空腹血糖受损患者动态血糖监测

目的探讨动态血糖监测系统运用于空腹血糖受损(IFG)患者的临床意义及护理特点,通过揭示IFG患者血糖波动特征及变化趋势为其防治提供线索.方法对12例空腹血糖受损患者进行3d的动态血糖监测,同时进行相关知识教育与护理.结果 12例空腹血糖受损患者均顺利完成监测,并且发现总时间的54.7%±18.6%血糖水平高于7.0mmol/L,血糖高峰期约为三餐后1.2±0.6h.结论动态血糖监测所提供的信息对于血糖波动特征及变化趋势的认识、完善血糖监测手段和协助制定IFG治疗策略是非常有帮助的,而加强护理是动态血糖监测系统顺利完成的保证.     

空腹血糖受损患者胰岛素抵抗状况的再评价

目的:研究切点调整后空腹血糖受损患者的胰岛素抵抗。方法:62例健康志愿者根据口服葡萄糖耐量试验结果分为正常糖耐量(NGT)组16例,单纯空腹血糖受损(IFG)组26例,伴糖耐量异常的空腹血糖受损(CGT)组15例。测定空腹血糖(FPG)、空腹胰岛素(FINS)、空腹C肽(FCp)、甘油三酯(TG)、胆固醇(CHO)以及口服葡萄糖耐量试验2h血糖(PPG)、胰岛素(PINS)、C肽(PCp)。用HOMA指数计算胰岛素敏感性和β细胞功能。结果:与NGT纽相比IFG与CGT组的HOMA-IR升高(P<0．05)。各组间HOMAβ无显著差异。结论:空腹血糖受损患者,无论其是否伴有糖耐量异常,均存在胰岛素抵抗状态。     

不同标准空腹血糖受损人群高血压分布特征及相关因素分析

目的:探讨2种标准空腹血糖受损人群高血压分布特征及相关危险因素.方法:时年龄>40岁3 828人进行流行病学调查,分析空腹血糖≥5.6 mmol/L和空腹血糖≥6.1 mmol/L者的血压状况.结果:空腹血糖≥5.6 mmol/L 627例中,高血压患病率为31.74%,男性(34.54%)高于女性(29.89%)(P<0.05),高血压前期患病率为47.05%,男性(51.41%)高于女性(44.18%)(P<0.05);Logistic回归结果分析显示,血压升高的危险因素为高血压家族史、腰围、总胆固醇升高和高密度脂蛋白胆固醇降低.空腹血糖≥6.1mmol/L 245例中,高血压患病率为31.43%,男性(34.55%)高于女性(28.89%)(P<0.05);高血压前期患病率为44.90%,男性(43.64%)低于女性(45.93%)(P>0.05);Logistic回归分析结果显示,血压升高的危险因素为年龄、高血压家族史、腰围和低密度脂蛋白胆固醇升高.结论:分别以空腹血糖≥5.6 mmol/L和≥6.1 mmol/L为诊断切点的空腹血糖受损人群高血压和高血压前期总患病率分别为78.79%和76.33%,可控危险因素主要是中心性肥胖和血脂代谢紊乱.     

空腹血糖受损患者动态血糖谱的分析

目的探讨空腹血糖受损（IFG）患者动态血糖谱的特点。方法将空腹血糖受损（IFG）患者18例为FPG组,糖耐量正常（NGT）者12例为NGT组,比较2组动态血糖谱的平均血糖值、3餐前1 h及3餐后2 h血糖水平、血糖漂移情况。结果IFG组的全天血糖平均值、血糖峰值、3餐前1 h血糖、3餐后2 h血糖均高于NGT组（P〈0.01）;IFG组血糖峰值,TPG≥7.8 mmol.L-1、TPG〈2.8 mmol.L-1的时间百分比均高于NGT组,血糖谷值低于NGT组（P〈0.01或P〈0.05）。结论IFG组患者整体血糖水平较NGT组高,血糖基线水平上移,IFG患者漂移幅度较NGT组大。     

2型糖尿病患者糖化血红蛋白和空腹血糖水平与视网膜病变相关性分析

目的 探讨2型糖尿病(T2DM)患者糖化血红蛋白(HbA1c)和空腹血糖(FPG)水平与视网膜病变(DR)的相关性.方法 对129例T2DM患者进行眼底检查或眼底血管荧光素造影检查,并依据眼底检查结果分组,确定T2DM无视网膜病变(NDR)组患者77例,DR组患者52例,其中非增生性视网膜病变(NPDR)组患者39例,增生性视网膜病变(PDR)组患者13例.所有研究对象HbA1c和FPG水平采用IE-HPLC法及葡萄糖氧化酶法进行定量测定,各组间进行统计学分析.结果 DR组HbA1c水平与NDR组和正常对照组比较差异有统计学显著性意义(P＜0.01),FPG水平也随着DR病情的发展和病变程度显著升高(P＜0.01).各组FPG与HbA1c相关性分析,DR组(NPDR组和PDR组)呈明显正相关(r=0.792);NDR组也呈明显正相关(r=0.684).结论 T2DM患者HbA1c和FPG水平与视网膜病变的发生、发展及病变程度有显著相关性,是糖尿病和并发症监控的重要监测指标.     

糖化血红蛋白、空腹血糖与糖尿病视网膜病变的关系

目的探讨糖尿病患者糖化血红蛋白(HbA1c)、空腹血糖(FBG)与糖尿病视网膜病变的关系。方法对本院115例2型糖尿病患者进行HbA1c、FBG检测并作眼底检查或荧光眼底血管造影。其中糖尿病正常眼底(NDR)组64例,糖尿病视网膜病变(DR)组51例。结果HbA1c水平DR组较NDR组高(P<0.01),HbA1c水平越高,DR的发生率越高(P<0.05),而FBG水平DR组与NDR组无显著性差异(P>0.05)。结论HbA1c测定可作为DR发生、发展的重要指标。     

空腹血糖受损的下限切点下调

1引言 2004年7月,中国糖尿病学会专门召开会议,主要讨论空腹血糖受损(impaired fasting glucose,IFG)的下限切点要不要从6.1 mmol/L下调到5.6mmol/L的问题.关于这问题的来龙去脉,现概述如下.     

空腹血糖受损患者血脂改变情况分析

目的探讨空腹血糖受损(impaired fasting glucose,IFG)患者血脂成分的改变情况。方法收集23例正常糖耐量(NGT)者和新诊断的44例IFG患者的临床资料,分别测定血脂谱。结果IFG患者血清甘油三酯(TG)水平显著高于NGT组(P<0.05),高密度脂蛋白—胆固醇(HDL-C)值明显低于NGT组(P<0.01)。结论新诊断的IFG患者已经存在血脂代谢异常。     

2003 ADA空腹血糖受损诊断标准在中老年患者中的评估

目的分析2003年美国糖尿病学会（ADA）空腹血糖受损（IFG）的空腹血糖（FPG）诊断标准下调对中老年糖调节受45（IGR）人群检出率的影响,并探讨区分糖调节正常与受损的FPG理想切点。方法3219例50岁以上台州农村人群分层整群随机抽样调查,空腹测毛细血管血糖。若FPG5．6mmol/L做OGTF检查。结果IFG患病率按新诊断切点5．6mmol/L为10．15％,按原切点6．1mmol/L为1．24％,两组比较,差异有统计学意义（X^2=83．55,P〈0．05）;空腹血糖受损合并糖耐量受损（IGT）患病率按新诊断切点5．6mmol／L为6．14％．按原切点6．1mmol／L为3．26％,两组比较,差异有统计学意义（X^2=10．78,P〈0．05）。计算不同FPG切点诊断IGR的约登指数,最大值对应的FPG为5．7mmol／l。结论IFG诊断标准下调后,IFG、IFG＋IGT检出率明显增加：非DM中老年人群中诊断IGR的FPG理想截定点为5．7mmol/L．     

空腹血糖受损与糖耐量减低患者的血脂水平分析

近年来,国外有杂志报道我国糖尿病（diabe．tesmellitus,DM）患病人数达9000多万,20岁以上成年人DM患病率达9．7％,更有1．48亿DM前期人群。国内针对DM前期患者的研究众多,但针对空腹血糖受损（impairedfastingglucose,IFG）与糖耐量减低（impairedglucosetolerance,IGT）患者血脂水平比较分析并不多。本研究分析了上海远郊地区部分体检人群中IFG与IGT患者的血脂情况,以期为预防IFG与IGT患者进入DM阶段提供较好的血脂监测指标。     

空腹血糖正常的原发性高血压患者糖代谢异常状况研究

目的研究原发性高血压伴有糖代谢异常患者的各项指标,为全面干预心血管危险因素提供依据。方法选择既往无糖代谢异常病史,空腹血糖〈5.6 mmol/L的原发性高血压患者398例,测定口服葡萄糖耐量试验（OGTT）后2小时血糖（2 hPG）水平。观察年龄、性别、体质量指数、血压、血脂、尿酸、动脉硬化等参数与OGTT后2hPG的关系。结果 398例患者中检出糖耐量减低99例（24.9%）;2型糖尿病52例（13.1%）。糖代谢异常的患者动脉硬化的比例（71.5%）高于血糖正常组（52.6%）。结论原发性高血压患者合并糖代谢异常的比例高,对于空腹血糖正常的原发性高血压患者,应常规行OGTT测定,以早期发现和干预糖代谢紊乱,减少动脉硬化的发生。     

空腹血糖受损人群葡萄糖负荷后血糖代谢特征及相关因素分析

目的:探讨空腹血糖受损人群葡萄糖负荷后血糖代谢特点及相关危险因素.方法:对3 828例≥40岁居民进行流行病学调查,筛查出的空腹血糖受损者行75 g葡萄糖粉负荷试验,分析葡萄糖负荷后2 h血糖代谢情况及其相关因素.结果:在空腹血糖受损人群中.糖耐量减低的患病率为41.22%,女性25.71%高于男性15.51%;2型糖尿病患病率为20.82%,女性11.84%高于男性8.98%.回归分析显示,空腹血糖受损人群葡萄糖负荷后2 h血糖升高的危险因素为空腹血糖、年龄和体质量指数.结论:空腹血糖受损阶段葡萄糖负荷后2h血糖代谢异常率高达62.04%,女性高于男性,其可控危险因素主要是超体质量.     

不同空腹血糖受损诊断标准下人群代谢特征比较

目的:从预测代谢性疾病的角度探讨空腹血糖受损(IFG)诊断下限从6.1 mmol/L下调至5.6 mmol/L的合理性.方法:比较正常糖代谢组(NGT,FPG＜ 5.6 mmol/L)、空腹血糖受损组1(IFG1,5.6 mmol/L≤FPG＜ 6.1 mmol/L)和空腹血糖受损组2(IFG2,6.1 mmol/L≤FPG＜ 7.0 mmol/L)之间代谢指标及发生代谢性疾病风险的差异.结果:与NGT组相比,IFG两组人群的血压、血脂等指标均显著升高(P＜0.05).与IFG1组相比,IFG2组仅部分代谢指标显著升高(P＜0.05).Logistic回归分析显示,与NGT组相比,IFG1与IFG2组发生中心性肥胖、高血压、高甘油三酯血症、代谢综合征的风险均升高(P＜0.05),而IFG两组间则无显著差异(P＞0.05).结论:从疾病早期防控的角度出发,将IFG诊断下限下调为5.6 mmol/L是合理的,应加强对人群空腹血糖的筛查.     

空腹血糖受损人群血脂水平变化及低密度脂蛋白胆固醇升高的相关因素分析

目的分析空腹血糖受损人群血脂代谢状况及低密度脂蛋白胆固醇升高的危险因素。方法对2 656例30~80岁汉族居民进行横断面调查,筛查血糖、血脂等相关项目,筛查空腹血糖受损人群,分析该人群血脂代谢状况及低密度脂蛋白胆固醇升高相关危险因素。结果空腹血糖受损人群中,高甘油三酯血症患病率34.7%,男性(38.2%)高于女性(28.3%)(P0.05);高胆固醇血症患病率59.2%,男性(61.2%)、女性(53.9%),差异无统计学意义(P0.05);高低密度脂蛋白血症患病率29.4%,男性(33.2%)高于女性(22.3%)(P0.05);低高密度脂蛋白血症患病率22.7%,男性(18.7%)低于女性(30.1%)(P0.05)。血脂代谢紊乱的总患病率63.7%。Logistic回归分析显示低密度脂蛋白胆固醇升高的危险因素为性别和胆固醇。结论空腹血糖受损人群存在血脂代谢紊乱低密度脂蛋白胆固醇升高的危险因素有性别和胆固醇。     

Cardiometabolic risk in impaired fasting glucose and impaired glucose tolerance: the Atherosclerosis Risk in Communities Study

OBJECTIVE: We compared and contrasted cardiovascular disease (CVD) risk factors, subclinical manifestations of CVD, incident coronary heart disease (CHD), and all-cause mortality by categories of impaired glucose regulation in nondiabetic individuals. RESEARCH DESIGN AND METHODS: The study included 6,888 participants aged 52-75 years who had no history of diabetes or CVD. All-cause mortality and incident CHD were ascertained over a median of 6.3 years of follow-up. RESULTS: Agreement between fasting and postchallenge glucose impairment was poor: 3,048 subjects (44%) had neither impaired fasting glucose (IFG) nor impaired glucose tolerance (IGT), 1,690 (25%) had isolated IFG, 1,000 (14%) had isolated IGT, and 1,149 (17%) had both IFG and IGT. After adjustment for age, sex, race, and center, subjects with isolated IFG were more likely to smoke, consume alcohol, and had higher mean BMI, waist circumference, LDL cholesterol, and fasting insulin and lower HDL cholesterol than those with isolated IGT, while subjects with isolated IGT had higher mean triglycerides, systolic blood pressure, and white cell counts. Measures of subclinical CVD and rates of all-cause mortality and incident CHD were similar in isolated IFG and isolated IGT. CONCLUSIONS: Neither isolated IFG nor isolated IGT was associated with a more adverse CVD risk profile.     

重视IFG、IGT的防治

糖耐量低减(impaired glucose tolerance，IGT)和空腹血糖异常(impaired fating glueose,IFG)均为糖尿病自然病程中的中间阶段。目前并未被确认为疾病状态，只认为是正常与疾病之间的一种高危状态，称前糖尿病状态(pre-diabetes)。大规模、前瞻性研究已证实：IGT和(或)IFG人群进展为临床糖尿病的危险显著高于正常糖耐量者(NGT)，年发病率约3％-10％，是临床糖尿病的主要后备人群；IGT和(或)IFG是冠心病、高血压及脑血管意外等疾病的重要危险因素；强化生活方式干预(饮食控制、运动)和一定的药物干预。可有效延缓和减少IGT／IFG人群的糖尿病危险。广东省1998年流行病学调查显示，20-74     

In vivo endothelial dysfunction characterizes patients with impaired fasting glucose

OBJECTIVE: The American Diabetes Association has recently defined a new category of abnormal glucose homeostasis called "impaired fasting glucose" (IFG), where glucose levels do not meet the criteria of diabetes but are too high to be considered normal. We determined whether endothelial dysfunction is a characteristic of subjects with IFG. RESEARCH DESIGN AND METHODS: In vivo vasodilatory responses to intra-arterial infusions of endothelium-dependent (acetylcholine [ACh]) and -independent (sodium nitroprusside [SNP]) vasoactive agents were determined in 17 IFG subjects (age 63 +/- 1 years, BMI 26.5 +/- 0.8 kg/m2, serum LDL cholesterol 3.5 +/- 0.2 mmol/l) with fasting plasma glucose levels of 117 +/- 1 mg/dl and in 12 subjects with normal fasting plasma glucose concentrations. RESULTS: The blood-flow response to the low dose of ACh was 46% (5.9 +/- 0.7 vs. 10.9 +/- 1.3 ml.dl-1.min-1, IFG vs. normal, P < 0.01) and to the high dose was 31% (9.1 +/- 1.2 vs. 13.2 +/- 1.5 ml.dl-1.min-1, P < 0.05, respectively) lower in the IFG than in the normal subjects. In contrast, blood-flow responses to both low (7.8 +/- 0.5 vs. 9.0 +/- 0.9 ml.dl-1.min-1, IFG vs. normal, NS) and high (11.6 +/- 1.2 vs. 12.3 +/- 1.3 ml.dl-1.min-1, NS, respectively) doses of SNP were comparable. The ratio of endothelium-dependent to -independent blood flow was 40% lower in the IFG (0.75 +/- 0.1) than in the normal (1.24 +/- 0.1, P < 0.001) subjects. Both fasting plasma glucose (r = -0.48, P < 0.01) and glycosylated hemoglobin (r = -0.42, P < 0.05) were inversely correlated with endothelium-dependent vasodilation but not with other parameters, such as weight, blood pressure, or lipids. CONCLUSIONS: We conclude that vascular dysfunction is associated with abnormal, although nondiabetic, glucose homeostasis.     

Impaired glucose tolerance and impaired fasting glucose

Impaired glucose tolerance and impaired fasting glucose form an intermediate stage in the natural history of diabetes mellitus. From 10 to 15 percent of adults in the United States have one of these conditions. Impaired glucose tolerance is defined as two-hour glucose levels of 140 to 199 mg per dL (7.8 to 11.0 mmol) on the 75-g oral glucose tolerance test, and impaired fasting glucose is defined as glucose levels of 100 to 125 mg per dL (5.6 to 6.9 mmol per L) in fasting patients. These glucose levels are above normal but below the level that is diagnostic for diabetes. Patients with impaired glucose tolerance or impaired fasting glucose have a significant risk of developing diabetes and thus are an important target group for primary prevention. Risk factors for diabetes include family history of diabetes, body mass index greater than 25 kg per m2, sedentary lifestyle, hypertension, dyslipidemia, history of gestational diabetes or large-for-gestational-age infant, and polycystic ovary syndrome. Blacks, Latin Americans, Native Americans, and Asian-Pacific Islanders also are at increased risk for diabetes. Patients at higher risk should be screened with a fasting plasma glucose level. When the diagnosis of impaired glucose tolerance or impaired fasting glucose is made, physicians should counsel patients to lose 5 to 7 percent of their body weight and engage in moderate physical activity for at least 150 minutes per week. Drug therapy with metformin or acarbose has been shown to delay or prevent the onset of diabetes. However, medications are not as effective as lifestyle changes, and it is not known if treatment with these drugs is cost effective in the management of impaired glucose tolerance.     

Effect of angiotensin receptor blockade on insulin sensitivity and endothelial function in abdominally obese hypertensive patients with impaired fasting glucose

AngII (angiotensin II) may contribute to cardiovascular risk in obesity via adverse effects on insulin sensitivity and endothelial function. In the present study, we examined the effects of ARB (angiotensin receptor blocker) therapy (losartan, 100?mg/day) on insulin sensitivity and endothelial function in 53 subjects with stage I hypertension, abdominal obesity and impaired fasting glucose. The study design was a randomized double-blinded parallel design placebo-controlled multi-centre trial of 8?weeks duration. We used the hyperinsulinaemic-euglycaemic clamp technique to measure insulin sensitivity (expressed as the 'M/I' value) and RH-PAT (reactive hyperaemia-peripheral arterial tonometry) to measure endothelial function. Additional measures included HOMA (homoeostasis model assessment)-B, an index of pancreatic β-cell function, and markers of inflammation [e.g. CRP (C-reactive protein)] and oxidative stress (e.g. F2-isoprostanes). ARB therapy did not alter insulin sensitivity [5.2 (2.7) pre-treatment and 4.6 (1.6) post-treatment] compared with placebo therapy [6.1 (2.9) pre-treatment and 5.3 (2.7) post-treatment; P value not significant], but did improve the HOMA-B compared with placebo therapy (P=0.05). ARB therapy also did not change endothelial function [RH-PAT, 2.15 (0.7) pre-treatment and 2.11 (0.7) post-treatment] compared with placebo therapy [RH-PAT, 1.81 (0.5) pre-treatment and 1.76 (0.7) post-treatment; P value not significant]. Markers of inflammation and oxidative stress were not significantly changed by ARB therapy. In conclusion, ARB therapy did not alter peripheral insulin sensitivity or endothelial function in this cohort of patients with essential hypertension, abdominal obesity and impaired fasting glucose, but did improve pancreatic β-cell function.