Quartile Of Glucose Research Articles

Does acute hyperglycemia add prognostic value to the GRACE score in individuals with non-ST elevation acute coronary syndromes?

Background It is not known in what extent admission glucose improves risk stratification of the GRACE Score in patients with non-ST-segment elevation acute coronary syndromes (ACS). We tested the hypothesis that admission glucose adds relevant prognostic information to the GRACE Score. Methods Consecutive patients admitted with ACS had plasma glucose measured at admission and cardiovascular events were defined as death, non-fatal myocardial infarction or non-fatal refractory angina during hospitalization. Results Among the 148 patients studied, 11.5% developed cardiovascular events. Patients in the forth quartile of admission glucose (≥ 175 mg/dl) had a greater incidence of events, compared with those in the first 3 quartiles (22% vs. 8.1%; RR = 2.7; 95%CI 1.1–6.4; P = 0.03). Plasma glucose remained a predictor of events, after adjustment for diabetes ( P = 0.03). After adjustment for the GRACE Score, glucose in the forth quartile lost its predictive value ( P = 0.29). Plasma glucose added to GRACE did not improve the C-statistics (0.82; 95%CI 0.75–0.88), as compared with the original Score (0.81; 95%CI 0.74–0.87). Net reclassification improvement by new score was − 0.03 ( P = 0.86), indicating no useful reclassification. Conclusion Despite its association with adverse events, admission plasma glucose does not improve GRACE's accuracy to predict in-hospital events in patients with ACS.

Association Between Hyperglycemia and Survival in Patients With Newly Diagnosed Glioblastoma

Hyperglycemia has been associated with poor outcomes in many disease states. This retrospective study assessed the association between hyperglycemia and survival in patients with newly diagnosed glioblastoma multiforme (GBM). PATIENTS AND METHODS; Between 1999 and 2004, before the standard use of temozolomide, 191 patients were accrued onto New Approaches to Brain Tumor Therapy CNS Consortium trials with similar eligibility criteria. Time-weighted mean glucose and mean glucocorticoid dose were calculated for each patient using all values collected regularly in follow-up. The primary outcome was survival. Mean glucose levels ranged between 65 and 459 mg/dL. These were divided into quartiles: quartile one (< 94 mg/dL), quartile two (94 to 109 mg/dL), quartile three (110 to 137 mg/dL), and quartile four (> 137 mg/dL). Median survival times for patients in quartiles one, two, three, and four were 14.5, 11.6, 11.6, and 9.1 months, respectively. The association between higher mean glucose and shorter survival persisted after adjustment for mean daily glucocorticoid dose, age, and baseline Karnofsky performance score (KPS). Compared with patients in the lowest mean glucose quartile, those in quartile two (adjusted hazard ratio [HR], 1.29; 95% CI, 0.85 to 1.96), quartile three (adjusted HR, 1.35; 95% CI, 0.89 to 2.06), and quartile four (adjusted HR, 1.57; 95% CI, 1.02 to 2.40) were at progressively higher risk of dying (P = .041 for trend). In these patients with newly diagnosed GBM and good baseline KPS, hyperglycemia was associated with shorter survival, after controlling for glucocorticoid dose and other confounders. The effect of intensive management of glucocorticoid-related hyperglycemia on survival deserves additional study in patients with GBM.

Interleukin-18 Is a Strong Predictor of Cardiovascular Events in Elderly Men With the Metabolic Syndrome

OBJECTIVE—The aim of this study was to investigate the role of inflammatory markers as potential predictors of cardiovascular events in subjects with and without the metabolic syndrome.RESEARCH DESIGN AND METHODS—This was a post hoc analysis from the Diet and Omega-3 Intervention Trial (DOIT), comprising 563 elderly men with (n = 221) and without (n = 342) metabolic syndrome. Circulating inflammatory markers were measured.RESULTS—During 3 years, 68 cardiovascular events were recorded. In the total population, C-reactive protein (CRP) (P < 0.001), interleukin-18 (IL-18) (P = 0.008), and IL-6 (P = 0.003) were elevated in subjects with events. In subjects with metabolic syndrome, IL-18 was the strongest predictor (adjusted odds ratio 2.9 [95% CI 1.1–7.8]). In subjects without metabolic syndrome, only CRP seemed to be an independent predictor (3.3 [1.5–7.3]). There was a significant interaction between fasting glucose and IL-18 (P = 0.008) and IL-6 (P = 0.024) but not CRP. Elevated fasting glucose (>6.2 mmol/l) markedly increased the predictive power of inflammatory markers (IL-18: 5.5 [1.4–21.1], IL-6: 3.5 [1.0–11.8], and CRP: 3.5 [1.0–11.9]). For IL-18, there was a stepwise increase in event rate by quartiles of fasting glucose.CONCLUSIONS—IL-18 was an independent predictor of cardiovascular events in subjects with metabolic syndrome and even more so in the presence of elevated fasting glucose. Our findings suggest a mutually potentiating effect of hyperglycemia and inflammation in cardiovascular risk prediction.

Impact of lowering the criterion for impaired fasting glucose on identification of individuals with insulin resistance. The GISIR database.

We assessed the accuracy of the American Diabetes Association (ADA)2003 definition of impaired fasting glucose (IFG) in identifying subjects with low insulin sensitivity, and determined cardiovascular risk factors in ADA2003 IFG subjects. This study included 930 non-diabetic Italian Caucasians from the GISIR database in which subjects underwent a hyperinsulinaemic-euglycaemic clamp performed with a standard technique. Low insulin sensitivity was defined as being in the lower quartile of glucose metabolized during the last hour of the clamp (M). Subjects were stratified in the following groups: normal fasting glucose (NFG) (<100 mg/dL), IFG100 (100-109 mg/dL), ADA1997 IFG110 (110-125 mg/dL), and ADA2003 IFG (100-125 mg/dL). The sensitivity of identifying subjects with low insulin sensitivity increased adopting the ADA2003 criterion. After Bonferroni correction for multiple comparisons, both IFG100 and ADA1997 IFG110 showed significantly higher body mass index (BMI), waist, systolic blood pressure (SBP) and diastolic blood pressure (DBP), triglyceride, fasting plasma insulin (FPI) and fasting plasma glucose (FPG), and lower insulin sensitivity as compared with NFG. As compared with IFG100, ADA1997 IFG110 showed significantly higher BMI, waist, SBP, FPI, FPG, and lower insulin sensitivity. ADA2003 IFG group showed significantly higher BMI, waist, SBP and DBP, triglyceride, cholesterol, FPI, and FPG, but lower HDL levels and insulin sensitivity compared with NFG subjects. Although neither the ADA2003 nor the ADA1997 definition of IFG appears to be particularly efficacious for the identification of subjects' low insulin sensitivity, lowering the criterion to the ADA2003 glucose threshold increased the sensitivity without affecting the specificity. ADA2003 IFG showed a worse cardiovascular risk profile compared with NFG.

Diabetes, Hyperglycemia, and Central Corneal Thickness: The Singapore Malay Eye Study

To examine the relationship of diabetes and hyperglycemia with central corneal thickness (CCT) in Malay adults in Singapore. Population-based cross-sectional study. Three thousand two hundred eighty Malay adults ages 40-80 years living in Singapore. The study population was selected using an age-stratified random sampling procedure of Malay 40- to 80-year-olds living in the southwestern part of Singapore. Participants had a standardized interview, examination, and ocular imaging at a centralized study clinic. Central corneal thickness was measured with an ultrasound pachymeter, and nonfasting serum glucose and glycosylated hemoglobin (Hb A(1C)) was obtained from all participants. Diabetes was defined as having nonfasting glucose levels of > or =200 mg/dl (11.1 mmol/l), a self-report of diabetic medication use, or physician diagnosis of diabetes. Central corneal thickness. Of the 3280 (78.7% response) participants, data on CCT were available on 3239 right eyes. Central corneal thickness was normally distributed, with a mean of 541.2 microm. There were 748 persons with diabetes (23.0%). After controlling for age and gender, central corneas were significantly thicker in persons with diabetes than in those without diabetes (547.2 microm vs. 539.3 microm, P<0.001) and, in the total population, with higher serum glucose (539.6, 540.2, 541.3, and 544.4, comparing increasing glucose quartiles; P = 0.023) and higher Hb A(1C) (537.8, 541.0, 541.4, and 545.5, comparing increasing Hb A(1C) quartiles; P<0.001) levels. In multiple linear regression models adjusting for age, intraocular pressure (IOP), body mass index, and axial length, persons with diabetes had, on average, central corneas 6.50 microm thicker than those of persons without diabetes. This population-based study among Malays showed that diabetes and hyperglycemia are associated with thicker central corneas, independent of age and IOP levels. These findings may have implications for understanding the relationship between diabetes and glaucoma.

Post‐challenge glucose predicts coronary atherosclerotic progression in non‐diabetic, post‐menopausal women1

We sought to determine whether fasting or post-challenge glucose were associated with progression of coronary atherosclerosis in non-diabetic women. We performed a post-hoc analysis of 132 non-diabetic women who underwent 75-g oral glucose tolerance testing. The primary outcome of interest was progression of atherosclerosis determined by baseline and follow-up coronary angiography, a mean of 3.1 +/- 0.9 years apart. We analysed the association of change in minimal vessel diameter (DeltaMD) by quartile of fasting and post-challenge glucose using mixed models that included adjustment for age, systolic blood pressure, total : high-density lipoprotein cholesterol ratio, current smoking, lipid-lowering and anti-hypertensive medication use and other covariates. At baseline, participants had a mean age of 65.7 +/- 6.7 years and a mean body mass index of 27.9 +/- 8.5 kg/m(2). Although there were no significant differences in atherosclerotic progression by fasting glucose category (P for trend across quartiles = 0.99), there was a significant inverse association between post-challenge glucose and DeltaMD (in mm) (Q1 : 0.01 +/- 0.03; Q2 : 0.08 +/- 0.03; Q3 : 0.13 +/- 0.03; Q4 : 0.11 +/- 0.03; P for trend = 0.02). In post-menopausal women without diabetes, post-challenge glucose predicts angiographic disease progression. These findings suggest that even modest post-challenge hyperglycaemia influences the pathogenesis of atherosclerotic progression.

Insulin Secretion and Insulin Sensitivity in Relation to Fasting Glucose in Healthy Subjects

This study evaluated insulin secretion and insulin sensitivity in healthy subjects with normal fasting glucose. A total of 148 healthy women (aged 53-70 years) underwent a glucose-dependent arginine stimulation test and a 2-h euglycemic-hyperinsulinemic clamp. In the arginine test, arginine (5 g) was injected intravenously under baseline (fasting) conditions and after raising the glucose levels to 15 and >28 mmol/l. From this test, the acute insulin response (AIR) to arginine during the three glucose levels (AIR1, AIR2, and AIR3) were estimated. The subjects were divided into quartiles of fasting glucose (n = 37 in each group [range <4.32; 4.33-4.84; 4.85-5.22; and 5.23-6.1 mmol/l, respectively). The results show that 1) AIR1 was higher in subjects in the two highest quartiles (P = 0.004), 2) AIR3 was higher in the quartile with the highest fasting glucose (P = 0.012), and 3) insulin sensitivity was reduced in subjects in the highest quartile (P = 0.026) compared with the lower quartiles. The results also show, in contrast, that AIR2 did not show a similar trend to be increased at higher fasting glucose. It is concluded that 1) raised fasting glucose (albeit still within normal values) augments baseline and maximal arginine-induced insulin secretion in healthy subjects, and 2) this is associated with reduced insulin sensitivity. This suggests that high, but still normal, fasting glucose may contribute to the augmented insulin secretion in subjects with low insulin sensitivity.

Blood glucose and the metabolism of cholesterol in coronary patients with and without simvastatin treatment

Background and aim of the study Association of blood glucose with cholesterol metabolism and with cholesterol lowering during simvastatin treatment has not been studied earlier in hypercholesterolemic subjects with coronary heart disease. Methods Baseline blood glucose was compared with cholesterol synthesis (e.g. ratios of squalene and lathosterol) and absorption (e.g. sitosterol ratio) without and with simvastatin for one year in 806 non-diabetes Finnish subjects of the Scandinavian Simvastatin Survival Study. Results Baseline blood glucose was positively correlated with the baseline synthesis and negatively with the absorption of cholesterol, and positively with the synthesis/absorption ratio (e.g. p = 0.001 for lathosterol/sitosterol). Simvastatin decreased serum cholesterol by about 29% irrespective of glucose level, cholesterol synthesis by up to 34%, especially in the highest glucose quartile, and increased cholesterol absorption by up to 49%, especially in the lowest glucose quartile ( p < 0.01 for all). The one-year synthesis/absorption ratio was decreased proportionately to the baseline glucose, e.g. for lathosterol/sitosterol by over 40% ( p < 0.001) in different glucose quartiles ( p < 0.001 between quartiles). Conclusions Baseline blood glucose level is related positively to cholesterol synthesis and negatively to that of absorption. Despite a marked glucose-related decrease in cholesterol synthesis with simvastatin, serum cholesterol reduction was not dependent on the baseline glucose level.

Pre-Type 1 Diabetes Dysmetabolism: Maximal Sensitivity Achieved with Both Oral and Intravenous Glucose Tolerance Testing

To determine the relationship of intravenous (IVGTT) and oral (OGTT) glucose tolerance tests abnormalities to diabetes development in a high-risk pre-diabetic cohort and to identify an optimal testing strategy for detecting preclinical diabetes. Diabetes Prevention Trial-Type 1 Diabetes (DPT-1) randomized subjects to oral (n = 372) and parenteral (n = 339) insulin prevention trials. Subjects were followed with IVGTTs and OGTTs. Factors associated with progression to diabetes were evaluated. Survival analysis revealed that higher quartiles of 2-hour glucose and lower quartiles of first phase insulin response (FPIR) at baseline were associated with decreased diabetes-free survival. Cox proportional hazards modeling showed that baseline body mass index (BMI), FPIR, and 2-hour glucose levels were significantly associated with an increased hazard for diabetes. On testing performed within 6 months of diabetes diagnosis, 3% (1/32) had normal FPIR and normal 2-hour glucose on OGTT. The sensitivities for impaired glucose tolerance (IGT) and low FPIR performed within 6 months of diabetes diagnosis were equivalent (76% vs 73%). Most (97%) subjects had abnormal IVGTTs and/or OGTTs before the development of diabetes. The highest sensitivity is achieved using both tests.

Association Between Blood Glucose and Long-Term Mortality in Patients With Acute Coronary Syndromes in the OPUS-TIMI 16 Trial

Hyperglycemia in the context of acute coronary syndrome (ACS) is a common observation, and existing data suggest that high glucose levels are associated with increased in-hospital mortality. We assessed the relation between random glucose and long-term mortality in 9,020 patients with ACS who were enrolled in the OPUS-TIMI 16 trial. A significant relation between glucose level and 10-month mortality was observed (2.7% in quartile 1 vs 7.0% in quartile 4, p <0.0001). After multivariable adjustment for co-morbidity, which included history of diabetes, this relation remained significant (quartile 4 vs 1, hazard ratio 1.70, 95% confidence interval 1.16 to 2.50, p = 0.006). These observations were similar in the TACTICS-TIMI 18 trial. In addition, we observed that B-type natriuretic peptide and troponin I levels increased across glucose quartiles in the OPUS-TIMI 16 trial (p values for trend = 0.002 and 0.0001, respectively) and the TACTICS-TIMI 18 trial (p values for trend = 0.006 and 0.0001, respectively). High blood glucose during ACS is an independent predictor of long-term mortality and is significantly correlated with prognostic biomarkers. Glucose levels during ACS may be an important addition to the risk stratification of patients with ACS and a potentially important target for therapy.

Insulin Resistance, Apoptosis, and Colorectal Adenoma Risk

Compelling evidence from epidemiologic studies indicates that elevated circulating insulin-like growth factor (IGF)-I, insulin resistance, and associated complications, such as elevated fasting plasma insulin, glucose and free fatty acids, glucose intolerance, increased body mass index, and visceral adiposity, are linked with increased risk of colorectal cancer. However, the role of insulin and markers of glucose control in the development of adenomas, precursors to colorectal cancer, has not been fully explored. We evaluated the relationship between plasma insulin, glucose, IGF-I, IGF-II, IGF-binding protein-3 (IGFBP-3), apoptosis, and colorectal adenomas in a case-control study. Participants were drawn from consenting patients undergoing colonoscopy at the University of North Carolina hospitals (Chapel Hill, NC). Participants were classified as cases or controls based on whether they had one or more colorectal adenomatous polyps. Fasting plasma insulin, IGF-I, IGF-II, and IGFBP-3 levels were assessed by ELISA. Glucose was measured by glucose hexokinase assay. Apoptosis was assessed by morphology on H&E-stained sections. Dietary and lifestyle information were obtained by telephone interview. Logistic regression was used to examine the association between adenoma status and insulin-IGF markers. Adenoma cases (n = 239) and adenoma-free controls (n = 517) provided rectal biopsies and/or blood samples and interview data. Consistent with prior findings, cases were more likely to be males, older, have higher waist-to-hip ratio, lower calcium intake, lower apoptosis, and less likely to report nonsteroidal anti-inflammatory drug use. Those in the highest quartile of insulin (adjusted odds ratio, 2.2; 95% confidence interval, 1.1-4.2) and glucose (adjusted odds ratio, 1.8; 95% confidence interval, 0.9-3.6) were more likely to have an adenoma compared with the lowest quartile. Similarly, subjects in the highest two quartiles of insulin were more likely to be in the lowest two quartiles of apoptosis. Overall, there were no significant differences between mean circulating levels of glucose, IGF-I, IGF-II, and IGFBP-3 among cases and controls and no association between these variables and apoptosis. The results provide novel evidence that elevated insulin and glucose are associated with increased adenoma risk and decreased apoptosis in normal rectal mucosa. These findings suggest that insulin may act early in the adenoma-carcinoma sequence to promote the development of colorectal adenoma by decreasing apoptosis in the normal mucosa.

Oxidative stress and glucose levels in a population‐based sample

To examine the relationship between markers of oxidative status and glucose on a population basis. We report here on a population-based sample of 1315 women and 981 men, aged 35-79 years, randomly selected from residents of Erie and Niagara Counties in western New York between 1996 and 1999. Thiobarbituric reactive substances (TBARS), erythrocyte glutathione (GSH) and plasma glutathione peroxidase (GSH-Px) were measured as markers of oxidative status. Study sample was categorized by quartiles of glucose, degree of abnormality of fasting glucose, and level of metabolic control in patients with diabetes. Men and women in the uppermost quartiles of glucose had higher levels of TBARS (men: Quartile 4 = 1.55 +/- 0.03, Quartile 1 = 1.36 +/- 0.03, women: 1.49 +/- 0.02, 1.30 +/- 0.02 nmol/ml) and lower levels of GSH (men: Quartile 4 = 1.57 +/- 0.03, Quartile 1 = 1.69 +/- 0.03, women: 1.71 +/- 0.03, 1.97 +/- 0.0 mmol/l packed RBCs). In women, compared with normal fasting glucose, impaired fasting glucose was associated with higher levels of TBARS (1.29 +/- 0.01 vs. 1.84 +/- 0.04 nmol/ml), lower levels of GSH (1.85 +/- 0.02 vs. 1.76 +/- 0.05 mmol/l packed RBCs), and higher GSH-Px activity (618.94 +/- 2.64 vs. 644.77 +/- 8.90 IU/l). In women, abnormal fasting glucose was associated with higher levels of TBARS (1.84 +/- 0.04 nmol/ml), lower levels of GSH (1.68 +/- 0.06 mmol/l packed RBCs), and higher levels of GSH-Px (647.72 +/- 9.87 IU/l) than normal or impaired fasting glucose. In men, abnormal fasting glucose was associated with higher TBARS (1.76 +/- 0.04 vs. 1.37 +/- 0.07 nmol/ml), and lower GSH (1.62 +/- 0.05 vs. 2.78 +/- 0.02 mmol/l packed RBCs), than normal fasting glucose. Poor metabolic control was associated with higher TBARS (men: 2.07 +/- 0.08 vs. 1.33 +/- 0.14 nmol/l, women: 2.02 +/- 0.09 vs. 1.35 +/- 0.18 nmol/l) and GSH-Px activity (men: 654.34 +/- 13.45 vs. 599.86 +/- 24.76, women: 660.61 +/- 13.25 vs. 579.42 +/- 27.42 IU/l). Glucose levels play a role in determining oxidative status in a population sample. The balance between oxidative and antioxidant processes appears to be sensitive to glucose levels with moderate elevations of glucose affecting the oxidative status.

Hyperinsulinaemia is associated with increased long-term mortality following acute myocardial infarction in non-diabetic patients?

To study the impact of disturbances in glucose metabolism on total mortality in non-diabetic patients with acute myocardial infarction. Four hundred and ninety four patients with a verified myocardial infarction and no history of diabetes were studied. The study population comprised a subgroup of patients screened for participation in the Trandolapril Cardiac Evaluation (TRACE) study. At baseline, fasting insulin, fasting glucose, glycosylated haemoglobin (HbA1c), and urinary albumin excretion were measured. Survival status was determined after 6-8 years. Patients with hyperinsulinaemia were more obese and more frequently suffered from hypertension, previous myocardial infarction and congestive heart failure. In a univariate regression analysis, values in the upper quartile of insulin, glucose, HbA1c, and urinary albumin were associated with an excess mortality risk (RR=1.8 (1.2-2.7), p=0.002; RR=1.6 (1.2-2.1), p=0.001; RR= 1.9 (1.3-2.9), p=0.001; RR=1.6 (1.2-2.1), p=0.02 respectively). However, only a high insulin level remained significant in a multivariable analysis (RR=1.54 (1.03-2.31), p=0.04) including baseline variables, left ventricular systolic function and in-hospital complications. High fasting plasma insulin is an independent risk factor of all-cause mortality in non-diabetic patients with acute myocardial infarction. This justifies future intervention studies aiming at reducing insulin resistance and using fasting insulin as the target variable.

Prediction of Type 2 diabetes in healthy middle-aged men with special emphasis on glucose homeostasis. Results from 22.5 years' follow-up.

To study the glucose disappearance rate and fasting blood glucose as predictors of Type 2 diabetes in a 22.5-year prospective follow-up of 1947 healthy non-diabetic men. Of a cohort of 2014 Caucasian men, the 1947 who had both fasting blood glucose < 110 mg/dl and an intravenous glucose tolerance test were included. A number of other physiological parameters were also determined at baseline. Multivariate Cox regression analyses were used to investigate the possible significance of the glucose disappearance rate and fasting blood glucose as predictors of Type 2 diabetes. After 22.5 years' follow-up, 143 cases of Type 2 diabetes had developed. Glucose disappearance rate and fasting blood glucose were moderately correlated (r = -0.32). Men in the lowest quartile of glucose disappearance rate and highest quartile of fasting blood glucose had markedly higher diabetes rates than all other men (P < 0.0001). After adjusting for each other, age, diabetes heredity, body mass index, physical fitness, triglycerides, cholesterol and blood pressure (Cox model), both glucose disappearance rate and fasting blood glucose remained major predictors of diabetes Glucose disappearance rate and fasting blood glucose are, in spite of low intercorrelation, major long-term predictors of Type 2 diabetes in healthy non-diabetic Caucasian men.

Fasting plasma glucose in non-diabetic elderly women predicts increased all-causes mortality and coronary heart disease risk.

To confirm the hypothesis that upper normal plasma glucose levels in non-diabetic subjects are independently predictive of mortality and cardiovascular disease (CVD). The study reports on 113 months' follow-up in a prospective study of CVD in the Australian elderly, The Dubbo Study. The cohort, first examined in 1988-89, consisted of 2805 men and women 60 years and older. Of the cohort, 2419 (86%) were defined as non-diabetic. The prediction of outcomes by quartile of fasting plasma glucose was examined in a Cox proportional hazards model, after linkage to hospital and death records. All-causes mortality increased progressively across quartile of fasting plasma glucose in both sexes, reaching statistical significance only in women. Coronary heart disease (CHD) incidence increased similarly, the increases being proportionately greater in women. Ischaemic stroke did not show a consistent gradient with fasting plasma glucose. After adjustment for age and other risk factors, all-causes mortality, CHD and ischaemic stroke incidence were not significantly related to plasma glucose in men. In women, all-causes mortality and CHD incidence showed a significant gradient with glucose quartile. Hazard Ratio (95% confidence intervals) for death in glucose Quartile IV (5.3-6.0 mmol/L) was 1.49 (1.03-2.14) and for CHD incidence was 1.52 (1.08-2.15). Subjects in the upper quartiles of fasting plasma glucose showed a clustering of overweight, hypertension, elevated serum triglycerides, reduced high density lipoprotein cholesterol and excess of small dense low density lipoprotein, suggestive of the Insulin Resistance Syndrome. Fasting plasma glucose levels in the upper normal range in non-diabetic elderly subjects appear to be associated with increased all-causes mortality and CHD, especially in women.

Perioperative glycemic control and the risk of infectious complications in a cohort of adults with diabetes.

Although hyperglycemia is hypothesized to increase the short-term risk of infection, this hypothesis has not been well tested in a clinical setting. This study was designed to assess the relationship of perioperative glycemic control to the subsequent risk of infectious complications. A total of 411 adults with diabetes who underwent coronary artery surgery from 1990 to 1995 in the cardiac surgery service of an urban university hospital were included in a nonconcurrent prospective cohort study based on chart review. Perioperative glycemic control was characterized by the mean of six capillary glucose measurements taken during the 36-h interval following surgery. The major outcomes studied were infections of leg and chest wounds, pneumonia, and urinary tract infections. Mean postoperative glucose levels ranged from 121 to 352 mg/dl and were divided into quartiles: quartile 1 (121-206 mg/dl), quartile 2 (207-229 mg/dl), quartile 3 (230-252 mg/dl), and quartile 4 (253352 mg/dl). After simultaneous adjustment for age, sex, race, underlying comorbidity, acute severity of illness, and the length of the stay in the surgical intensive care unit, patients with higher mean capillary glucose readings were at increased risk of developing infections. Compared with people in the lowest quartile of postoperative glucose, those in quartiles 2 (relative odds of infection [95% CI] = 1.17 [0.57-2.40]), 3 (1.86 [0.94-3.68]), and 4 (1.78 [0.86-3.47]) were at progressively higher risk for infection (P = 0.05 for trend). In patients with diabetes who undergo coronary artery surgery, postoperative hyperglycemia is an independent predictor of short-term infectious complications. Physicians should consider a glucose concentration target of < or =200 mg/dl to reduce the risk of infection.

Increased blood glucose and insulin, body size, and incident colorectal cancer.

Abdominal obesity--an elevated level of visceral adipose tissue--has been linked to colorectal cancer. Furthermore, elevated levels of visceral adipose tissue have been associated with hyperinsulinemia, and insulin is a growth factor in the colon. We assessed whether waist circumference, a surrogate measure of visceral adipose tissue, and metabolic parameters associated with visceral adipose tissue were related to colorectal cancer. In the Cardiovascular Health Study cohort, we examined the relationship of baseline measurements of body size, glucose, insulin, and lipoproteins to incident colorectal cancer. All P values are two-sided. Among 5849 participants, 102 incident cases of colorectal cancer were identified. Individuals in the highest quartile of fasting glucose had a nearly twofold increased risk of colorectal cancer (relative risk [RR] = 1.8; 95% confidence interval [CI] = 1.0-3.1), and the linear trend RR (LT RR = 1.2; 95% CI = 1.0-1.5) for fasting glucose level was statistically significant (P =. 02). Glucose and insulin levels 2 hours after oral glucose challenge also exhibited statistically significant associations with colorectal cancer (2-hour glucose levels: RR = 2.4 [95% CI = 1.2-4. 7]/LT RR = 1.3 [95% CI = 1.0-1.6; P =.02]; 2-hour insulin levels: RR = 2.0 [95% CI = 1.0-3.8]/LT RR = 1.2 [95% CI = 1.0-1.5; P =.04]). Analysis of fasting insulin levels suggested a threshold effect, with values above the median associated with colorectal cancer (RR = 1.6; 95% CI = 1.1-2.4; P =.02). Higher levels of waist circumference were also statistically significantly associated with colorectal cancer (RR = 1.9; 95% CI = 1.1-3.3; P =.02). These data provide, to our knowledge, the first direct evidence of an association between elevated visceral adipose tissue level, its associated metabolic effects, and colorectal cancer.

Fasting blood glucose: an underestimated risk factor for cardiovascular death. Results from a 22-year follow-up of healthy nondiabetic men.

Because of the available conflicting epidemiological data, we investigated the possible impact of fasting blood glucose as a risk factor for cardiovascular death in nondiabetic men. This study reports the results from a 22-year prospective study on fasting blood glucose as a predictor of cardiovascular death. Of the 1,998 apparently healthy nondiabetic men (aged 40-59 years), a total of 1,973 with fasting blood glucose < 110 mg/dl were included in the study in which also a number of conventional risk factors were measured at baseline. After 22 years of follow-up, 483 men had died, 53% from cardiovascular diseases. After dividing men into quartiles of fasting blood glucose level, it was found that men in the highest glucose quartile (fasting blood glucose > 85 mg/dl) had a significantly higher mortality rate from cardiovascular diseases compared with those in the three lowest quartiles. Even after adjusting for age, smoking habits, serum lipids, blood pressure, forced expiratory volume in 1 s, and physical fitness (Cox model), the relative risk of cardiovascular death for men with fasting blood glucose > 85 mg/dl remained 1.4 (95% CI 1.04-1.8). Noncardiovascular deaths were unrelated to fasting blood glucose level. Fasting blood glucose values in the upper normal range appears to be an important independent predictor of cardiovascular death in nondiabetic apparently healthy middle-aged men.

Effects of diabetes and level of glycemia on all-cause and cardiovascular mortality. The San Antonio Heart Study.

Although the level of hyperglycemia is clearly a risk factor for microvascular complications in diabetic patients, its role in macrovascular complications remains controversial. We followed 4,875 subjects (65% Mexican-American) for 7-8 years to investigate the effects of diabetes and hyperglycemia on all-cause and cardiovascular disease (CVD) mortality. These end points were also analyzed according to quartiles of baseline fasting plasma glucose among diabetic participants. The Cox proportional hazards model was used to estimate the relative risks (RRs) for all-cause and CVD mortality. Diabetes was significantly associated with increased all-cause mortality (RR [95% CI] = 2.1 [1.3-3.5] in men; 3.2 [1.9-5.4] in women) and increased CVD mortality (3.2 [1.4-7.1] in men; 8.5 [2.8-25.2] in women). Among diabetic subjects, those in quartile 4 had a 4.2-fold greater risk of all-cause mortality (P < 0.001) and a 4.7-fold greater risk of CVD mortality (P = 0.01) than those in quartiles 1 and 2 combined. After further adjustment for other potential risk factors, subjects in quartile 4 had a 4.9-fold greater risk of all-cause mortality and a 4.9-fold greater risk of CVD mortality than those in quartiles 1 and 2. In addition, hypertension, current smoking, and cholesterol > 6.2 mmol/l were significant predictors of CVD mortality using Cox models. We conclude that diabetes is a predictor of both all-cause and CVD mortality in the general population and that both hyperglycemia and common CVD risk factors are important predictors of all-cause and CVD mortality in diabetic subjects.