Abstract:Objective: This study was designed to evaluate the association between skin autofluorescence (AF), an indicator of advanced glycation end-products (AGEs), and foot ulcers in subjects with diabetes. Methods: In this study, 195 Chinese diabetic subjects were examined. Their feet were examined regardless of whether an ulcer was present or not. Skin AF was measured with an AGE reader. Demographic characteristics and blood data were recorded. Results: The mean values of skin AF were 2.29±0.47 for subjects without foot ulcers, and 2.80±0.69 for those with foot ulcers, a significant difference (P<0.05). Skin AF was strongly correlated with age and duration of diabetes. After adjusting for these factors, multivariate logistic regression showed that skin AF was independently associated with foot ulcerations. Conclusions: Skin AF is independently associated with diabetic foot ulcerations. It might be a useful screening method for foot ulceration risk of diabetic patients.

We aimed to determine the relationship between lower extremity peripheral arterial disease (PAD), 10-year coronary heart disease (CHD), and stroke risks in patients with type 2 diabetes (T2DM) using the UKPDS risk engine. We enrolled 1178 hospitalized T2DM patients. The patients were divided into a lower extremity PAD group (ankle-brachial index ≤ 0.9 or >1.4; 88 patients, 7.5%) and a non-PAD group (ankle-brachial index > 0.9 and ≤1.4; 1090 patients, 92.5%). Age; duration of diabetes; systolic blood pressure; the hypertension rate; the use of hypertension drugs, ACEI /ARB, statins; CHD risk; fatal CHD risk; stroke risk; and fatal stroke risk were significantly higher in the PAD group than in the non-PAD group (P < 0.05 for all). Logistic stepwise regression analysis indicated that ABI was an independent predictor of 10-year CHD and stroke risks in T2DM patients. Compared with those in the T2DM non-PAD group, the odds ratios (ORs) for CHD and stroke risk were 3.6 (95% confidence interval (CI), 2.2–6.0; P < 0.001) and 6.9 (95% CI, 4.0–11.8; P < 0.001) in those with lower extremity PAD, respectively. In conclusion, lower extremity PAD increased coronary heart disease and stroke risks in T2DM.

BackgroundThe effects of brain natriuretic peptide (BNP) on the risk of cardiovascular disease and atherosclerosis have been studied. However, little information is available regarding peripheral arterial disease (PAD), particularly among subjects with type-2 diabetes mellitus (T2DM). The aim of our study was to assess the potential relationship between BNP levels and PAD among T2DM patients.MethodsThe study cohort was 507 T2DM outpatients in which BNP levels were measured. Cross-sectional associations between BNP levels (in tertiles) and PAD were examined.ResultsCompared withT2DM patients without PAD, BNP levels were markedly higher in patients with PAD (p = 0.001). Correlation analyses showed that the BNP level was negatively correlated with the ankle–brachial index (r = −0.453, p = 0.033). At a cutoff value of 78.2 pg/ml, the BNP level showed a sensitivity of 71.9%, a specificity of 68.1%, and a positive predictive value of 84.3% for a diagnosis of PAD. The area under the receiver-operating characteristic curve increased significantly if BNP levels were incorporated into a predictive model of the potential risk factors for PAD (0.85 vs 0.81, p = 0.029).ConclusionsBNP is a potential and promising biomarker for PAD screening in T2DM patients.

PRIMARY ALDOSTERONISM (PA) is characterized by overproduction of the mineralocorticoid hormone aldosterone by adrenal glands. According to recent reports, it appears to be the most common cause of secondary persistent hypertension, and may account for about 8~13% of unselected hypertensives [1] and as high as 20% of resistant hypertensives [2,3]. The inappropriately high production of aldosterone causes suppression of plasma renin, sodium retention, hypertension, cardiovascular damage, and potassium excretion [4]. Elevated blood pressure combined with the proinflammatory and profibrotic effects of aldosterone To date, although the genetic basis of familial hyperaldosteronism has been more clearly, the exact pathogenesis of sporadic forms of the disease remains unknown. Among a number of studied susceptibility genes, the aldosterone synthase gene (CYP11B2) is the most commonly studied. The CYP11B2 gene situates on chromosome 8q24.3 and encodes aldosterone synthase, which is the key rate-limiting enzyme for the final stage of aldosterone synthesis pathway and pri- Original