强化干预对脑卒中并存糖耐量异常患者治疗依从性的影响

目的探讨强化护理干预对脑卒中并存糖耐量异常患者依从性的影响。方法将210例脑卒中并存糖耐量异常患者随机分为观察组和对照组各105例。两组住院期间均接受相同的健康教育,但观察组接受护理人员的监督,确保干预措施的强化和落实。测评两组出院时依从性情况及出院后6个月的血糖。结果观察组患者出院时治疗依从性显著高于对照组(均P<0.01),出院后6个月血糖控制情况显著优于对照组(P<0.01)。结论强化干预可提高脑卒中并存糖耐量异常患者治疗依从性,有利于血糖控制。     

Metabolic characteristics of individuals with impaired fasting glucose and/or impaired glucose tolerance.

With the release of the new 1997 American Diabetes Association diagnostic criteria, a new category was introduced, termed "impaired fasting glucose" (IFG). The metabolic abnormalities of individuals with IFG, compared with those with impaired glucose tolerance (IGT) (World Health Organization criteria), remain to be elucidated. We assessed insulin action (hyperinsulinemic clamp), insulin secretion (25-g intravenous glucose tolerance test), and endogenous glucose output (EGO) (3-(3)H-glucose) in 434 nondiabetic Pima Indians with either normal (NFG; <6.1 mmol/l) or impaired (IFG; 6.1-7.0 mmol/l) fasting glucose and with either normal (NGT; 2-h glucose <7.8 mmol/l) or impaired (IGT; 2-h glucose 7.8-11.1 mmol/l) glucose tolerance: NFG/NGT (n = 307), IFG/NGT (n = 11), NFG/IGT (n = 98), and IFG/IGT (n = 18). Compared with the NFG/NGT group, individuals with IFG/NGT had lower maximal insulin-stimulated glucose disposal (M; -20%, P < 0.01), a lower acute insulin response (AIR) to intravenous glucose (-33%, P < 0.05), and higher EGO (8%, P = 0.055). Individuals with NFG/IGT also had lower M (-21%, P < 0.001) and lower AIR (-8%, P < 0.05), but normal EGO (-1%, NS). Individuals with IFG/IGT showed the most severe abnormalities in M (-27%), AIR (-51%), and EGO (+13%) (all P < 0.001 compared with NFG/NGT). These group differences could be explained by the observation that AIR and EGO, but not M, were more strongly related to the fasting than to the 2-h glucose concentration. Thus, Pima Indians with isolated IFG and isolated IGT show similar impairments in insulin action, but those with isolated IFG have a more pronounced defect in early insulin secretion and, in addition, increased EGO. More severe metabolic abnormalities are present in Pima Indians with combined IFG and IGT.     

团队干预对妊娠期糖耐量异常孕妇妊娠结局的影响

目的 探讨团队干预对妊娠期糖耐量异常孕妇的血糖、体重指数、妊娠结局的影响.方法 将60例GIGT孕妇随机分为对照组和观察组各30例.对照组孕妇行常规产前检查、孕妇学校学习、产科营养门诊就诊;观察组在此基础上实施团队干预,由产科医师、内分泌科医师、营养师、护士组成的团队,根据每位孕妇的年龄、体重指数、孕周、血糖水平、胎儿宫内生长情况制定个性化的食谱、运动方案,利用各种渠道提供一对一咨询服务和个性化指导.结果 观察组分娩结束当天的餐后2 h血糖、体质量显著低于对照组,分娩孕周显著长于对照组,新生儿出生体质量显著重于对照组新生儿(P<0.05,P<0.01).观察组无一例妊娠糖尿病发生,胎膜早破仅2例;对照组发生妊娠糖尿病2例、妊娠高血压4例、早产7例、胎膜早破9例、娩出巨大儿3例.结论 团队干预可有效地控制妊娠期糖耐量异常孕妇的血糖、体质量,减少妊娠并发症发生.     

Microvascular complications of impaired glucose tolerance

Impaired glucose tolerance (IGT) serves as a marker for the state of insulin resistance and predicts both large- and small-vessel vascular complications, independent of a patient's progression to diabetes. Patients with IGT are at significantly increased risk for death and morbidity due to myocardial infarction, stroke, and large-vessel occlusive disease. IGT is more predictive of cardiovascular morbidity than impaired fasting glucose, probably because it is a better surrogate for the state of insulin resistance. IGT is also independently associated with traditional microvascular complications of diabetes, including retinopathy, renal disease, and polyneuropathy, which are the topics of this review. Inhibition of nitric oxide-mediated vasodilation, endothelial injury due to increased release of free fatty acids and adipocytokines from adipocytes, and direct metabolic injury of endothelial and end-organ cells contribute to vascular complications. Early detection of IGT allows intensive diet and exercise modification, which has proven significantly more effective than drug therapy in normalizing postprandial glucose and inhibiting progression to diabetes. To what degree intervention will limit recognized complications is not known.     

Effects of insulin on brain glucose metabolism in impaired glucose tolerance

OBJECTIVE

Insulin stimulates brain glucose metabolism, but this effect of insulin is already maximal at fasting concentrations in healthy subjects. It is not known whether insulin is able to stimulate glucose metabolism above fasting concentrations in patients with impaired glucose tolerance.

RESEARCH DESIGN AND METHODS

We studied the effects of insulin on brain glucose metabolism and cerebral blood flow in 13 patients with impaired glucose tolerance and nine healthy subjects using positron emission tomography (PET). All subjects underwent PET with both [¹⁸F]fluorodeoxyglucose (for brain glucose metabolism) and [¹⁵O]H₂O (for cerebral blood flow) in two separate conditions (in the fasting state and during a euglycemic-hyperinsulinemic clamp). Arterial blood samples were acquired during the PET scans to allow fully quantitative modeling.

RESULTS

The hyperinsulinemic clamp increased brain glucose metabolism only in patients with impaired glucose tolerance (whole brain: +18%, P = 0.001) but not in healthy subjects (whole brain: +3.9%, P = 0.373). The hyperinsulinemic clamp did not alter cerebral blood flow in either group.

CONCLUSIONS

We found that insulin stimulates brain glucose metabolism at physiological postprandial levels in patients with impaired glucose tolerance but not in healthy subjects. These results suggest that insulin stimulation of brain glucose metabolism is maximal at fasting concentrations in healthy subjects but not in patients with impaired glucose tolerance.Peripheral insulin resistance is a hallmark of metabolic syndrome and type 2 diabetes, but it is unclear if the brain also shows insulin resistance. Peripheral insulin crosses the blood-brain barrier via an active transport mechanism and binds to insulin receptors on neurons and glial cells. Insulin has a catabolic effect; in addition, it influences memory functions by modulating neurotransmitter release and synaptic plasticity (1–4). Therefore, determining whether insulin resistance also occurs in the brain in metabolic syndrome is important (5). Obese individuals have a decreased cerebrospinal fluid–to–plasma insulin ratio (6), diminished catabolic responses to intranasal insulin (7), and decreased cortical brain activity after insulin (8), suggesting brain insulin resistance (1,5). However, these indirect studies do not establish the relationship between insulin and brain glucose metabolism, which is important given the role of the brain in glucose sensing (9).Direct evidence on the effects of insulin on the brain may be obtained with positron emission tomography (PET) and ¹⁸F-labeled fluorodeoxyglucose ([¹⁸F]FDG). Studies in healthy subjects have shown that brain glucose metabolism does not increase after increasing plasma insulin concentrations above physiological fasting levels (10,11) but decreases after decreasing plasma insulin concentration below physiological fasting levels (12,13), suggesting that the insulin effect is already saturated at fasting concentrations in healthy subjects. In contrast, Anthony et al. (12) recently demonstrated that reducing plasma insulin does not reduce brain glucose metabolism in patients with impaired glucose tolerance. However, it is not known whether insulin stimulates brain glucose metabolism above fasting levels in these patients or whether this effect is already saturated at fasting levels, as in healthy subjects (12,13).To characterize the dose-response relationship of plasma insulin and brain glucose metabolism in patients with impaired glucose tolerance, we used [¹⁸F]FDG PET to measure brain glucose metabolism in two conditions (in the fasting state and during a euglycemic-hyperinsulinemic clamp) in both healthy subjects and patients with impaired glucose tolerance. [¹⁸F]FDG is a glucose analog that is taken up in the brain and trapped after phosphorylation; thus, the measured signal approximates uptake of glucose. The euglycemic-hyperinsulinemic clamp allows close monitoring and adjustment of plasma glucose while inducing a constant insulin stimulation. In a subset of subjects, we also measured the effects of insulin on cerebral blood flow with [¹⁵O]H₂O PET.     

Differences in insulin resistance in nondiabetic subjects with isolated impaired glucose tolerance or isolated impaired fasting glucose

Both impaired glucose tolerance (IGT) (as defined by the 1985 World Health Organization criteria) and impaired fasting glucose (IFG) (as defined by the 1997 American Diabetes Association criteria) represent intermediate metabolic states between normal and diabetic glucose homeostasis. Cardiovascular disease may be related to postglucose load rather than fasting glycemia, i.e., IGT rather than IFG. We hypothesized that subjects with IGT may be more insulin resistant and have higher levels of common cardiovascular risk factors than those with isolated IFG. In the Insulin Resistance Atherosclerosis Study (IRAS), we studied S(i) and first-phase insulin secretion (acute insulin response [AIR]), as derived from a frequently sampled intravenous glucose tolerance test, as well as common cardiovascular risk factors in four different glucose tolerance categories (NFG/NGT [n = 654], NFG/IGT [n = 255], IFG/NGT [n = 59], and IFG/IGT [n = 102]) among nondiabetic subjects. Subjects with isolated postchallenge hyperglycemia (NFG/IGT) had lower S(i) (means +/- SE: 2.10 +/- 0.04 vs. 2.59 +/- 0.13 x 10(-4) min(-1). microU(-1). ml(-1); P = 0.005), lower proinsulin levels (34.4 +/- 1.8 vs. 42.0 +/- 4.5 pmol/l; P = 0.03), higher AIR (273.1 +/- 18.1 vs. 215.9 +/- 30.0 pmol/l; P = 0.04), higher C-reactive protein (2.49 +/- 0.3 vs. 1.49 +/- 0.5 mg/l; P = 0.0015), and higher triglyceride levels (137.7 +/- 5.5 vs. 108.4 +/- 8.9 mg/dl; P = 0.0025) than subjects with isolated fasting hyperglycemia (IFG/NGT). The relation of insulin resistance to glucose tolerance category was consistently seen in women and men and across the three ethnic groups of the IRAS (non-Hispanic whites, African Americans, and Hispanics). Nondiabetic individuals with isolated postchallenge hyperglycemia (IGT) are more insulin resistant than individuals with isolated fasting hyperglycemia (IFG). The risk factor pattern (including increased insulin resistance) seen in isolated IGT identifies a subgroup of nondiabetic individuals who are likely to benefit from early intervention.     

Management of patients with impaired glucose tolerance following esophagectomy in carcinoma of the esophagus]

We demonstrated the effectiveness of the "sliding scale" insulin infusion in diabetic patients undergoing esophagectomy. Fifty-eight patients were followed after esophagectomy to clarify differences in energy expenditure and caloric contributions of substrates. Energy expenditure was measured by indirect calorimetry on the 1st, 3rd, 5th, and 7th days after esophagectomy. Out of 58 patients, 7 were divided into diabetic (D), 30 into borderline (B), 21 into normal (N), according to a 75 g oral glucose tolerance test, preoperatively. Forty-four patients underwent esophagectomy by means of right thoracotomy, and blunt esophagectomy was done on 14 patients. The results were as follows: 1) No relation was found between postoperative morbidity and severity of glucose intolerance. 2) There was no significant difference in changes in energy expenditure following operation among groups D, B, and N. No difference was found in ratio of caloric intake to energy expenditure among groups D, B, and N. Caloric contributions of substrates seemed to be comparable among groups D, B, and N. These results suggest that "sliding scale" insulin infusion with total parenteral nutrition enable us to control not only blood glucose level but energy metabolism following esophagectomy in diabetic patients.     

Polyneuropathy with impaired glucose tolerance: Implications for diagnosis and therapy

Opinion statement Prediabetes is associated with a length-dependent polyneuropathy that typically is sensory predominant and painful. A diagnosis of prediabetes should be sought in patients with otherwise idiopathic sensory-predominant neuropathy by doing a 2-hour oral glucose tolerance test. Fasting plasma glucose of 100 to 125 mg/dL or 2-hour glucose 140 to 199 mg/dL (impaired glucose tolerance) constitutes prediabetes. Most patients with neuropathy associated with prediabetes (NAP) are obese and show metabolic manifestations of insulin resistance, including hyperlipidemia and hypertension. Appropriate treatment addresses hyperglycemia, insulin resistance, and neuropathic pain. Professionally administered individualized diet and exercise counseling (modeled on the Diabetes Prevention Program) has been shown to be more effective than glucose-lowering medications in preventing progression from impaired glucose tolerance to diabetes, and is the mainstay of treatment for all patients with NAP. The goals of this therapy should be a 5% to 7% reduction in weight and an increase to 30 minutes of moderate exercise five times weekly. Patients with prediabetes are at increased risk for myocardial infarction, stroke, and peripheral vascular disease. Therefore, risk reduction with control of hypertension and hyperlipidemia is essential. Neuropathic pain troubles nearly every patient with NAP, and often limits aerobic exercise. No trials have specifically addressed the patient population with NAP, and neuropathic pain treatment closely follows recommendations for diabetic neuropathy. Gabapentin, lamotrigine, and tricyclic antidepressants are well-validated first-line therapies. Adjunctive therapy with opioids, nonsteroidal anti-inflammatory drugs often are necessary. Diet and exercise seem to reduce neuropathic pain in patients with NAP.     

强化考核式健康教育对肾移植患者遵医行为的影响

目的探讨强化考核式健康教育对加强肾移植患者遵医行为的影响。方法将160例肾移植患者按入院时间分为对照组(76例)和观察组(84例)。对照组采用常规健康教育,如集中教育、召开座谈会、家访及个别指导、热线电话咨询;观察组在对照组教育的基础上增加术后及出院前2次强化考核,针对考核结果调整健康教育内容。结果观察组患者术后6个月未按量服药、忘记记录尿量等10项不良事件发生率显著低于对照组(均P<0.05)。结论强化考核式健康教育可促进肾移植患者的遵医行为,减少不良事件的发生。     

Prevalence of complications among second-generation Japanese-American men with diabetes, impaired glucose tolerance, or normal glucose tolerance

In a study sample of 229 second-generation Japanese-American (Nisei) men, 79 with normal glucose tolerance, 72 with impaired glucose tolerance (IGT), and 78 with non-insulin-dependent diabetes, we have determined prevalence rates for certain conditions (ischemic heart disease, peripheral vascular disease, hypertension, retinopathy, neuropathy, and nephropathy) associated with diabetes. All subjects participated in a 75-g oral glucose tolerance test. World Health Organization (WHO) diagnostic criteria and information from the subject's medical history and personal physician were used to classify the subjects. Retinopathy was observed only in diabetic men in the study sample (11.5% of diabetic men). Furthermore, it was observed only in men who were receiving drug treatment for diabetes--40.0% of insulin-treated and 17.2% of sulfonylurea-treated men. Electrophysiologic evidence of peripheral neuropathy was observed in 46.2% of diabetic men and in 4.0% of nondiabetic (normal and IGT) men. For diabetic men with fasting serum glucose greater than or equal to 140 mg/dl, 63.8% had peripheral neuropathy and 19.1% had retinopathy, whereas for diabetic men with fasting serum glucose less than 140 mg/dl, 19.4% had neuropathy and none had retinopathy. For diabetic men with a diabetes duration of greater than or equal to 10 yr, 72.7% had neuropathy and 31.8% had retinopathy; with a diabetes duration of 5-9 yr, 70.6% had neuropathy and 11.8% had retinopathy; and with a diabetes duration of less than 5 yr, 20.5% had neuropathy and none had retinopathy. Nephropathy was distinctly uncommon, and among the measurements of kidney function, only proteinuria was clearly abnormal with diabetes. Prevalence rates of hypertension, peripheral vascular disease, and ischemic heart disease were highest in Nisei men with diabetes, lowest in men with normal glucose tolerance, and intermediate in men with IGT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased urinary excretion of N-acetylglucosaminidase in subjects with impaired glucose tolerance

N-acetylglucosaminidase (NAG) is a lysosomal enzyme produced by renal proximal tubular cells and has been widely used as a marker, which indicates a degree of renal tubular damage. An increase in urinary NAG excretion is though to result from the renal tubular damage. The aim of this study was to evaluate whether even mild hyperglycemia causes an increase in urinary excretion of NAG, which is a renal tubular protein. We examined urinary NAG excretion in overnight urine in 22 Japanese men with impaired glucose tolerance (IGT) for more than two years (IGT group) and 41 healthy control subjects matched in age, gender, BMI and blood pressure (control group). Urinary NAG excretion levels of IGT group and control group were 2.89 (1.23-7.97) and 2.22 (0.60-4.93) U/g creatinine, median (range), respectively. The IGT group showed significantly higher urinary excretion of NAG compared to the control group (p < 0.01). Several studies have indicated that plasma proteins filtered through the glomerular capillary may have intrinsic renal toxicity. Recently, we have reported that urinary excretion of plasma proteins (ceruloplasmin, IgG4 and IgG) with molecular radii of approximately 45-55 A is increased in subjects with IGT compared to healthy control subjects with normal glucose tolerance. Considering the present result together with our recent finding, we suggest that increased urinary excretion of NAG in the mildly hyperglycemic subjects may be due to the adverse effects of the plasma proteins highly filtered through the glomerular capillary on tubular cells.     

Pathogenesis of pre-diabetes: mechanisms of fasting and postprandial hyperglycemia in people with impaired fasting glucose and/or impaired glucose tolerance

Thirty-two subjects with impaired fasting glucose (IFG) and 28 subjects with normal fasting glucose (NFG) ingested a labeled meal and 75 g glucose (oral glucose tolerance test) on separate occasions. Fasting glucose, insulin, and C-peptide were higher (P < 0.05) in subjects with IFG than in those with NFG, whereas endogenous glucose production (EGP) did not differ, indicating hepatic insulin resistance. EGP was promptly suppressed, and meal glucose appearance comparably increased following meal ingestion in both groups. In contrast, glucose disappearance (R(d)) immediately after meal ingestion was lower (P < 0.001) in subjects with IFG/impaired glucose tolerance (IGT) and IFG/diabetes but did not differ in subjects with IFG/normal glucose tolerance (NGT) or NFG/NGT. Net insulin action (S(i)) and insulin-stimulated glucose disposal (S(i)*) were reduced (P < 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in subjects with NFG/NGT or IFG/NGT. Defective insulin secretion also contributed to lower postprandial R(d) since disposition indexes were lower (P < 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in subjects with NFG/NGT and IFG/NGT. We conclude that postprandial hyperglycemia in individuals with early diabetes is due to lower rates of glucose disappearance rather than increased meal appearance or impaired suppression of EGP, regardless of their fasting glucose. In contrast, insulin secretion, action, and the pattern of postprandial turnover are essentially normal in individuals with isolated IFG.     

脑卒中吞咽障碍患者的摄食管理临床研究

目的提高脑卒中吞咽障碍患者吞咽功能训练效果,降低卒中相关性肺炎发生率。方法将136例脑卒中吞咽障碍(洼田饮水试验Ⅱ～Ⅴ级)患者随机分为两组各68例。对照组行脑卒中吞咽障碍常规饮食护理;观察组采取食物稠度及一口量精细评估,制订个体化进食方案,动态评价与方案调整等措施进行摄食管理。结果观察组吞咽功能恢复程度显著优于对照组,卒中相关性肺炎发生率显著低于对照组(P0.05,P0.01)。结论精细评估、个体化护理及全程追踪可提高脑卒中吞咽障碍训练效果,降低相关并发症。     

糖耐量低减患者动态血压与尿白蛋白排泄率的关系

目的 探讨糖耐量低减(IGT)患者尿白蛋白排泄率(UAE)与不同血压指标的关系。方法 对44例IGT患者均进行动态血压(ABPM)监测,心血管自主神经功能测试,UAE测定。结果 与UAE正常组比较,UAE增高组ABPM多项指标增高,夜间血压降低幅度减少,24小时血压曲线平坦。UAE与夜间舒张压(DBP)、收缩压(SBP)负荷、DBP负荷、24hDBP以及24hSBP呈显著正相关,与昼夜血压差值呈显著负相关。结论 UAE增高的IGT患者已经开始出现血压的异常改变。     

糖耐量减低患者血清肝细胞生长因子水平及相关因素分析

目的观察糖耐量减低（IGT）患者血清肝细胞生长因子（HGF）水平。方法选取IGT患者（IGT组）、2型糖尿病（T2DM）患者（T2DM组）及健康对照者（NC组）各30例,分别测定血清HGF、空腹血糖（FBG）、餐后2h血糖（2hPG）、糖化血红蛋白（GHbA1C）、空腹胰岛素（FINS）、收缩压（SBP）、舒张压（DBP）等指标,并对HGF的相关因素进行分析。结果IGT组与T2DM组血清HGF水平均高于对照组[分别为（413．22±102．48）、（422．76±126．77）、（120．45±25．11）ng／L]（P〈0．05）,IGT组与T2DM组比较差异无统计学意义（P〉0．05）;FBG与HGF呈正相关（r=0．326,P〈0．05）,多元回归分析显示,HGF与DBP具有高度相关性（r=4．730,P〈0．05）。结论血清HGF水平在IGT阶段即升高,表明存在血管内皮功能异常。     

Intensive lifestyle intervention or metformin on inflammation and coagulation in participants with impaired glucose tolerance

Increases in subclinical inflammation (C-reactive protein [CRP]) and impaired coagulation have been associated with increased obesity and insulin resistance. Only a few small studies have examined the effect of lifestyle changes, such as weight loss, increased physical activity, and insulin-sensitizing intervention on inflammation and coagulation. The Diabetes Prevention Program (DPP) clinical trial studied the effect of an intensive lifestyle intervention or metformin on progression to diabetes relative to placebo in 3,234 adults with impaired glucose tolerance. The effects of these interventions on CRP and fibrinogen at 12 months are examined in this report. Metformin reduced CRP in women compared with the placebo group. In men, the median changes in CRP from baseline to 1 year were -33% in the lifestyle group, -7% in the metformin group, and +5% in the placebo group. In women, the changes in CRP from baseline to follow-up were -29% in the lifestyle group, -14% in the metformin group, and 0% in the placebo group. In the lifestyle group weight loss rather than increased physical activity seems to account for most of the changes in CRP. Only modest reductions (although significant) were seen in fibrinogen levels in the lifestyle group relative to the metformin and placebo group. Lifestyle intervention reduced levels of nontraditional cardiovascular risk factors relative to both placebo and to a lesser degree to metformin.     

Insulin secretion and action in subjects with impaired fasting glucose and impaired glucose tolerance: results from the Veterans Administration Genetic Epidemiology Study

This study was conducted to observe changes in insulin secretion and insulin action in subjects with impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT). A total of 319 subjects were studied with an oral glucose tolerance test (OGTT). Fasting plasma glucose and insulin concentrations were measured at baseline and every 30 min during the OGTT. Fifty-eight subjects also received a euglycemic-hyperinsulinemic clamp. Insulin sensitivity was calculated as the total glucose disposal (TGD) during the last 30 min of the clamp. Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated from fasting plasma glucose and insulin concentrations. Subjects with IFG had TGD similar to normal glucose-tolerant subjects, while subjects with IGT and combined IFG/IGT had significantly reduced TGD. HOMA-IR in subjects with IFG was similar to that in subjects with combined IFG/IGT and significantly higher than HOMA-IR in subjects with IGT or NGT. Insulin secretion, measured by the insulinogenic index (DeltaI(0-30)/DeltaG(0-30)) and by the ratio of the incremental area under the curve (AUC) of insulin to the incremental AUC of glucose (0-120 min), was reduced to the same extent in all three glucose-intolerant groups. When both measurements of beta-cell function were adjusted for severity of insulin resistance, subjects with IGT and combined IFG/IGT had a significantly greater reduction in insulin secretion than subjects with IFG. Subjects with IGT and IFG have different metabolic characteristics. Differences in insulin sensitivity and insulin secretion may predict different rates of progression to type 2 diabetes and varying susceptibility to cardiovascular disease.     

不同年龄糖耐量异常患者骨密度变化的关联研究

目的观察不同年龄段糖耐量异常(IGT)患者骨密度(BMD)的变化及其关联因素。方法在我院进行健康体检的30~73岁人群,选取290例糖耐量异常者做为实验组,290例年龄、性别相匹配的糖耐量正常(NGT)者做为对照组,对两组骨密度,空腹血糖、餐后2小时血浆葡萄糖及糖化血红蛋白(HbA1c)水平进行检测,比较两组骨密度、空腹血糖、餐后2小时血糖、HbA1c变化水平,分析两组间在不同年龄段骨密度的变化及其关联因素。结果 IGT组与NGT组的骨密度、餐后2小时血糖、HbA1c水平比较有统计学意义(P0.05),而两组间空腹血糖比较无统计学意义(P0.05),随着增龄两组间骨密度均呈下降趋势,其中60岁以上的男性IGT患者BMD明显低于同龄NGT者(P0.05),50岁以上女性IGT患者BMD明显低于同龄NGT者(P0.05)。结论随着增龄,及餐后2小时血糖的影响,糖耐量异常患者较糖耐量正常患者更易发生骨质疏松,且有性别差异,女性年龄较男性提前。