Difference in sarcopenia prevalence and associated factors according to 2010 and 2018 European consensus (EWGSOP) in elderly patients with type 2 diabetes mellitus.

OBJECTIVES: The aim of this study was to establish the prevalence of sarcopenia and associated factors in elderly patients with type 2 diabetes mellitus (DM) according to 2010 (EWGSOP1) and 2018 (EWGSOP2) European consensus. DESIGN: Cross-sectional study. PARTICIPANTS: Elderly outpatients ≥60 years with type 2 DM and able to walk were recruited at the DM ambulatory care center of a public hospital in Porto Alegre from 2017 to 2018. MATERIALS AND METHODS: The diagnosis of sarcopenia was performed according to EWGSOP1 and EWGSOP2. Muscle mass (MM) was assessed using bioelectrical impedance (BIA). Muscle strength (MS) was assessed using the handgrip strength (HS) test and physical performance (PP) by timed-up-and-go (TUG) test. RESULTS: We included 242 patients with 68.3 ± 5.6 years, 54% women, 78% white, DM duration 14(8-22) years, BMI 29.5 ± 4.5 kg/m2, and HbA1c 7.8 ± 1.5%. Overall prevalence of sarcopenia was 21%. In EWGSOP1 it was 16.9%. The GLM Poisson model was used to assess sarcopenia. Male sex increased the prevalence of sarcopenia by 33% (3.330 [1.747-6.350]; p < .001), and walking >5401 steps/day had a protective effect of 70% for the prevalence of sarcopenia (0.306 [0.127-0.739]; p = .029). Finally, age had an impact of 6% on prevalence of sarcopenia (1.06 [1.015-1.108]; p = .009) according to EWGSOP1. On the other hand, the prevalence was 7%, women had more sarcopenia (88%), and BMI was lower in the sarcopenic group when defined according to EWGSOP2. CONCLUSIONS: The prevalence of sarcopenia was more than double when comparing EWGSOP1 (16.9%) and EWGSOP2 (7%). We believe that the difference in prevalence is due to modifications in MM and MS criteria. According to EWGSOP1, walking may have protective role in the prevalence of sarcopenia in elderly type 2 DM individuals.

Effect of dietary lipids on circulating adiponectin: a systematic review with meta-analysis of randomised controlled trials.

Different dietary interventions have been identified as potential modifiers of adiponectin concentrations, and they may be influenced by lipid intake. We identified studies investigating the effect of dietary lipids (type/amount) on adiponectin concentrations in a systematic review with meta-analysis. A literature search was conducted until July 2013 using databases such as Medline, Embase and Scopus (MeSH terms: 'adiponectin', 'dietary lipid', 'randomized controlled trials (RCT)'). Inclusion criteria were RCT in adults analysing adiponectin concentrations with modification of dietary lipids. Among the 4930 studies retrieved, fifty-three fulfilled the inclusion criteria and were grouped as follows: (1) total dietary lipid intake; (2) dietary/supplementary n-3 PUFA; (3) conjugated linoleic acid (CLA) supplementation; (4) other dietary lipid interventions. Diets with a low fat content in comparison to diets with a high-fat content were not associated with positive changes in adiponectin concentrations (twelve studies; pooled estimate of the difference in means: -0·04 (95% CI -0·82, 0·74) µg/ml). A modest increase in adiponectin concentrations with n-3 PUFA supplementation was observed (thirteen studies; 0·27 (95% CI 0·07, 0·47) µg/ml). Publication bias was found by using Egger's test (P= 0·01) and funnel plot asymmetry. In contrast, CLA supplementation reduced the circulating concentrations of adiponectin compared with unsaturated fat supplementation (seven studies; -0·74 (95% CI -1·38, -0·10) µg/ml). However, important sources of heterogeneity were found as revealed by the meta-regression analyses of both n-3 PUFA and CLA supplementation. Results of new RCT would be necessary to confirm these findings.

Endothelial dysfunction and serum fatty acid composition in patients with type 2 diabetes mellitus.

The aim of this study was to evaluate the possible association between serum fatty acids composition and endothelial dysfunction in patients with type 2 diabetes mellitus. A cross-sectional study was conducted with 125 normo- or microalbuminuric type 2 diabetes mellitus patients with serum creatinine <1.5 mg/dL. Serum fatty acids composition (gas chromatography), serum levels of endothelin-1 (ET-1) (enzyme-linked immunosorbent assay), fibrinogen, serum C-reactive protein, lipids, homeostasis model assessment resistance index (HOMA-R), and 24-hour urinary albumin excretion rate were measured. Serum levels of ET-1 were positively correlated with saturated fatty acids (r = 0.257, P = .025) and negatively correlated with polyunsaturated fatty acids (PUFAs) (r = -0.319, P = .005). Serum ET-1 levels were also positively correlated with systolic blood pressure, waist circumference, total cholesterol levels, triglycerides, and HOMA-R. In multiple linear regression models, only saturated fatty acids (R(2) = 0.317, P = .002) or PUFAs (R(2) = 0.314, P = .001) remained associated with ET-1 levels. Models were adjusted for systolic blood pressure, HOMA-R, waist circumference, triglycerides, body mass index, and smoking habit. The serum total PUFA levels showed an inverse correlation with urinary albumin excretion rate (r = -0.248, P = .012). In conclusion, in type 2 diabetes mellitus patients, the serum fatty acids composition was independently related to endothelial function evaluated by serum ET-1. Saturated fatty acids were associated with endothelial dysfunction (high levels of ET-1), whereas PUFAs had a protective role in endothelial function.

Parenteral nutrition as a risk factor for central venous catheter-related infection.

BACKGROUND: The role of parenteral nutrition (PN) therapy as an independent risk factor for central venous catheter (CVC)-related infection in nonselected adult patients is not well established. The aim of this study was to evaluate PN as a risk factor for central venous catheter-related infection in nonselected adult patients in a general university hospital. METHODS: Patients using central venous catheters, exposed or nonexposed to PN, were prospectively followed for development of central venous catheter-related infection. RESULTS: One hundred fifty-three patients were studied; 28 developed central venous catheter-related infection. Patients with central venous catheter-related infection presented higher frequency of PN use than patients without infection (60.7 vs 34.4%; p = .010). Multivariate Cox analysis showed that PN (relative risk (RR) = 3.30; 95% confidence interval [CI], 1.30-8.34; p = .012) was the only risk factor for central venous catheter-related infection. Malnutrition (RR = 0.45; 95% CI, 0.15-1.34; p = .152), days of hospitalization before central venous catheter insertion (RR = 1.00; 95% CI, 0.98-1.02; p = .801), and sustained hyperglycemia (RR = 0.49; 95% CI, 0.98-1.21; p = .091) were not significant in the model. Multiple logistic regression revealed that mal-nutrition (odds ratio [OR] = 8.05; 95% CI, 1.85-35.03; p = .005), central venous catheter indication for surgical-related pathology (OR = 7.26; 95% CI, 2.51-21.04; p < .001), sustained hyperglycemia (OR = 4.34; 95% CI, 1.79-10.52; p = .001), and days of hospitalization before central venous catheter insertion (OR = 1.04; 95% CI, 1.01-1.07; p = .004) were associated with PN use after adjustment for Assessment Score Intervention System score (OR = 0.33; 95% CI, 0.14-0.80; p = .014). CONCLUSIONS: PN therapy is an independent risk factor for central venous catheter-related infection in nonselected hospitalized adult patients.

Diabetic nephropathy: diagnosis, prevention, and treatment.

Diabetic nephropathy is the leading cause of kidney disease in patients starting renal replacement therapy and affects approximately 40% of type 1 and type 2 diabetic patients. It increases the risk of death, mainly from cardiovascular causes, and is defined by increased urinary albumin excretion (UAE) in the absence of other renal diseases. Diabetic nephropathy is categorized into stages: microalbuminuria (UAE >20 microg/min and < or =199 microg/min) and macroalbuminuria (UAE > or =200 microg/min). Hyperglycemia, increased blood pressure levels, and genetic predisposition are the main risk factors for the development of diabetic nephropathy. Elevated serum lipids, smoking habits, and the amount and origin of dietary protein also seem to play a role as risk factors. Screening for microalbuminuria should be performed yearly, starting 5 years after diagnosis in type 1 diabetes or earlier in the presence of puberty or poor metabolic control. In patients with type 2 diabetes, screening should be performed at diagnosis and yearly thereafter. Patients with micro- and macroalbuminuria should undergo an evaluation regarding the presence of comorbid associations, especially retinopathy and macrovascular disease. Achieving the best metabolic control (A1c <7%), treating hypertension (<130/80 mmHg or <125/75 mmHg if proteinuria >1.0 g/24 h and increased serum creatinine), using drugs with blockade effect on the renin-angiotensin-aldosterone system, and treating dyslipidemia (LDL cholesterol <100 mg/dl) are effective strategies for preventing the development of microalbuminuria, in delaying the progression to more advanced stages of nephropathy and in reducing cardiovascular mortality in patients with type 1 and type 2 diabetes.

ACE and PC-1 gene polymorphisms in normoalbuminuric Type 1 diabetic patients: a 10-year prospective study.

The aim of this study was to analyze the role of ACE gene insertion/deletion (I/D) and PC-1 gene K121Q polymorphisms in the changes of glomerular filtration rate (GFR), urinary albumin excretion rate (UAER), and blood pressure (BP) levels in a cohort of normoalbuminuric Type 1 diabetic patients. This is a 10.2+/-2.0-year prospective study of 30 normotensive normoalbuminuric Type 1 diabetic patients. UAER (immunoturbidimetry), GFR ((51)Cr-EDTA single injection technique), GHb (ion exchange chromatography), and BP levels were measured at baseline and at 1.7+/-0.6-year intervals. The presence of ACE gene I/D and PC-1 gene K121Q polymorphisms was determined by polymerase chain reaction (PCR) and restriction enzyme techniques. Three patients developed diabetic nephropathy (DN), all carriers of allele D. The presence of allele D was the only predictor (R(2)=.15, F=4.92, P=.035) of the observed GFR decline (-0.29+/-0.34 ml/min/month, P<.05). UAER increased during the study (log UAER=0.0275+/-0.042 microg/min/month, P=.002) and was associated with baseline UAER levels only (R(2)=.17, F=5.72, P=.024). A significant increase (P<.05) in cases of hypertension and retinopathy were observed in ID/DD (n=19) and not in II patients (n=11). Patients with the KQ/QQ genotype (n=8) presented a significant increase (P=.045) in new cases of retinopathy. In conclusion, the presence of the ACE gene D allele in this sample of normoalbuminuric normotensive Type 1 diabetic patients was associated with a higher proportion of microvascular complications and hypertension.