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Objective We compared the pain accompanying the injection of high-concentration (300 units/mL) insulin glargine (U300G) with that accompanying the injection of conventional (100 units/mL) insulin glargine (U100G). Methods U100G was switched to U300G at basically the same dosage. Visual analog scales were used to assess the quality of life (QOL). The primary outcome was the change in the pain accompanying injections in those using ≥30 units of U100G compared with those using <30 units at baseline. Standardized mean differences (Cohen's d) were used to measure the effect size. Patients Adult patients with type 2 diabetes mellitus using U100G. Results One hundred and eight patients were recruited. The numbers of patients who used U100G at ≥30 units, 20 to <30 units, 10 to <20 units, and <10 units were 13, 14, 34, and 47, respectively. The improvement in the pain score was not significant for ≥30 units compared with <30 units (-50.3±24.0 vs. -40.4±28.5, p=0.25, d=0.38), but a significant difference was observed for ≥20 units compared with <20 units (-50.8±22.7 vs. -38.4±29.1, p=0.03, d=0.48), as well as for ≥10 units compared with <10 units (-48.1±25.0 vs. -33.0±29.7, p<0.01, d=0.56). When all patients were analyzed together, significant improvements in the pain score (-41.5±28.0, p<0.01), ease of use score (-37.5±32.2, p<0.01), force needed to inject score (-46.5±28.6, p<0.01), and preference for U300G compared with U100G score (-45.8±33.1, p<0.01) were observed. Conclusion There is possibility that switching from U100G to U300G might be associated with better QOL for patients who require insulin glargine injections. To prove this hypothesis, a randomized controlled trial (preferably double-blinded) will be required in the future.

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UNLABELLED: Aims/Introduction: The aim of the present study was to evaluate the efficacy of replacing neutral protamine Hagedorn insulin (NPH) with the long-acting insulin analogue, detemir, in clinical practice. MATERIALS AND METHODS: We carried out a retrospective study to compare the effects of replacing NPH with detemir in basal-bolus insulin therapy in Japanese patients with type 1 diabetes. A total of 19 patients were enrolled in the study, and changes in hemoglobin A1c (HbA1c), insulin dose, bodyweight, fasting blood glucose levels (FBG), within-patient variability in FBG and prevalence in hypoglycemia were monitored for 12 weeks before replacement and during three periods after replacement; 1-12 weeks (period 1), 13-24 weeks (period 2) and 25-36 weeks (period 3). RESULTS: HbA1c values improved significantly in periods 2 and 3. Despite the total insulin dose remaining unchanged throughout the study, the basal insulin dose increased from 0.24 to 0.27 IU/kg/day in period 2 and 0.28 IU/kg/day in period 3. Bodyweight decreased from 61.8 to 60.8 kg in period 1, whereas FBG improved throughout the study. Within-patient variability in FBG was lower with detemir treatment than with NPH, despite the number of hypoglycemic episodes increasing significantly after replacement. CONCLUSIONS: These findings show that the weight loss observed in patients was independent of the reduction in calorie intake resulting from less frequent hypoglycemic attacks. In Japanese patients with diabetes who received NPH, replacing NPH with detemir led to improvements in glycemic control without any weight gain. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2010.00066.x, 2010).

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The aim of this study was to evaluate relationships between serum estradiol concentration and carotid atherosclerosis in addition to major cardiovascular risk factors in men with type 2 diabetes mellitus because previous reports concerning the role of estrogen on atherosclerosis in men are conflicting. Serum estradiol concentrations were measured in 305 consecutive men with type 2 diabetes mellitus. Relationships were evaluated between serum estradiol concentration and carotid atherosclerosis, as determined by ultrasonographically evaluated intima-media thickness (IMT) and plaque score, in a subgroup of 144 diabetic patients, as well as major cardiovascular risk factors, including age, blood pressure, and lipid concentrations. An inverse correlation was found between serum estradiol concentration and IMT (r = -0.174, P = .0369), but no correlation was found between serum estradiol concentration and plaque score. Patients with serum estradiol concentrations in the lowest tertile displayed significantly higher IMT compared with patients in the highest tertile (P = .0083). Serum estradiol concentration was not a determinant of IMT (beta = -.121, P = .1396) in the multiple regression analysis. An inverse correlation was found between serum estradiol concentration and triglyceride concentration (r = -0.136, P = .0186). In conclusion, serum estradiol concentration is inversely associated with carotid atherosclerosis as determined by ultrasonographically evaluated IMT in men with type 2 diabetes mellitus.

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A case of hypereosinophilic syndrome (HES) with a rare complication of Buerger's disease-like large arterial occlusion (AO) was successfully treated with emergent percutaneous transluminal angioplasty and anticoagulants plus corticosteroid. By reviewing 15 reported cases of HES with AO including the present case, we found man predominance but no other consistent characteristics in HES with AO, such as age, smoking history, eosinophil counts or previous treatments, thus, predicting AO in HES patients appears to be difficult. Vessel intervention should be considered as a treatment option, since treatment delay in some patients has resulted in the amputation of extremities.

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Advanced diabetic nephropathy is characterized by abnormal synthesis of extracellular matrix (ECM) proteins, such as collagen I (COL I). The present experiments were designed to test the hypothesis that the presence of abnormal ECM proteins may be responsible for increased generation of reactive oxygen species (ROS) that are thought to have an important role in the pathogenesis of diabetic nephropathy. SV40 MES 13 murine mesangial cells were plated on COL I or collagen IV (COL IV) for 3 h at 5.5 or 25 mM D-glucose concentration. Increased intracellular ROS generation and reduced intracellular nitric oxide (NO) production was measured in cells attached to COL I compared with cells attached to COL IV. Treatment with N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME), an inhibitor of NO synthase, reduced this difference in ROS generation between cells attached to either COL I or IV. The results using antibodies against integrins also indicated that an alpha(2) integrin-mediated pathway was involved in the different response in ROS generation caused by ECM proteins. These results suggest that contact between altered ECM proteins that are present in advanced diabetic nephropathy and mesangial cells has the potential to increase intracellular oxidative stress, leading to progressive glomerular damage.

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We recently found that serum dehydroepiandrosterone sulfate (DHEA-S) concentration correlated inversely with the degree of urinary albumin excretion in a cross-sectional study. We therefore performed an observational study to investigate the relationship between serum DHEA-S concentrations and changes in urinary albumin excretion in male patients with type 2 diabetes to answer the question as to whether DHEA is a causal rather than simply coincidental intermediate linking urinary albumin excretion to cardiovascular disease (CVD). The relationship between serum DHEA-S concentration and changes in urinary albumin excretion was investigated in 207 consecutive male patients with type 2 diabetes. Baseline serum DHEA-S concentration and urinary albumin excretion were measured in 2003. After 12 months, urinary albumin excretion was measured and any changes in urinary albumin excretion were calculated. Patients were divided into tertiles according to DHEA-S concentration. Greater changes in urinary albumin excretion were seen in patients with low DHEA-S concentration (29.6+/-7.6mg/g creatinine) than in patients with high DHEA-S concentration (5.1+/-3.6mg/g creatinine, P=0.0091). An inverse correlation was observed between serum DHEA-S concentration and changes in urinary albumin excretion (r=-0.193, P=0.0052). Multiple regression analysis demonstrated that HbA1c (beta=0.241, P=0.0009), and serum DHEA-S concentration (beta=-0.195, P=0.0054) were independent determinants of changes in urinary albumin excretion. In conclusion, serum DHEA-S concentration was inversely correlated with changes in urinary albumin excretion, which may indicate causality in the increased CVD mortality in male patients with type 2 diabetes and low DHEA-S concentration.

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Macrovascular disease is the most common cause of morbidity and mortality in diabetic patients. With the increasing numbers of patients with type 2 diabetes, a simple, noninvasive method is needed to detect atherosclerosis. Augmentation represents the difference between the second and first peaks of the central arterial pressure waveform in systole and is a measure of systemic arterial stiffness, which causes the pressure wave to rebound. We investigated whether augmentation could serve as a marker of atherosclerosis in patients with type 2 diabetes. Central arterial pressure and degree of its augmentation by pulse wave rebound were measured sphygmographically in 208 consecutive patients with type 2 diabetes and 117 healthy control subjects. The relationship between augmentation and carotid atherosclerosis detected by carotid ultrasonography was investigated in a subgroup of 81 diabetic patients. Augmentation was greater in diabetic patients than control subjects (13.2+/-6.9 vs. 9.4+/-5.7 mm Hg, P<0.0001). The positive correlation between augmentation and intima-media thickness (r=0.309, P=0.0051) and between augmentation and plaque score (r=0.304, P=0.0059) were found in patients with type 2 diabetes. Augmentation was greater in diabetic patients with cardiovascular disease (n=47) than without (n=161; 15.1+/-8.4 vs. 12.6+/-6.3 mm Hg, P=0.031). Augmentation of central arterial pressure is a reliable marker for atherosclerosis in patients with type 2 diabetes. This simple, noninvasive determination would permit large-scale, early screening for atherosclerosis in patients with type 2 diabetes, who are at increased risk for cardiovascular disease.

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BACKGROUND/AIMS: Glomerular infiltration with monocytes/macrophages has been implicated in the pathogenesis of diabetic nephropathy. In this study, we evaluated the relationship between the genetic polymorphism in leukocyte-endothelial adhesion molecule-1 (LECAM-1) and diabetic nephropathy in patients with type 2 diabetes mellitus. METHODS: We determined the frequency of the LECAM-1 P213S genotype in 102 diabetic patients with diabetic nephropathy, 90 diabetic patients with no evidence of diabetic nephropathy, and 200 healthy control individuals. RESULTS: The frequency of the LECAM-1 213PP genotype and P allele in patients with diabetic nephropathy was significantly higher than that in patients without nephropathy (genotype 68% vs. 53%, chi(2)=6.78, P=.034; allele 83% vs. 72%, chi(2)=6.26, P=.012). The LECAM-1 P213 genotype was associated with a 1.86-fold increased risk for nephropathy independently of other risk factors. CONCLUSION: The data suggest that the LECAM-1 213PP genotype is a genetic risk factor for the development of nephropathy in type 2 diabetes mellitus.

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