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OBJECTIVE-To assess prospectively the effect of benchmarking on quality of primary care for patients with type 2 diabetes by using three major modifiable cardiovascular risk factors as critical quality indicators. RESEARCH DESIGN ANDMETHODS-Primary care physicians treating patients with type 2 diabetes in six European countries were randomized to give standard care (control group) or standard care with feedback benchmarked against other centers in each country (benchmarking group). In both groups, laboratory tests were performed every 4 months. The primary end point was the percentage of patients achieving preset targets of the critical quality indicators HbA1c, LDL cholesterol, and systolic blood pressure (SBP) after 12 months of follow-up. RESULTS-Of 4,027 patients enrolled, 3,996 patients were evaluable and 3,487 completed 12 months of follow-up. Primary end point of HbA1c target was achieved in the benchmarking group by 58.9 vs. 62.1% in the control group (P = 0.398) after 12 months; 40.0 vs. 30.1% patients met the SBP target (P < 0.001); 54.3 vs. 49.7% met the LDL cholesterol target (P = 0.006). Percentages of patients meeting all three targets increased during the study in both groups, with a statistically significant increase observed in the benchmarking group. The percentage of patients achieving all three targets at month 12 was significantly larger in the benchmarking group than in the control group (12.5 vs. 8.1%; P, 0.001). CONCLUSIONS-In this prospective, randomized, controlled study, benchmarking was shown to be an effective tool for increasing achievement of critical quality indicators and potentially reducing patient cardiovascular residual risk profile. [ABSTRACT FROM AUTHOR]

Presents information on a study which determined the distribution of plasma total homocysteine concentration in type 2 diabetes and its relationship to chronic complications and insulin resistance. Methodology; Results of the study; Conclusions.

Adequate comparisons of the relative performance of different tests of beta-cell function are not available. We compared discrimination of commonly used in vivo tests of beta-cell function across a range of glucose tolerance in seven subjects with normal glucose tolerance (NGT), eight subjects with impaired glucose tolerance (IGT), and nine subjects with type 2 diabetes. In random order, each subject underwent two of each of the following tests: 1) frequently sampled 0.3-g/kg intravenous glucose tolerance test (FSIVGTT) with MinMod analysis; 2) homeostasis model assessment (HOMA) from three samples at 5-min intervals with a model incorporating immunoreactive or specific insulin measurements; and 3) continuous infusion of 180 mg x min(-1) x m(-2) glucose with model assessment (CIGMA) of three samples at 50, 55, and 60 min (1-h CIGMA) and at 110, 115, and 120 min (2-h CIGMA). The discrimination of each test was assessed by the ratio of the within-subject SD to the underlying between-subject SD, the discriminant ratio (DR). The degree to which tests measured the same physiological variable was assessed using Pearson's correlation coefficient adjusted for attenuation due to test imprecision. An unbiased line of equivalence, taking into account the imprecision of both tests, was used to compare results. Beta-cell function assessed from HOMA and beta-cell function assessed from CIGMA (CIGMA%beta) (using immunoreactive insulin) had higher DRs than first-phase intravenous glucose tolerance test-derived incremental insulin peak, area, insulin-to-glucose index, and acute insulin response to glucose from FSIVGTT-MinMod. CIGMA%beta (immunoreactive insulin) had the highest DR. FSIVGTT-derived first-phase insulin response tests correlated only moderately with HOMA and CIGMA. Using specific rather than immunoreactive insulin for HOMA and CIGMA did not improve discriminatory power. Simple tests such as HOMA and CIGMA, using immunoreactive insulin, offer better beta-cell function discrimination across subjects with NGT, IGT, and type 2 diabetes than measurements derived from FSIVGTT first-phase insulin response. [ABSTRACT FROM AUTHOR]

Coronary artery disease (CAD) is a major cardiovascular (CV) complication in type 2 diabetes (T2DM) populations with metabolic syndrome (MS) phenotype, while T2DM is increasingly recognized as a major co-morbidity in CAD patients. It is not established whether those overlapping populations share a similar macrovascular phenotype. We therefore compared the clinical and biochemical characteristics of patients with both T2DM and CAD followed either in the cardiac or diabetes out/inpatient clinics. From a cohort of 385 patients with T2DM and CAD, we analyzed 314 patients followed in the cardiology clinic (CC) and compared this group to 71 patients followed in the diabetes clinic (DC) from the same university hospital. Data are expressed as means (1SD) or proportions (%). Age, sex, family CV history, blood pressure, smoking exposure and aspirin use were similar in both groups, as were BMI, abdominal circumference and MS (ATP III definition) prevalence. MS severity was lesser in CC, 38% of whom scored at the lowest (3/5) category vs. 18% in DC (p<0.05). The CC group was less often treated with statins/fibrates (44/13 vs. 63/40%), glitazones (2 vs. 10%) and insulin (20 vs. 60%), and more often with beta-blockers (74 vs. 61%) as compared to the DC group (all p<0.05). HbA1c and serum creatinine were higher in DC (8.0 vs. 7.4% and 1.38 vs. 1.12 mg/dL respectively; p<0.05). LDL-C was lower in DC (102 vs. 116 mg/dL), while triglycerides were higher (211 vs. 174 mg/dL; p<0.05). BNP [27 (45) vs. 16 (15)] and Big-ET-1 [9.3 (4.8) vs. 7.7 (2.9)] were higher in CC than in DC (p<0.05). Peripheral artery disease was more prevalent in DC as compared to CC (28 vs. 17%; p<0.05), as a result of a markedly higher stroke prevalence recorded in DC (24 vs. 8% in CC; p<0.001). Our results indicate that patients with both CAD and T2DM followed in the diabetes clinic have a markedly higher stroke prevalence than those followed in the cardiology clinic, despite similar conventional risk factors such as BMI, blood pressure, smoking exposure and family CV history. This unexpected and unreported divergence warrants further investigations regarding established and putative stroke determinants in these seemingly overlapping populations. [ABSTRACT FROM AUTHOR]

Nebivolol is a BP-lowering drug that combines β-blocking with vascular NO-release, ensuring peripheral vasodilation with lesser peripheral resistance. This unique dual action provides higher intra-class tolerability, making it a suitable choice for hypertensive subjects with type 2 diabetes (T2DM) as mono-or add-on therapy. No assessment is yet available on the potential impact of nebivolol's properties on Quality of Life (QoL), efficacy and tolerability in non-diabetic and in T2DM hypertensive subjects. The QoLaN Study included 1620 poorly-controlled hypertensive subjects (followed by 133 GPs) in whom nebivolol was introduced as monotherapy (n=587), add-on (n=460) or switch (n=421), or compared with a control group (n=152). The multicentre, prospective, open trial had a 2-month mean follow-up and this analysis of QoLaN compares 370 non-diabetic (NDH) and 90 T2DM (T2H) hypertensive subjects in whom nebivolol was introduced as add-on therapy, with graded questionnaire's assessment of QoL (at entry and after 2 months) related to modifiable items potentially affected by BP-lowering therapy. NDH and T2H had similar age (64 (12) years; mean (ISD)), age at hypertension diagnosis, sex ratio, systolo/diastolic BP values pre-nebivolol (NDH : 162/96 (16/8) vs. 162/95 (14/9) mm Hg in T2H) and post-nebivolol BP decrements (at 2-month : NDH: -23/-13 (16/8) vs. -25/-14 (15/9) mm Hg in T2H). Both in NDH and T2H groups, the following items were favorably-unfavorably rated (% of subjects at 2-month): headache: 39-10 (NDH) and 43-11 (T2H); fatigue: 59-6 (NDH) and 51-13 (T2H); coughing: 28-6 (NDH) and 11-9 (T2H); peripheral edema: 19-8 (NDH) and 30-11 (T2H); dyspnoea: 18-6 (NDH) and 9-11 (T2H); satisfaction with sexual life: 28-12 (NDH) and 33-19 (T2H); satisfaction with professional life: 30-15 (NDH) and 39-20 (T2H); and satisfaction with current BP therapy: 58-14 (NDH) and 47-15 (T2H). The QoLaN study demonstrates that adding nebivolol in GP practices to poorly-controlled hypertensive subjects brings about a marked improvement in BP values, both in non-diabetic and in T2DM subjects, alongside beneficial shifts in the ratings of a QoL questionnaire pertaining to modifiable items affected by BP-lowering therapy. [ABSTRACT FROM AUTHOR]

The aim of the study is (1) to determine the clinical phenotype of adolescent and adult patients with cystic fibrosis (CF), according to heterozygnsity or homozygosity for CFTR gene ΔF 508 mutation, and (2) to analyse their characteristics according to glucose tolerance status. Seventy-six CF patients with CFTR gene ΔF 508 mutation including 33 heterozygous and 43 homozygous individuals were studied. They were stratified according to normal (NGT, n = 51) or abnormal (AGH; prediabetes [IFG-IGT] or diabetes, n = 25) glucose homeostasis status. We measured using HOMA (Homeostasis Model Assessment) the β-cell function (HOMA-B) and insulin sensitivity (HOMA-S), allowing for defining a [BxS] product. Pancreatic exocrine insufficiency was inferred from requirements for oral pancreatic supplementation. Clinical effects of insulin therapy on weight and lung function were also recorded. An AGH was observed in 24 and 40% of heterozygous and homozygous subjects respectively. Patients with AGH were older than those with NGT (29 ± 10 vs. 23 ± 8 years, mean ± SD; p=8.006) and their B function was lower (93 ± 49 vs. 125 ± 51%, p=0.011). HOMA-S values were comparable in NGT and AGH individuals. A lower hyperbolic BxS product was observed in AGH, although non-significant when adjusted for error propagation. Pancreatic insufficiency was observed in 52 and 100% of ΔF 508 hetero- and homozygous patients respectively, (p=0.001). In subjects With AGH, HbA[sub 1C] was lowered from 7,3 ± 1,3 to 6,8 ± 1,2% after insulin therapy. This treatment also significantly improved nutritional status (p=0.030) and lung function (p=0.046). Prediabetes and diabetes represent frequent co-morbidities in young adults who carry the CFTR gene ΔF 508 mutation in the homozygous or heterozygous state. Impairment of insulin secretion, as shown by HOMA, is a hallmark of this condition, in the absence of common-type insulin resistance. Given the high prevalence of abnormal glucose tolerance, screening for (pre) diabetes is mandatory. Insulin supplementation in diabetic CFTR gene ΔF 508 subjects seems a rational therapy based on pathophysiological mechanism as well as on response to therapy. [ABSTRACT FROM AUTHOR]

The article discusses a study comparing adiposity, metabolic syndrome (MS) prevalence and insulin sensitivity in first generational Sub-Saharan Africa migrants with type 2 diabetes mellitus (T2DM) from Bantu extraction living in Belgium and white Caucasians with T2DM. The diastolic blood pressure of the Bantu group was higher than the Caucasians. White subjects showed higher MS and macroangiopathy prevalence. It concludes that Bantu diabetics have similar insulin resistance than the other group.

Adiponectin plasma levels are inversely correlated with insulin resistance and central fat, as well as with development of peripheral and coronary artery disease (CAD) and acute vascular complications. Transient ischemic attacks (TIA) and ischemic strokes are frequently observed in type 2 diabetes mellitus but the relationship between TIA, stroke and adiponectin levels are yet poorly documented in this condition. We analyzed 156 type 2 diabetes male patients (>90% white caucasians; age [mean (1SD)]: 64 (11) years) in whom overall TIA/stroke prevalence was 13% (TIA/stroke+; n=21; TIA/stroke-;' n=135). Mean age was 67 (10) in TIA/stroke+ vs. 63 (12) years in TIA/stroke- (NS). Each group was compared with respect to clinico-biochemical phenotype, plasma adiponectin levels, fat mass and vasoactive Nt-pro-atrial and brain natriuretic peptides (Nt-proANP and Nt-proBNP). Data are listed in the Table and expressed as means (1SD) or proportions. Our results clearly demonstrate that TIA/stroke prevalence is associated not only with systolic blood pressure (BP) and homocysteine levels, but also with elevated vasoactive peptides Nt-proANP and Nt-proBNP. On the other hand, the higher fat mass observed in patients with TIA/stroke was associated with paradoxically higher plasma adiponectin, suggesting a lack (or loss) of association between adiponectin, fat mass and stroke prevalence in white caucasian males with type 2 diabetes mellitus. [ABSTRACT FROM AUTHOR]

Objective: We sought to determine the clinical phenotype of adolescent/adult patients with cystic fibrosis, according to heterozygosity or homozygosity for cystic fibrosis transmembrane regulator (CFTR) deltaF508 mutation, and to analyze their characteristics according to glucose tolerance status., Research Design and Methods: A total of 76 cystic fibrosis patients with CFTR deltaF508 mutation (33 heterozygous and 43 homozygous) stratified according to normal glucose tolerance (NGT) (n = 51) or abnormal glucose homeostasis (AGH) (impaired fasting glucose, impaired glucose tolerance, or diabetes; n = 25) had their homeostasis model assessment (HOMA) of beta-cell function and of insulin sensitivity and hyperbolic product (beta-cell function x insulin sensitivity [B x S]) measured. Pancreatic exocrine insufficiency was inferred from pancreatine requirements. Clinical effects of insulin therapy on weight and lung function were recorded., Results: AGH was observed in 24 and 40% of heterozygous and homozygous subjects, respectively. AGH patients were older than NGT patients (mean +/- SD age 29 +/- 10 vs. 23 +/- 8 years, P = 0.006), and their beta-cell function was lower (93 +/- 49 vs. 125 +/- 51%, P = 0.011). Insulin sensitivity values were comparable in NGT and AGH patients. A lower B x S product was observed in AGH, although it was nonsignificant when adjusted for error propagation. Pancreatic insufficiency was observed in 52 and 100% of heterozygous and homozygous patients (P = 0.001)., Conclusions: Pre-diabetes and diabetes represent frequent comorbidities in CFTR deltaF508 mutation in the homozygous or heterozygous states. Impairment of insulin secretion, as shown by HOMA, is an important determinant when compared with the magnitude of compensation from insulin sensitivity. Given the high prevalence of abnormal glucose tolerance, screening for (pre-)diabetes is mandatory. Insulin supplementation in diabetic subjects with CFTR deltaF508 mutation seems a rational therapy for consideration, although this does not preclude that therapy directed toward insulin resistance could also interact.