporosis and fragility fractures. The mechanisms underlying low bone strength are not fully understood but could include impaired accrual of peak bone mass and diabetic complications, such as nephropathy. Type 1 diabetes mellitus (T1DM) affects the skeleton more severely than type 2 diabetes mellitus (T2DM), probably because of the lack of the bone anabolic actions of insulin and other pancreatic hormones. Bone mass can remain high in patients with T2DM, but it does not protect against fractures, as bone quality is impaired. The class of oral antidiabetic drugs known as glitazones can promote bone loss and osteoporotic fractures in postmenopausal women and, therefore, should be avoided if osteoporosis is diagnosed. A physically active, healthy lifestyle and prevention of diabetic complications, along with calcium and vitamin D repletion, represent the mainstay of therapy for osteoporosis in patients with T1DM or T2DM. Assessment of BMD and other risk factors as part of the diagnostic procedure can help design tailored treatment plans. All osteoporosis drugs seem to be effective in patients with diabetes mellitus. Increased awareness of osteoporosis is needed in view of the growing and aging population of patients with diabetes mellitus.     

Quality of life associated with diabetes mellitus in an adult population

To ascertain the quality of life associated with the health state of diabetes mellitus using utility value analysis. Consecutive adult patients with diabetes mellitus for at least 1 year and a mean age of 61.7 years (range 21-85 years) were interviewed in a cross-sectional fashion using standardized research methodology. Utility analysis values were obtained employing the time tradeoff method and were correlated with clinical parameters of the sample group, as well as with co-morbidities using the heteroscedastic Student's t-test and multivariate linear regression. The chi(2) distribution to test for independence was used to compare sample subgroups. With a sample of 292 patients, the mean, patient-preference-based, time tradeoff utility value associated with the health state of diabetes mellitus was 0.88 (standard deviation (SD)=0.17; 95% confidence interval (CI), 0.86-0.90). Repeat analysis confirmed the reproducibility of the data. Thus, the average diabetic was willing to trade away 12% of his or her remaining life in return for a diabetic-free health state. Factors associated with a significant decrease in diabetic-associated quality of life included: (1) the requirement for insulin (p=0.05), (2) the presence of depression (p=0.01), (3) the presence of diabetic retinopathy (p=0.03) and the presence of co-morbidities in general (p=0.01). The health state of diabetes mellitus has a significant effect upon patient, preference-based quality of life. The presence of diabetic co-morbidities and dependence upon insulin appear to decrease quality of life. The utility value associated with the health state of diabetes mellitus is of substantial importance for use in the calculation of cost-effective analyses.     

A combination of the aldose reductase inhibitor, statil, and the prostaglandin E1 analogue, OP1206.alpha CD, completely improves sciatic motor nerve conduction velocity in streptozocin-induced chronically diabetic rats.

In view of the possible implication of multifactorial mechanisms in the pathogenesis of diabetic neuropathy, the aldose reductase inhibitor (ARI), Statil, which ameliorates abnormal sorbitol or myo-inositol metabolism in diabetic nerves, and the prostaglandin E1 (PGE1) analogue, OP1206.alpha CD (OP), which improves diabetic vascular derangements, were administered simultaneously for 2 months to streptozocin (STZ)-induced diabetic rats with 5 months' duration of diabetes, and the effects on sciatic motor nerve conduction velocity (MNCV), Na(+)-K(+)-adenosine triphosphatase (ATPase) activity, and morphology of myelinated nerve fibers (MNF) were compared with the effects of a monotherapy with OP. The combination regimen ameliorated abnormal nerve sorbitol and myo-inositol levels and normalized decreased MNCV and enzyme activity. In contrast, neither sorbitol nor myo-inositol metabolism was ameliorated, and only insufficient improvement of MNCV and morphology of MNF was obtained with a monotherapy with OP. In addition, the combination therapy reversed both a decrease in the percent of large MNF and an increase in the percent of small MNF in diabetic rats, whereas a monotherapy with OP reversed only a decrease in the percent of large MNF. The results might suggest that a multiple-drug therapy with different mechanisms of action has greater effects on diabetic neuropathy than a single-drug therapy and is worthy of clinical consideration.