Obstructive sleep apnea syndrome and chronic kidney disease: a new cardiorenal risk factor

Clinical and experimental studies revealed that sleep apnea might be an insidious risk factor for the progression of kidney disease and development of cardiovascular events by exacerbating well-known risk factors, namely hypertension, type 2 diabetes mellitus and obesity. Furthermore, sleep apnea also has a negative impact on endothelial function. Therefore, sleep apnea might be defined as a new cardiorenal risk factor. In this review, we aimed to summarize the evidences supporting the complex inter-relations between sleep apnea and development and progression of chronic kidney disease.     

Abnormal cardiac and metabolic measures correlate significantly with lower performance and activity in overweight chronic liver disease

People with Hepatitis C (HCV) and non‐alcoholic fatty liver disease (NAFLD) in the United States follow national trends toward a sedentary lifestyle and are increasingly at risk for hypertension. The intent of this study was to identify potential correlates of exercise tolerance in people with two types of chronic liver disease (CLD)‐NAFLD and HCV. Measures included cardiac output, oxygen consumption and stroke volume, blood pressure, distance walked in 6 minutes, clinical laboratory tests, and medications influencing the autonomic nervous system, patient self‐reports of activity, fatigue, and health‐related quality of life (HRQL). A total of 67 patients completed the 6‐minute walk test [45.1% Female, Age 51.7 ± 8.0 years, Body Mass Index 32.8 ± 5.9, 60% HCV]. At baseline, 70% had either diastolic (DBP) or systolic blood pressure outside normal range. Performance and cardiorespiratory measures correlated strongly with one another, but not with activity. Patients with abnormal DBP reported significantly lower maximum activity (MAS; r = −.254, P = .041, CI = −0.51 to −0.010; MAS 70.6 vs 82.5), significantly higher DBP post‐6‐minute walk test (r = .524, P = .0001, CI = 0.287‐0.762) and significantly lower overall HRQL items related to physical domains (r = .273, P = .029, CI = −0.518 to −0.029). Mental‐domain HRQL and depression measures did not correlate significantly with blood pressure. This study reports a significant correlation between both pre‐hypertensive and hypertensive DBP, poor physical‐domain self‐reports, HRQL, and performance in CLD patients.     

Esophagus adenocarcinoma in a young patient with celiac disease; Is celiac disease a predisposing factor for esophagus adenocarcinoma as well as squamous cell carcinoma?

We report a 36-year-old female with longstanding oily diarrhea and new-onset dysphagia that was diagnosed as celiac disease and esophagus adenocarcinoma. Celiac is a multisystemic autoimmune disease associated with a longstanding inflammatory process, especially in the gastrointestinal tract. This chronic inflammation may lead to a modest increase in neoplasia risk. There is a modest increased risk of malignancy in celiac disease, particularly adenocarcinoma and T-cell lymphoma of the small intestine and squamous cell carcinoma (SCC) of the esophagus, mouth, and pharynx. Although there is an association between SCC of the esophagus and celiac disease, there are no reports in the English literature about a relationship between celiac disease and esophageal adenocarcinoma. This case shows that as well as SCC, adenocarcinoma of the esophagus may also occur in patients with longstanding celiac disease.     

D-dimer level predicts in-hospital mortality in patients with infective endocarditis: A prospective single-centre study

Background

Increased circulating D-dimer levels have been correlated with adverse outcomes in various clinical conditions. To our knowledge, the association of on-admission D-dimer and in-hospital mortality in infective endocarditis (IE) has not been investigated. We hypothesized that increased on-admission D-dimer levels would correlate with adverse outcomes when prospectively studied in patients with IE.

Methods

In this prospective study, a total of 157 consecutive patients with the definite IE diagnosis met the inclusion criteria and underwent testing for on-admission D-dimer and CRP assays. The outcome measure was in-hospital death from any cause.

Results

In-hospital mortality occurred in 40 (26%) patients. Increased levels of plasma D-dimer (5.1 ± 1.7 vs 1.9 ± 0.8, p < 0.001), CRP [45(13-98) vs 12(5–28), p < 0.001] were found in dead patients compared with those survived. In addition to S. aureus infection, increased leukocyte count, end-stage renal disease, LVEF < 50%, vegetation size of > 10 mm, perivalvular abscess, on-admission D-dimer (HR: 1.32; 95% CI: 1.24-1.40; p < 0.001) and CRP (HR: 1.18; 95% CI: 1.09-1.36; p = 0.001) levels were significantly associated with in-hospital mortality. Furthermore, the sensitivity and specificity of D-dimer ≥ 4.2 mg/L in predicting in-hospital death in IE were 86% and 85%, respectively. Moreover, the sensitivity and specificity of CRP levels ≥ 13.6 mg/L were 72% and 69%, respectively.

Conclusion

Our findings suggest that on-admission D-dimer level may be a simple, available and valuable biomarker that allows us to identify high-risk IE patients for in-hospital mortality. D-dimer ≥ 4.2 mg/L, CRP ≥ 13.6 mg/L were independently associated with IE related in-hospital death.     

Early mitochondrial adaptations in skeletal muscle to diet-induced obesity are strain dependent and determine oxidative stress and energy expenditure but not insulin sensitivity

This study sought to elucidate the relationship between skeletal muscle mitochondrial dysfunction, oxidative stress, and insulin resistance in two mouse models with differential susceptibility to diet-induced obesity. We examined the time course of mitochondrial dysfunction and insulin resistance in obesity-prone C57B and obesity-resistant FVB mouse strains in response to high-fat feeding. After 5 wk, impaired insulin-mediated glucose uptake in skeletal muscle developed in both strains in the absence of any impairment in proximal insulin signaling. Impaired mitochondrial oxidative capacity preceded the development of insulin resistant glucose uptake in C57B mice in concert with increased oxidative stress in skeletal muscle. By contrast, mitochondrial uncoupling in FVB mice, which prevented oxidative stress and increased energy expenditure, did not prevent insulin resistant glucose uptake in skeletal muscle. Preventing oxidative stress in C57B mice treated systemically with an antioxidant normalized skeletal muscle mitochondrial function but failed to normalize glucose tolerance and insulin sensitivity. Furthermore, high fat-fed uncoupling protein 3 knockout mice developed increased oxidative stress that did not worsen glucose tolerance. In the evolution of diet-induced obesity and insulin resistance, initial but divergent strain-dependent mitochondrial adaptations modulate oxidative stress and energy expenditure without influencing the onset of impaired insulin-mediated glucose uptake.