Non-diabetic Hyperglycaemia Research Articles

Longitudinal changes in insulin sensitivity, insulin secretion, beta cell function and glucose effectiveness during development of non-diabetic hyperglycemia in a Japanese population.

Since there had been no previous studies of alterations in insulin sensitivity, glucose-stimulated insulin secretion, beta cell function and glucose effectiveness during the development of non-diabetic hyperglycemia in Asian populations, we conducted a longitudinal study of such changes in 244 Japanese adults with normal glucose tolerance (median BMI 23.3 kg/m2 and age 51 yrs). The median follow-up period was 3.3 yrs. One hundred and eighty-two subjects maintained normal glucose tolerance (nonprogressors). After excluding the 3 subjects who progressed to diabetes, we analyzed the 59 who developed non-diabetic hyperglycemia (progressors), of which 31 progressed to impaired fasting glucose and 28 to impaired glucose tolerance. Whole body insulin sensitivity was estimated by ISIMatsuda, glucose-stimulated insulin secretion by [δIRI0-30/δPG0-30] and Stumvoll indices, hepatic insulin sensitivity by quantitative insulin sensitivity check index (QUICKI) and 1/fasting IRI, beta cell function by oral disposition index (DIO) ([δIRI0-30/δPG0-30]∙[ISIMatsuda]), and glucose effectiveness by an OGTT-derived index (SgIO). ISIMatsuda (p <0.05), [δIRI0-30/δPG0-30], DIO and SgIO (both p <0.01), but not QUICKI, 1/fasting IRI, or Stumvoll-1st and -2nd phases, were lower in the progressors at baseline. This group was also characterized by the following: 1) ISIMatsuda, DIO and SgIO were reduced by 34%, 32% and 11%, respectively (all p <0.01); 2) QUICKI and 1/fasting IRI diminished by 21% and 5%, respectively (both p <0.01); and 3) no significant changes were found in [δIRI0-30/δPG0-30], Stumvoll-1st and -2nd phases or BMI during the follow-up. In the nonprogressors, no indices changed significantly during the follow-up. Our study concluded that during the transition from normal glucose tolerance to non-diabetic hyperglycemia in this non-obese population, whole body insulin sensitivity, hepatic insulin sensitivity, beta cell function, and glucose effectiveness were all attenuated, but no significant changes in glucose-stimulated insulin secretion occurred. Also of note is the fact that the transition took place without any accompanying increase in BMI.Electronic supplementary materialThe online version of this article (doi:10.1186/2193-1801-3-252) contains supplementary material, which is available to authorized users.

The effects of vitamin D₂ or D₃ supplementation on glycaemic control and related metabolic parameters in people at risk of type 2 diabetes: protocol of a randomised double-blind placebo-controlled trial.

BackgroundThe global prevalence of type 2 diabetes is increasing. Effective strategies to address this public health challenge are currently lacking. A number of epidemiological studies have reported associations between low concentrations of 25-hydroxy vitamin D and the incidence of diabetes, but a causal link has not been established. We investigate the effect of vitamin D supplementation on the metabolic status of individuals at increased risk of developing type 2 diabetes.Methods/designIn a randomised double-blind placebo-controlled trial individuals identified as having a high risk of type 2 diabetes (non-diabetic hyperglycaemia or positive diabetes risk score) are randomised into one of three groups and given 4 doses of either placebo, or 100,000 IU Vitamin D2 (ergocalciferol) or 100,000 IU Vitamin D3 (cholecalciferol) at monthly intervals. The primary outcome measure is the change in glycated haemoglobin level between baseline and 4 months. Secondary outcome measures include blood pressure, lipid levels, apolipoproteins, highly sensitive C-reactive protein, parathyroid hormone (PTH) and safety of supplementation. and C-reactive protein. The trial is being conducted at two sites (London and Cambridge, U.K.) and a total of 342 participants are being recruited.DiscussionTrial data examining whether supplementation of vitamin D improves glycaemic status and other metabolic parameters in people at risk of developing type 2 diabetes are sparse. This trial will evaluate the causal role of vitamin D in hyperglycaemia and risk of type 2 diabetes. Specific features of this trial include recruitment of participants from different ethnic groups, investigation of the relative effectiveness and safety of vitamin D2 and D3 and an evidence based approach to determination of the dose of supplementation.Trial registrationEudraCT2009-011264-11; ISRCTN86515510

Targets for Glycemic Control

Targets for Glycemic Control

Call for consistent coding in diabetes mellitus using the Royal College of General Practitioners and NHS pragmatic classification of diabetes

The prevalence of diabetes is increasing with growing levels of obesity and an aging population. New practical guidelines for diabetes provide an applicable classification. Inconsistent coding of diabetes hampers the use of computerised disease registers for quality improvement, and limits the monitoring of disease trends. To develop a consensus set of codes that should be used when recording diabetes diagnostic data. The consensus approach was hierarchical, with a preference for diagnostic/disorder codes, to define each type of diabetes and non-diabetic hyperglycaemia, which were listed as being completely, partially or not readily mapped to available codes. The practical classification divides diabetes into type 1 (T1DM), type 2 (T2DM), genetic, other, unclassified and non-diabetic fasting hyperglycaemia. We mapped the classification to Read version 2, Clinical Terms version 3 and SNOMED CT. T1DM and T2DM were completely mapped to appropriate codes. However, in other areas only partial mapping is possible. Genetics is a fastmoving field and there were considerable gaps in the available labels for genetic conditions; what the classification calls 'other' the coding system labels 'secondary' diabetes. The biggest gap was the lack of a code for diabetes where the type of diabetes was uncertain. Notwithstanding these limitations we were able to develop a consensus list. It is a challenge to develop codes that readily map to contemporary clinical concepts. However, clinicians should adopt the standard recommended codes; and audit the quality of their existing records.

Fasting glucose, obesity, and coronary artery calcification in community-based people without diabetes.

OBJECTIVEOur objective was to assess whether impaired fasting glucose (IFG) and obesity are independently related to coronary artery calcification (CAC) in a community-based population.RESEARCH DESIGN AND METHODSWe assessed CAC using multidetector computed tomography in 3,054 Framingham Heart Study participants (mean [SD] age was 50 [10] years, 49% were women, 29% had IFG, and 25% were obese) free from known vascular disease or diabetes. We tested the hypothesis that IFG (5.6–6.9 mmol/L) and obesity (BMI ≥30 kg/m2) were independently associated with high CAC (>90th percentile for age and sex) after adjusting for hypertension, lipids, smoking, and medication.RESULTSHigh CAC was significantly related to IFG in an age- and sex-adjusted model (odds ratio 1.4 [95% CI 1.1–1.7], P = 0.002; referent: normal fasting glucose) and after further adjustment for obesity (1.3 [1.0–1.6], P = 0.045). However, IFG was not associated with high CAC in multivariable-adjusted models before (1.2 [0.9–1.4], P = 0.20) or after adjustment for obesity. Obesity was associated with high CAC in age- and sex-adjusted models (1.6 [1.3–2.0], P < 0.001) and in multivariable models that included IFG (1.4 [1.1–1.7], P = 0.005). Multivariable-adjusted spline regression models suggested nonlinear relationships linking high CAC with BMI (J-shaped), waist circumference (J-shaped), and fasting glucose.CONCLUSIONSIn this community-based cohort, CAC was associated with obesity, but not IFG, after adjusting for important confounders. With the increasing worldwide prevalence of obesity and nondiabetic hyperglycemia, these data underscore the importance of obesity in the pathogenesis of CAC.

Index of glucose effectiveness derived from oral glucose tolerance test

Aim of this study was to formulate an index for glucose effectiveness (Sg), SgIo, based on 3-point (0, 30 and 120 min) 75 g oral glucose tolerance test (OGTT). The equation for SgI(O) was developed in the Chikuma cohort (n = 502). Firstly, post-loading plasma glucose without insulin action and Sg (PPG-without insulin and Sg) was calculated as follows: fasting plasma glucose (mg/dl) + [0.75 × 75,000]/[0.19 × BW(kg) × 10]. Secondly, 'PPG-without insulin/with Sg' was obtained from inverse correlation between log(10)DI(O) and 2-h post-glucose plasma glucose at OGTT (2hPG) in each glucose tolerance category: DI(O) denotes oral disposition index, a product of the Matsuda Index and δIRI(0-30)/δPG(0-30). Thirdly, expected 2hPG (2hPG(E)) of a given subject was obtained from the regression, and the ratio of 2hPG to 2hPG(E) (2hPG/2hPG(E)) was determined as an adjustment factor. Lastly, SgI(O) ([mg/dl]/min) was calculated as [PPG-without insulin and Sg]-[PPG-without insulin / with Sg] x [(2hPG) / 2hPG(E)]. SgI(O) was validated against Sg obtained by frequently sampled intravenous glucose tolerance test in the Jichi cohort (n = 205). Also, the accuracy of prediction of Sg by SgIo was tested by the Bland-Altman plot. SgI(O) was 3.61 ± 0.73, 3.17 ± 0.74 and 2.15 ± 0.60 in subjects with normal glucose tolerance (NGT), non-diabetic hyperglycemia and diabetes, respectively, in the Chikuma cohort. In the Jichi cohort, SgI(O) was significantly correlated with Sg in the entire group (r = 0.322, P < 0.001) and in subjects with NGT (r = 0.286, P < 0.001), and SgIo accurately predicted Sg. In conclusion, SgI(O) could be a simple, quantitative index for Sg.

Hormonal Association and Sexual Dysfunction in Patients with Impaired Fasting Glucose: A Cross-Sectional and Longitudinal Study

The category of impaired fasting glucose (IFG) denotes a state of nondiabetic hyperglycemia, considered a risk factor for the further development of diabetes mellitus (DM) and cardiovascular (CV) diseases. The aim of the present study is to evaluate the impact of IFG on sexual health in men. In addition, its effect on CV morbidity and mortality will also be addressed. A consecutive series of 3,451 men (mean age 57.3 ± 10.1 years) attending our outpatient clinic for sexual dysfunction was retrospectively studied. A subset of this sample (N = 1,687) was enrolled in a longitudinal study. Several clinical, biochemical (including testosterone), and instrumental (penile color Doppler ultrasound) factors were evaluated. IFG was defined by fasting glucose concentrations between 5.6 and 6.9 mmol/L (100-125 mg/dL). A higher threshold (6.1-6.9 mmol/L, 110-125 mg/dL) was also considered. Among the patients studied, 747 (21.7%) had DM. In addition, 659 (19.1%) subjects were classified as IFG. Patients with IFG, however defined, more often had severe ED, reduced penile blood flow, and overt hypogonadism when compared with patients with normal glucose levels. In addition, men with ED and IFG show poorer blood pressure and lipid profile with an overall increase in CV risk. Unadjusted incidence of major adverse CV events was significantly associated with baseline DM, whereas there was a trend toward higher risk also for IFG, but this did not reach statistical significance. Conversely, both IFG and DM were significantly associated with a higher risk of fatal and nonfatal cerebral events. Checking glucose and testosterone levels is mandatory in subjects with ED because testosterone substitution in impotent IFG subjects might ameliorate not only their sexual life but also their overall health.

The 30-year cardiovascular risk profile of South Africans with diagnosed diabetes, undiagnosed diabetes, pre-diabetes or normoglycaemia : the Bellville, South Africa pilot study

The aim of this pilot study was to assess the 30-year risk for cardiovascular disease (CVD) in the South Africa population of mixed-ancestry in individuals with non-diabetic hyperglycaemia, and undiagnosed and self-reported diabetes. Participants were drawn from an urban community of the Bellville South suburb of Cape Town. In total, 583 subjects without a history of CVD were eligible for lifetime CVD risk estimation. Gender-specific prediction for CVD risk was calculated using the 30-year CVD interactive risk calculator. High CVD risk (> 20%) was evident in normoglycaemic and younger subjects (under 35 years). The significant predictors of CVD were sibling history of diabetes, and triglyceride, low-density lipoprotein cholesterol and glycated haemoglobin levels (p < 0.001). The high lifetime risk in normoglycaemic and younger subjects may be considered a warning that CVD might take on epidemic proportions in the near future in this country. We recommend the inclusion of education on CVD in school and university curricula.

Insulin secretion and insulin sensitivity on the oral glucose tolerance test (OGTT) in middle-aged Japanese

The aim of this study was to assess the changes in insulin secretion and insulin sensitivity in relation to fasting and 2-hour plasma glucose (PG) levels and to assess the independent contributions of their impairments to non-diabetic hyperglycemia. A total of 2157 Japanese workers (mean age 52.6±7.3 years and mean BMI 23.9±3.2 kg/m(2)) underwent an oral glucose tolerance test (OGTT). Of these subjects, 1125 had normal glucose tolerance (NGT), 525 subjects had isolated impaired fasting glucose (IFG), 159 subjects had isolated impaired glucose tolerance (IGT), 263 subjects had combined IFG and IGT, and 85 subjects had newly diagnosed type 2 diabetes. Insulinogenic index and Matsuda insulin sensitivity index (ISI) were significantly attenuated in subjects with normal but slightly elevated fasting PG, or in subjects with normal but slightly elevated 2-hour PG. Whereas, InsAUC(120)/GluAUC(120) was not significantly decreased in those subjects, and significant decrease of it was observed exclusively in subjects with abnormal fasting PG (≥ 106 mg/dL) or abnormal 2-hour PG (≥ 221 mg/dL). Using multiple regression analyses, both Matsuda ISI and insulinogenic index were independently correlated with PG concentrations in subjects with IFG and/or IGT, while Matsuda ISI alone was independently correlated with fasting PG concentrations in normoglycemic subjects. In conclusion, both insulinogenic index and Matsuda ISI were significantly attenuated in subjects with normal but slightly elevated PG. Lowering of Matsuda ISI was likely to be a strong contributor to 'elevation of fasting PG within the normal range' in this population.

Hyperbolic correlation between insulin sensitivity and insulin secretion fades away in lean subjects with superb glucose regulation

The relationship between insulin sensitivity (Si) and insulin secretion (β) was analyzed in 533 health examinees. The subjects underwent a 75 g oral glucose tolerance test, with plasma glucose (PG) and immunoreactive insulin (IRI) determined at fasting, 30 min and 120 min, and were classified according to the current criteria as normal glucose tolerance (NGT, n=328), non-diabetic hyperglycemia (NDH, n=113) including impaired fasting glucose and impaired glucose tolerance, and diabetes mellitus (DM, n=72). NGT was subdivided by fasting PG (FPG) tertile, ≤4.9, 5.0-5.4 and 5.5-6.0 mM, into NGT(FPG1), NGT(FPG2) and NGT(FPG3), or by body mass index (BMI) tertile, ≤21.8, 21.9-24.4 and ≥24.5 kg/m², into NGT(BMI1), NGT(BMI2) and NGT(BMI3). As an index of Si and β, Matsuda index=10,000/sqrt[FPG·FIRI·2hPG·2hIRI] and δIRI₀₋₃₀/δPG₀₋₃₀, were employed respectively: FIRI, 2hPG and 2hIRI denote fasting IRI, 2h-post glucose PG and IRI, respectively. Correlation between Si and β was evaluated by Spearman's rank correlation and the parameters for [β]=a·[Si](b) were obtained by standardized major axis (SMA) regression. Si-β correlation was strongest in NDH (Spearman's rho=-0.546, SMA regression r²=0.277), intermediate in DM (rho=-0.432, r²=0.193) and weakest in NGT (rho=-0.201, r²=0.039). Spearman's rho for the Si-β correlation was significantly lower in NGT than in NDH (p=0.003). Si-β correlation was significant in NGT(FPG3), NGT(FPG2) and NGT(BMI3), but not in NGT(FPG1), NGT(BMI2) and NGT(BMI1). The slope, b, was -1.184˜-1.530 without significant differences between any groups. In conclusion, the hyperbolic Si-β correlation was weaker in NGT than in NDH and absent in NGT subjects belonging to the lowest FPG or BMI tertile.

Impact of hypertension, overall obesity and abdominal obesity on diabetes incidence in Shanghai residents with different glucose levels

The impact of hypertension, overall obesity and abdominal obesity, individually or collectively, on diabetes incidence over a period of 5 years in residents with different glucose levels is diverse, with abdominal obesity having an impact in both non-diabetic hyperglycaemia and normal groups.

The prevalence of undiagnosed diabetes in non-cardiac surgery patients, an observational study

Given that preoperative hyperglycemia is associated with poor outcomes and many non-diabetic patients have high plasma glucose (PG) levels, the purpose of our study was to estimate the prevalence of undiagnosed diabetes among non-cardiac surgery patients and to identify predictors of hyperglycemia in non-diabetics. We included all non-cardiac surgery patients with complete records in the Clinical Database of the Anesthesiology Institute at the Cleveland Clinic during January 2007 to April 2009, and we estimated the prevalence of undiagnosed diabetes and impaired fasting glucose (IFG) among the non-diabetic patients. The mean glucose levels for known diabetics and undiagnosed diabetics were compared using two-tailed Student's t tests, and we assessed the association between PG levels and demographic variables within the non-diabetics. Of the 39,434 patients analyzed, 5,511 (14%) were known diabetics. Of the 33,923 known non-diabetics, 3,426 (10 %) were undiagnosed diabetics and another 3,549 (11%) had IFG. Thus, 6,975 patients (21%) of the non-diabetic patients presented with abnormally high glucose. Previously undiagnosed diabetics had higher preoperative glucose levels compared with known diabetics, with a mean ± standard deviation (SD) of 161 ± 48 vs 146 ± 67 mg·dL⁻¹ (8.9 ± 2.7 vs 8.1 ± 3.7 mmoL·L⁻¹), respectively. The difference remained highly significant after adjusting for body mass index, age, sex, and American Society of Anesthesiologists (ASA) physical status (P < 0.001). Among non-diabetics, older age, obesity, male sex, and a higher ASA physical status were collectively significant predictors of hyperglycemia, with a c-statistic (95% confidence interval) of 0.67 (0.66-0.68). A significant proportion of non-cardiac surgery patients have previously undiagnosed diabetes and pre-diabetes. Previously undiagnosed patients have higher fasting glucose levels compared with diabetic patients. Further studies should be conducted to identify the implications of these findings on patient outcomes.

Non-diabetic hyperglycaemia and cardiovascular risk: moving beyond categorisation to individual interpretation of absolute risk

Non-diabetic hyperglycaemia is usually not considered at all or is viewed as a binary risk category in isolation from other factors when quantifying cardiovascular risk. We argue that hyperglycaemia should be considered as a continuous risk factor and only in the context of other vascular risk factors. To examine the potential impact of hyperglycaemia on cardiovascular disease (CVD) risk, we calculated the absolute CVD risk in groups defined by different levels of HbA(1c) and other CVD risk factors. We used data on 10,144 men and women from the European Prospective Investigation of Cancer-Norfolk cohort to calculate CVD rates across levels of HbA(1c) in groups characterised by different levels of traditional risk factors. We found significant differences in CVD rates across levels of HbA(1c) in groups defined by different levels of the other risk factors. CVD rates for non-diabetic individuals with an HbA(1c) of <5.5% increased from 0.6 (95% CI 0.3-1.2) to 29.6 (95% CI 14.8-59.1) per 1,000 person-years when traditional CVD risk factors were added sequentially to the lowest risk reference group. In most cases, non-diabetic individuals with an HbA(1c) of <5.5% and high values for all other CVD risk factors had substantially higher absolute CVD rates than those with an HbA(1c) of 6.0% to 6.4% but with no other raised CVD risk factors (29.6 [95% CI 14.8-59.1] and 2.5 [95% CI 0.4-18.1], respectively). A history of diabetes significantly increased CVD risk over the non-diabetic hyperglycaemia range. Comparisons of CVD rates across tertiles of total cholesterol:HDL-cholesterol ratio or mean systolic blood pressure in groups characterised by different levels of other risk factors showed similar findings. In people with non-diabetic hyperglycaemia, cardiovascular risk is highly dependent on the presence of other CVD risk factors. Attention should be given not to whether an individual has 'pre-diabetes', 'hypertension' or 'hypercholesterolaemia', but to an integrated assessment of CVD risk, based on the combination of risk factors present and potential benefits of treatment.

Non-diabetic hyperglycaemia correlates with angiographic coronary artery disease prevalence and severity

Aim The role of glycaemia as a coronary artery disease (CAD) risk factor is controversial, and the optimal glucose level is still a matter of debate. For this reason, we assessed the prevalence and severity of angiographic CAD across hyperglycaemia categories and in relation to haemoglobin A 1c (HbA 1c) levels. Methods We studied 273 consecutive patients without prior revascularization undergoing coronary angiography for suspected ischaemic pain. CAD severity was assessed using three angiographic scores: the Gensini's score; extent score; and arbitrary index. Patients were grouped, according to 2003 American Diabetes Association criteria, into those with normal fasting glucose (NFG), impaired fasting glucose (IFG) and diabetes mellitus (DM). Results CAD prevalence was 2.5-fold higher in both the IFG and DM groups compared with the NFG group. Deterioration of glycaemic profile was a multivariate predictor of angiographic CAD severity (extent score: P = 0.027; arbitrary index: P = 0.007). HbA 1c levels were significantly higher among CAD patients ( P = 0.016) and in those with two or more diseased vessels ( P = 0.023) compared with the non-CAD group. HbA 1c levels remained predictive of CAD prevalence even after adjusting for conventional risk factors, including DM (adjusted OR: 1.853; 95% CI: 1.269–2.704). Conclusion Non-diabetic hyperglycaemia, assessed either categorically by fasting glucose categories or continuously by HbA 1c levels, correlates with the poorest angiographic outcomes.

One case of hemichorea associated with non-diabetic hyperglycemia

One case of hemichorea associated with non-diabetic hyperglycemia

Hyperglycemia in diabetics and non-diabetics: Effect on the risk for and severity of pneumococcal pneumonia

We sought to determine whether poor glucose control among diabetics is associated with increased risk for pneumococcal pneumonia and whether elevated admitting plasma glucose (APG) levels are associated with increased severity of this infection in diabetic and non-diabetic patients. We compared hemoglobin A(1c) (HbA(1c)) in diabetics who had pneumococcal pneumonia with diabetic case-controls who did not have pneumonia. In patients with pneumococcal pneumonia, we related APG to disease severity as determined by SMART-COP score, need for ICU admission, and mortality at 7 and 30 days. Fifty-three of 233 patients with pneumococcal pneumonia (22.7%) were diabetic. Diabetics with pneumonia had poorer glycemic control than diabetic case-controls (HbA(1c) 8.2% vs. 7.2%, respectively, P<0.01). In pneumococcal pneumonia patients, SMART-COP scores, need for ICU admission, and mortality increased in proportion to the APG. These findings were attributable to the significant association between hyperglycemia and severity in non-diabetics. Poor glycemic control predisposes diabetics to pneumococcal pneumonia but, among diabetics, the degree of hyperglycemia at admission is not associated with increased disease severity. In contrast, among non-diabetics with pneumococcal pneumonia, hyperglycemia is a marker for severe disease and increased mortality, perhaps reflecting massive release of cytokines and glucocorticosteroids in overwhelming infection.

The threshold for definition of impaired fasting glucose in a Japanese population

We examined whether the cut-off value of fasting plasma glucose (FPG) for diagnosing impaired fasting glucose (IFG) should be lowered, using data from a large Japanese population. A retrospective cohort study was conducted from 1998 to 2006. Follow-up (2002-2006) data were merged with baseline (1998-2002) data, yielding 11 129 persons who had participated on both occasions. Among these, 10 475 persons who did not have diabetes (known diabetes or defined as FPG > or = 7.0 mmol/l) or suspected diabetes (glycated haemoglobin > or = 6.4%) were analysed. During follow-up of an average of 5.4 years, 279 (5.2%) out of 5372 men and 98 (1.9%) out of 5103 women developed diabetes. According to the three baseline FPG categories (< 5.6, 5.6-6.1 and 6.2-6.9 mmol/l), 28/3401 (0.8%), 91/1456 (6.3%) and 160/515 (31.1%), respectively, in men and 13/4231 (0.3%), 30/695 (4.3%) and 55/177 (31.1%), respectively, in women developed diabetes. The optimal cut-off FPG value to predict diabetes was 5.7 mmol/l for both men (sensitivity 84.2%, specificity 76.9%) and women (81.6%, 91.0%). However, lowering the cut-off from 6.1 to 5.7 mmol/l increased the prevalence of IFG 2.7-fold in men and 3.0-fold in women. Lowering the value further to 5.6 mmol/l increased the prevalence of IFG 3.8-fold in men and 4.9-fold in women. It may be reasonable to retain the conventional lower FPG limit for IFG and treat FPG values of 5.6-6.1 mmol/l as non-diabetic hyperglycaemia, considering the four- to fivefold increase in individuals classified as IFG when the new cut-off is applied.

Metabolic syndrome, aging, physical inactivity, and incidence of type 2 diabetes in general African population

The first objective of this study was to determine the baseline prevalence of metabolic syndrome and its individual components using the NCEP-R/ATPIII criteria, IDF criteria for Europe, and IDF criteria for Africa: waist circumference of at least 94 cm for men and women. The second objective was to investigate the incidence and the determinants of type 2 diabetes in a prospective cohort of 807 non-diabetic Central Africans aged >or= 40 years from December 2004 to September 2008. During 3,156 person-years of median follow up, there were 93 type 2 diabetes cases (11.5%), corresponding to an incidence of 29 (95% CI 15-43) per 1,000 person-years. The independent predictors of incident type 2 diabetes were age >or= 45 years, physical inactivity, non-diabetic hyperglycaemia and metabolic syndrome regardless of criteria used. In conclusion, urgent prevention strategies are needed to curb the type 2 diabetes epidemic in Africa.

Continuous relationships between non-diabetic hyperglycaemia and both cardiovascular disease and all-cause mortality: the Australian Diabetes, Obesity, and Lifestyle (AusDiab) study

Hyperglycaemia is a risk factor for cardiovascular disease (CVD) and all-cause mortality in individuals without diabetes. We investigated: (1) whether the risk of all-cause and CVD mortality extended continuously throughout the range of fasting plasma glucose (FPG), 2 h plasma glucose (2hPG) and HbA(1c) values; and (2) the ability of these measures to improve risk prediction for mortality. Data on 10,026 people aged >or=25 years without diagnosed diabetes were obtained from the population-based Australian Diabetes, Obesity and Lifestyle study. Between 1999 and 2000, FPG, 2hPG and HbA(1c) were assessed and all-cause (332 deaths) and CVD (88 deaths) mortality were obtained after 7 years. Both 2hPG and HbA(1c) exhibited linear relationships with all-cause and CVD mortality, whereas FPG showed J-shaped relationships. The adjusted HR (95% CI) for all-cause mortality per SD increase was 1.2 (1.1-1.3) for 2hPG and 1.1 (1.0-1.2) for HbA(1c). The HR for FPG <5.1 mmol/l (per SD decrease) was 2.0 (1.3-3.0); for FPG >or=5.1 mmol/l (per SD increase) the HR was 1.1 (1.0-1.2). Corresponding HRs for CVD mortality were 1.2 (1.0-1.4), 1.2 (1.0-1.3), 4.0 (2.1-7.6) and 1.3 (1.1-1.4). The discriminative ability of each measure was similar; no measure substantially improved individual risk identification over traditional risk factors. In individuals without diagnosed diabetes, 2hPG and FPG, but not HbA(1c) were significant predictors of all-cause mortality, whereas all measures were significant predictors of CVD mortality. However, these glucose measures did not substantially improve individual risk identification.

Repercusiones y manejo de la hiperglucemia peroperatoria en cirugía cardiaca

Surgery produces a neuroendocrine stress response that affects resistance to insulin, reduces insulin secretion, and increases the release of glucose from the liver. This situation can trigger hyperglycemia in both diabetics and nondiabetics. Hyperglycemia has been linked to an increase in the morbidity and mortality among patients who undergo cardiac surgery, and the benefits of correcting hyperglycemia in this setting by means of intensive insulin therapy are well documented. This review discusses various aspects of hyperglycemia, particularly the evidence supporting stricter control of this condition in patients undergoing cardiac surgery. Furthermore, based on the available data and recommendations, and our clinical experience, we suggest therapeutic strategies to improve the control of hyperglycemia in these patients.