This study has assessed the protective efficacy of
Heart failure is a disease affecting millions of patients each year, and is responsible for burdening the world with high mortality rates. More concerns come from its numerous hospital readmissions (with an estimated number of 2.6 million per year which makes it one of the leading diseases responsible for national healthcare expenditures). Despite drastic improvement of therapies in recent years, heart failure remains a progressive disease. Thus, more attention has been given to finding potential biomarkers involved in the pathological mechanisms of this disease that would potentially lead to faster diagnosis and improved prognosis. One of the emerging biomarkers that has just recently come into the spotlight is galectin-3. It was associated in recent clinical trials with both the progression and severity of heart failure. Ventricular remodelling and myocardial fibrosis are essential for heart failure development and are linked to poor outcomes. An ever-growing body of evidence places galectin-3 as an important link between inflammation and fibrosis, which play a prominent role in cardiac remodelling.This review sums up the most relevant experimental and clinical studies about galectin-3 and its potential prognostic value in heart failure. The article also provides a better understanding of this molecule's involvement in heart failure pathology by modulating cardiac fibrosis. It also weighs whether the available data on galectin-3 are consistent enough to reduce readmissions and mortality while improving diagnosis and future therapies for heart failure, versus the possibility that it is simply"another brick in the wall?"
Galectin-3 can predict long-term mortality in patients with AHF. The results of our study suggest a possible relation between left ventricular remodeling and increasing galectin-3 levels.
BackgroundHeart failure is accompanied by abnormalities in ventricular-vascular interaction due to increased myocardial and arterial stiffness. Galectin-3 is a recently discovered biomarker that plays an important role in myocardial and vascular fibrosis and heart failure progression.ObjectivesThe aim of this study was to determine whether galectin-3 is correlated with arterial stiffening markers and impaired ventricular-arterial coupling in decompensated heart failure patients.MethodsA total of 79 inpatients with acute decompensated heart failure were evaluated. Serum galectin-3 was determined at baseline, and during admission, transthoracic echocardiography and measurements of vascular indices by Doppler ultrasonography were performed.ResultsElevated pulse wave velocity and low arterial carotid distensibility are associated with heart failure in patients with preserved ejection fraction (p = 0.04, p = 0.009). Pulse wave velocity, carotid distensibility and Young’s modulus did not correlate with serum galectin-3 levels. Conversely, raised galectin-3 levels correlated with an increased ventricular-arterial coupling ratio (Ea/Elv) p = 0.047, OR = 1.9, 95% CI (1.0‑3.6). Increased galectin-3 levels were associated with lower rates of left ventricular pressure rise in early systole (dp/dt) (p=0.018) and raised pulmonary artery pressure (p = 0.046). High galectin-3 levels (p = 0.038, HR = 3.07) and arterial pulmonary pressure (p = 0.007, HR = 1.06) were found to be independent risk factors for all-cause mortality and readmissions.ConclusionsThis study showed no significant correlation between serum galectin-3 levels and arterial stiffening markers. Instead, high galectin-3 levels predicted impaired ventricular-arterial coupling. Galectin-3 may be predictive of raised pulmonary artery pressures. Elevated galectin-3 levels correlate with severe systolic dysfunction and together with pulmonary hypertension are independent markers of outcome.
Background and Objectives: Bronchial asthma (BA) and chronic obstructive pulmonary disease (COPD) are not only common obstructive respiratory conditions but also major causes of morbidity and mortality worldwide. There is, however, a surprising lack of blood-based biomarkers for separating between these pulmonary disorders. The aim of this study was to assess the practical relevance of using serum YKL-40, single or combined, for this purpose. Materials and Methods: Subjects included Romanian patients with BA (n = 24) or COPD (n = 27). YKL-40, fibrinogen, pre-treatment C-reactive protein (CRP), post-treatment CRP, erythrocyte sedimentation rate, interleukin 6 (IL-6), procalcitonin (PCT), absolute neutrophil count, neutrophil percentage, absolute lymphocyte count, lymphocyte percentage, absolute eosinophil count, and eosinophil percentage were measured and compared between these patients. Results: This is the first study investigating the clinical significance of serum YKL-40 in delineating between COPD and BA in Caucasian populations. Only fibrinogen and YKL-40 levels were different between COPD and BA, with the measured values being significantly elevated. These patients exhibited distinct inflammatory profiles. Using the upper quartiles of these variables for the pooled study population (YKL-40: 5100 pg/mL; fibrinogen: 552 mg/dL) as cut-off values, subjects were classified into high or low groups. High YKL-40 adults revealed significantly increased PCT levels. High fibrinogen subjects, by contrast, showed significantly elevated IL-6 concentrations and pre-treatment CRP levels. Low YKL-40 and fibrinogen patients showed the absence of COPD. Conclusions: Combined use of serum YKL-40 and fibrinogen may be useful for identifying the absence of COPD.
This method can avoid the saponification of the FA methyl esters and can analyze for the first time simultaneously neutral monosaccharides, FAs and cholesterol from a drop of blood.
This article presents an observational randomized prospective study done on 65 patients, who underwent major surgical interventions in the field of orthopedic surgery-total hip replacement or general surgery � total colectomy. The level of albuminemia in these cases were determined before the surgical intervention, after 6 hours of the intervention and after 24 h of the intervention. The measurements of the plasmatic concentration of the pro-inflammatory cytokines Tumor Necrosis factor -alpha (TNF-alpha) and interleukin 6 (IL6) were simultaneously done with the determination of the plasmatic levels of albumin. Values of hemoglobin and hematocrit were determined 24 h after the surgical procedure in order to exclude hemodilution, which could lead to a possible drop in the levels of plasmatic albumin. After the collection of the data, the statistical work was done and it consisted of descriptive statistics, correlation and comparison tests as well as statistical validation tests. Obtained results indicate that IL-6 plays a major role comparatively with that of TNF-alfa, regarding the decrease of the plasmatic level of albumin, and due to this, the primordial cause for hypoalbuminemia is an acute hepatic phase reaction. Supplemental permeability of the capillary wall under the action of TNF alpha has a secondary role, but could lead to a faster decrease in plasmatic albumin in the first hours after the surgical procedure.
Background and objectives: Bronchial asthma is a heterogeneous, multifactorial pulmonary disease characterized by variable airway obstruction caused by chronic inflammation. Our study investigates the clinical relevance of MBL plasma levels in accordance with IgE values in children who attended a pediatric consult for respiratory symptoms with bronchial asthma. Materials and Methods: The study population consists of patients <18-years-old and included 43 patients with bronchial asthma and 64 age-matched healthy subjects as a control group. We used the ELISA Human MBL Immunoassay kit and the electrochemiluminescence immunoassay (ECLIA) kit for IgE determination. Results: Our results show significantly different distributions of patients in the bronchial asthma group and control group. The measured values were within the normal range for most controls, while the bronchial asthma patients displayed higher values of plasma MBL and IgE levels. We observed a wider heterogeneity in MBL concentrations in bronchial asthma patients when compared to the healthy age-matched controls. Our results also suggest a potential clinical usefulness of plasma MBL concentrations in accordance with IgE and eosinophil cells levels in the diagnosis of bronchial asthma, and our results may suggest a prognostic role of MBL in the evolution of asthmatic disease; however, further studies are necessary to confirm these findings. Conclusions:We can say that plasma MBL concentrations present a relative diagnostic role for bronchial asthma in pediatric patients and may suggest a more severe disease progression; however, further studies are needed to elucidate the role played by MBL in the determination and evolution of this disease.
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