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Objective: To compare outcomes in patients with type 2 diabetes initiating insulin lispro mix 75/25 (75% insulin lispro protamine suspension and 25% lispro) or insulin glargine therapy, stratified by baseline oral antihyperglycemic agent (OHA) use., Methods: We performed a post hoc analysis of 6-month data from the DURABLE clinical trial, which enrolled patients with hemoglobin A1c (A1C) levels >7.0% treated with 2 or more OHAs (metformin, sulfonylurea, and thiazolidinedione), and randomly assigned them to treatment with twice-daily insulin lispro 75/25 or once-daily glargine., Results: In both insulin treatment groups, metformin/thiazolidinedione-treated patients had significantly greater improvement in A1C levels (-2.19% to -2.36%), lower end point A1C values, and lower rates of occurrence of hypoglycemia in comparison with metformin/sulfonylurea-treated patients (all P<.05). Patients treated with sulfonylurea/thiazolidinedione or metformin/sulfonylurea/thiazolidinedione did not differ significantly from metformin/sulfonylurea-treated patients in A1C change (-1.56% to -1.84%) or rates of occurrence of hypoglycemia., Conclusion: In these post hoc analyses, patients with type 2 diabetes initiating premixed or basal insulin therapy and treated concomitantly with the OHA combination of metformin/thiazolidinedione at baseline demonstrated significantly greater A1C improvement with less hypoglycemia in comparison with patients treated with metformin/sulfonylurea.

Background: diabetes and CHF are common comorbidities in hospitalized patients but the relationship between glycaemic control, glycaemic variability, and mortality in patients with both conditions is unclear., Methods: we used administrative data to retrospectively identify patients with a diagnosis of CHF who underwent frequent glucose assessments. TWMG was compared with other measures of glycaemic control and a time-weighted measure of glycaemic variability, the glycaemic lability index. The outcome was hospital mortality., Results: a total of 748 patients were included in the final analysis. Time-weighted mean glucose was higher than unadjusted mean glucose (137 + /- 44.7 mg/dL versus 167 + /- 54.9, p < 0.001), due in part to shorter sampling intervals at higher glucose levels. Hypoglycaemia, defined as a glucose level < 70 mg/dL, occurred during 6.3% of patient-days in survivors and 8.4% of patient-days among nonsurvivors (p = 0.05). Time-weighted mean glucose was similar (128 + /- 33.1 mg/dL versus 138 + /- 45.1 mg/dL) in nonsurvivors versus survivors, p = 0.19). However, relatively few patients had were significantly elevated readings. Median GLI was higher in nonsurvivors compared with that in survivors (18.1 versus 6.82, p = 0.0003). Increasing glycaemic lability index (odds ratio 1.32, 95% confidence interval 1.05-1.65), and hypoglycaemia (odds ratio 2.21, 95% confidence interval 1.07-4.65), were independently associated with higher mortality in logistic regression analysis. Respiratory failure was associated with mortality, but not standard deviation of glucose., Conclusions: future studies analysing glycaemic control should control for variable sampling intervals. In this analysis, glycaemic lability index was independently associated with increased mortality, independent of hypoglycaemia. Prospective studies are needed to evaluate these findings., (2010 John Wiley & Sons, Ltd.)

Objective: To determine the relationship between inpatient glycemic control and hospital readmission in patients with congestive heart failure (CHF)., Methods: We used an electronic data collection tool to identify patients with a discharge diagnosis of CHF who underwent point-of-care glucose assessments. Timeweighted mean glucose (TWMG), hemoglobin A1c, and glycemic lability index (GLI) served as glycemic indicators, and readmission for CHF was determined at 30 days and between 30 and 90 days., Results: The analysis included 748 patients. After adjustment for significant covariates, log-transformed increasing TWMG (odds ratio 3.3; P = .03) and log-transformed hemoglobin A1c (odds ratio 5.5; P = .04) were independently associated with higher readmission for CHF between 30 and 90 days, but not by 30 days. Renal disease, African American race, and year of hospital admission were also significantly associated with readmission, but GLI was not. There was no significant difference in TWMG when analyzed on the basis of race or renal status. We noted a decrease in TWMG (P = .004) and a trend for reduction in readmission rates between 30 and 90 days (P = .06) after hospital-wide interventions were implemented to improve glycemic control, but no significant difference was detected in GLI or hypoglycemia., Conclusion: Increasing glucose exposure, but not glycemic variability, was associated with higher risk of readmission between 30 and 90 days in patients with CHF. Prospective studies are needed to confirm or refute these results.

Results of randomised controlled trials of tight glycaemic control in hospital inpatients might vary with population and disease state. Individualised therapy for different hospital inpatient populations and identification of patients at risk of hyperglycaemia might be needed. One risk factor that has received much attention is the presence of pre-existing diabetes. So-called stress hyperglycaemia is usually defined as hyperglycaemia resolving spontaneously after dissipation of acute illness. The term generally refers to patients without known diabetes, although patients with diabetes might also develop stress hyperglycaemia-a fact overlooked in many studies comparing hospital inpatients with or without diabetes. Investigators of several studies have suggested that patients with stress hyperglycaemia are at higher risk of adverse consequences than are those with pre-existing diabetes. We describe classification of stress hyperglycaemia, mechanisms of harm, and management strategies.

Content: Recent studies have reported hemoglobin A(1c) (A1c) differences across racial/ethnic groups. Our diverse population allows for further investigation of potential differences in measurements of glycemia., Objectives: Our objectives were to describe and explore baseline racial/ethnic differences in self-monitored plasma glucose profiles, A1c, and 1,5-anhydroglucitol (1,5-AG) in patients with type 2 diabetes enrolled in the Assessing DURAbility of Basal vs. Lispro Mix 75/25 Insulin Efficacy trial., Design, Setting, Patients: The trial enrolled 2094 patients with type 2 diabetes, ages 30-80 yr, from 11 countries., Main Outcome Measures: Estimated mean plasma glucose (MPG), A1c, and 1,5-AG were compared among racial/ethnic groups before and after adjusting for factors affecting glycemia: age, sex, duration of diabetes, body mass index, and MPG., Results: Baseline estimated MPG +/- sd was 220.0 +/- 82.0 mg/dl, mean A1c was 9.0 +/- 1.3%, and 1,5-AG was 5.0 +/- 4.1microg/ml. Estimated MPG did not differ between Caucasian and non-Caucasian groups. A1c was higher in Hispanics (9.4 +/- 1.4%; P < 0.001), Asians (9.2 +/- 1.4%; P < 0.01), and patients of other racial/ethnic groups (9.7 +/- 1.5%; P < 0.001) compared with Caucasians (8.9 +/- 1.2%). Paradoxically, 1,5-AG was higher for Asian (5.7 +/- 4.6 microg/ml) and African patients (6.2 +/- 5.4 microg/ml) vs. Caucasians (4.9 +/- 3.9 microg/ml) (P < 0.01). After adjusting for factors affecting glycemia, A1c was higher (all P

1,5-anhydroglucitol (1,5-AG) is a validated marker of short-term glycemic control. It is a metabolically inert polyol that competes with glucose for reabsorption in the kidneys. Otherwise stable levels of 1,5-AG are rapidly depleted as blood glucose levels exceed the renal threshold for glucosuria. 1,5-AG more accurately predicts rapid changes in glycemia than hemoglobin A1C (A1C) or fructosamine. It is also more tightly associated with glucose fluctuations and postprandial glucose. Thus, 1,5-AG may offer complementary information to A1C. This review will summarize the limitations of current methods of assessing glycemic control, assess the data to support 1,5-AG as a glycemic marker and highlight the scenarios by which 1,5-AG may fill the gap in assessing glycemic control.

Objective: Postprandial hyperglycemia is often inadequately assessed in diabetes management. Serum 1,5-anhydroglucitol (1,5-AG) drops as serum glucose rises above the renal threshold for glucose and has been proposed as a marker for postprandial hyperglycemia. The objective of this study is to demonstrate the relationship between 1,5-AG and postprandial hyperglycemia, as assessed by the continuous glucose monitoring system (CGMS) in suboptimally controlled patients with diabetes., Research Design and Methods: Patients with type 1 or type 2 diabetes and an HbA(1c) (A1C) between 6.5 and 8% with stable glycemic control were recruited from two sites. A CGMS monitor was worn for two consecutive 72-h periods. Mean glucose, mean postmeal maximum glucose (MPMG), and area under the curve for glucose above 180 mg/dl (AUC-180), were compared with 1,5-AG, fructosamine (FA), and A1C at baseline, day 4, and day 7., Results: 1,5-AG varied considerably between patients (6.5 +/- 3.2 mug/ml [means +/- SD]) despite similar A1C (7.3 +/- 0.5%). Mean 1,5-AG (r = -0.45, P = 0.006) correlated with AUC-180 more robustly than A1C (r = 0.33, P = 0.057) or FA (r = 0.38, P = 0.88). MPMG correlated more strongly with 1,5-AG (r = -0.54, P = 0.004) than with A1C (r = 0.40, P = 0.03) or FA (r = 0.32, P = 0.07)., Conclusions: 1,5-AG reflects glycemic excursions, often in the postprandial state, more robustly than A1C or FA. 1,5-AG may be useful as a complementary marker to A1C to assess glycemic control in moderately controlled patients with diabetes.

Fibroblast growth factors (FGFs) have been previously implicated in urodele limb regeneration. Here, we examined expression of FGF-1 by blastema cells and neurons and investigated its involvement in wound epithelial formation and function and in the trophic effect of nerves. Neurons innervating the limb and blastema cells in vivo and in vitro expressed the FGF-1 gene. The peptide was present in blastemas in vivo. Wound epithelium thickened when recombinant newt FGF-1 was provided on heparin-coated beads, demonstrating that the FGF-1 was biologically active and that the wound epithelium is a possible target tissue of FGF. FGF-1 did not stimulate accessory limb formation. FGF-1 was as effective as 10% fetal bovine serum in maintaining proliferative activity of blastema cells in vitro but was unable to maintain growth of denervated, nerve-dependent stage blastemas when provided on beads or by injection. FGF-1 had a strong stimulating effect on blastema cell accumulation and proliferation of limbs inserted into the body cavity that were devoid of an apical epithelial cap (AEC). These results show that FGF-1 can signal wound epithelium cap formation and/or function and can stimulate mesenchyme accumulation/proliferation in the absence of the AEC but that FGF-1 is not directly involved in the neural effect on blastema growth., (Copyright 2002 Wiley-Liss, Inc.)