No abstract

Adverse-outcomes related to sarcopenia are mostly mentioned as physical disability. As the other skeletal muscles, respiratory muscles may also be affected by sarcopenia. Respiratory muscle strength is known to affect pulmonary functions. Therefore, we aimed to investigate the relations between extremity muscle strength, respiratory muscle strengths and spirometric measures in a group of male nursing home residents. Among a total of 104 male residents, residents with obstructive measures were excluded and final study population was composed of 62 residents. Mean age was 70.5 ± 6.7 years, body mass index: 27.7 ± 5.3 kg/m2 and dominant hand grip strength: 29.7 ± 6.5 kg. Hand grip strength was positively correlated with maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) (r = 0.35, p < 0.01 and r = 0.26, p < 0.05, respectively). In regression analysis, the only factor related to MIP was hand grip strength; among spirometric measures only parameter significantly related to grip strength was peak cough flow (PCF). The association of PCF with grip strength disappeared when MIP alone or "MIP and MEP" were included in the regression analysis. In the latter case, PCF was significantly associated only with MIP. We found peripheric muscle strength be associated with MIP and PCF but not with MEP or any other spirometric parameters. The relation between peripheral muscle strength and PCF was mediated by MIP. Our findings suggest that sarcopenia may affect inspiratory muscle strength earlier or more than the expiratory muscle strength. Sarcopenia may cause decrease in PCF in the elderly, which may stand for some common adverse respiratory complications.

Endothelial-specific molecule 1 (endocan) is expressed in endothelial cells. We investigated the relationship between acute coronary syndrome (ACS) and serum endocan levels. We included 30 individuals as a control group and 53 patients diagnosed with ACS. The severity of coronary artery disease was assessed by a modified Gensini stenosis and SYNTAX scoring system. There was a significant difference in serum endocan levels between the control group and the ACS group (0.75 ± 0.13 vs 0.86 ± 0.25 ng/mL, P = .014). There was also a significant difference in serum endocan levels between diabetic patients with ACS and nondiabetic patients with ACS (1.02 ± 0.33 vs 0.81 ± 0.21 ng/mL, P = .016). There was no significant correlation between serum endocan level, Gensini, and SYNTAX score (r = .11, P = .53 and r = .16, P = .37). Endocan, a new biomarker of endothelial pathology, is significantly increased in patients with ACS.

Endothelial-specific molecule 1 (endocan) is expressed by endothelial cells and may have a major role in the regulation of cell adhesion and in the pathogenesis of inflammatory disorders. We aimed to assess change in endocan levels after 3 months of lifestyle change recommendations and guideline-based treatment. Diabetic patients (n = 77) who had neither chronic kidney disease nor chronic inflammatory disease were included. After baseline evaluation, the patients were advised lifestyle changes, and their medical treatment was determined individually according to recommendations of the American Diabetes Association (ADA) guidelines. At the end of third month patients were reevaluated. Baseline endocan levels were significantly increased in the study group compared with the control group. The third-month laboratory workup showed significant reductions in hemoglobin A1c, urinary albumin-to-creatinine ratio (UACR), and endocan levels. Only δ-UACR was independently correlated with δ-endocan in multivariate linear regression analysis. Our findings suggest that serum endocan concentrations are elevated in patients with type 2 diabetes and decrease following anti-hyperglycemic treatment. Furthermore, decrease in endocan concentrations might be associated with improved glycemic control and reductions in UACR.

Baseline proteinuria was significantly correlated with ∆%GFR per year. Hypertension and proteinuria were found to be the major treatable risk factors for the progression of CKD in ADPKD patients.