179 research outputs found
Μελέτη της σχέσης των επιπέδων της galectin-3 με τη νεφρική λειτουργία και τα επίπεδα της neutrophil gelatinase-associated lipocalin σε ασθενείς με καρδιακή ανεπάρκεια.
Εισαγωγή: Η νεφρική λειτουργία μπορεί να επηρεαστεί σημαντικά στους ασθενείς με καρδιακή ανεπάρκεια (ΚΑ). Η Neutrophil Gelatinase-Associated Lipocalin (NGAL) είναι ένας βιοδείκτης νεφρικής βλάβης που σχετίζεται με την εξέλιξη της νεφρικής δυσλειτουργίας.
Σκοπός: Να διερευνήσουμε την πιθανή ύπαρξη συσχέτισης μεταξύ των δεικτών νεφρικής βλάβης και των επιπέδων της Γκαλεκτίνης-3 του πλάσματος, ενός διαμεσολαβητή της μυοκαρδιακής ίνωσης και αναδιαμόρφωσης, σε ασθενείς με χρόνια καρδιακή ανεπάρκεια.
Υλικό και μέθοδος: Στη μελέτη συμπεριλήφθηκαν 115 άτομα με σταθερή χρόνια καρδιακή ανεπάρκεια ισχαιμικής αιτιολογίας με μειωμένο κλάσμα εξώθησης της αριστερής κοιλίας. Μετρήθηκαν τα επίπεδα της Γκαλεκτίνης-3 του πλάσματος, του β-νατριουρητικού πεπτιδίου (BNP), του NGAL και του παράγοντα νέκρωσης των όγκων-a (TNF-a). Η κάθαρση κρεατινίνης (CrCl) υπολογίστηκε με τη χρήση του τύπου των Cockcroft-Gault.
Αποτελέσματα: Τα επίπεδα του NGAL στο πλάσμα συσχετίστηκαν θετικά με τα επίπεδα της Γκαλεκτίνης-3 (rho=0.26, p=0.04), του BNP (rho=0.30, p=0.005) και του TNF-a (rho=0.24, p=0.01), ενώ συσχετίστηκαν αρνητικά με το κλάσμα εξώθησης της αριστερής κοιλίας (rho=-0.31, p=0.02). Το NGAL συσχετίστηκε επίσης θετικά με την κρεατινίνη του πλάσματος, ενώ συσχετίστηκε αντιστρόφως με την κάθαρση κρεατινίνης (CrCl). Μετά από προσαρμογή για πιθανούς συγχυτικούς παράγοντες όπως η ηλικία, το φύλο, ο διαβήτης, η υπέρταση, η κάθαρση κρεατινίνης και το BNP, το NGAL συσχετίστηκε ανεξάρτητα και ισχυρά μόνο με τα επίπεδα της Γκαλεκτίνης-3 του πλάσματος.
Συμπεράσματα: Στην παρούσα μελέτη διαπιστώσαμε πως υπάρχει θετική συσχέτιση μεταξύ των επιπέδων του NGAL και της Γκαλεκτίνης-3 του πλάσματος σε ασθενείς με καρδιακή ανεπάρκεια. Τα ευρήματα αυτά υποδηλώνουν την πιθανή συσχέτιση μεταξύ της νεφρικής βλάβης, την μυοκαρδιακής ίνωσης και αναδιαμόρφωσης του μυοκαρδίου στην καρδιακή ανεπάρκεια, ενώ καταδεικνύουν την αξία της παρακολούθησης της νεφρικής λειτουργίας στους ασθενείς με καρδιακή ανεπάρκεια.Background: Renal function may be impaired in heart failure (HF) patients. Neutrophil Gelatinase-Associated Lipocalin (NGAL) is a biomarker of renal injury associated with the progression of the disease.
Objectives: To examine the association of renal injury with Galectin-3, a mediator of myocardial fibrosis and remodeling, in patients with chronic HF.
Methods: We consecutive enrolled 115 subjects with stable ischemic HF with reduce ejection fraction. Serum levels of Galectin-3, b-type natriuretic peptide (BNP), NGAL and tumor necrosis factor alpha (TNFa) were measured. Creatinine clearance (CrCl) was estimated using Cockcroft-Gault formula.
Results: NGAL levels were positive correlated with Galectin-3 levels (rho=0.26, p=0.04), with BNP levels (rho=0.30, p=0.005), with TNF-a levels (rho=0.24, p=0.01) and inversely correlated with left ventricle ejection fraction (rho=-0.31, p=0.02). NGAL levels were also positively correlated with Creatinine levels and inversely associated with CrCl. After adjustment for many confounders including age, gender, diabetes mellitus, hypertension, CrCl and BNP; NGAL was independently associated with Galectin-3 levels.
Conclusions: In the present study we found a positive correlation between NGAL and Galectin-3 in patients with heart failure. These findings reveal the potential association between renal injury and myocardial fibrosis and remodeling in heart failure and highlight the importance of renal function monitoring in patients with HF
The Role of Inflammation in Diabetes: Current Concepts and Future Perspectives
Diabetes is a complex metabolic disorder affecting the glucose status of the human body. Chronic hyperglycaemia related to diabetes is associated with end organ failure. The clinical relationship between diabetes and atherosclerotic cardiovascular disease is well established. This makes therapeutic approaches that simultaneously target diabetes and atherosclerotic disease an attractive area for research. The majority of people with diabetes fall into two broad pathogenetic categories, type 1 or type 2 diabetes. The role of obesity, adipose tissue, gut microbiota and pancreatic beta cell function in diabetes are under intensive scrutiny with several clinical trials to have been completed while more are in development. The emerging role of inflammation in both type 1 and type 2 diabetes (T1D and T1D) pathophysiology and associated metabolic disorders, has generated increasing interest in targeting inflammation to improve prevention and control of the disease. After an extensive review of the possible mechanisms that drive the metabolic pattern in T1D and T2D and the inflammatory pathways that are involved, it becomes ever clearer that future research should focus on a model of combined suppression for various inflammatory response pathways
Cystatin C as an Early Biomarker of Nephropathy in Patients with Type 2 Diabetes
This study was done to evaluate clinical usefulness of cystatin C levels of serum and urine in predicting renal impairment in normoalbuminuric patients with type 2 diabetes and to evaluate the association between albuminuria and serum/urine cystatin C. Type 2 diabetic patients (n = 332) with normoalbuminuria (n = 210), microalbuminuria (n = 83) and macroalbuminuria (n = 42) were enrolled. Creatinine, urinary albumin levels, serum/urine cystatin C and estimated glomerular filtration rate (eGFR by MDRD [Modification of Diet in Renal Disease] and CKD-EPI [Chronic Kidney Disease Epidemiology Collaboration] equations) were determined. The cystatin C levels of serum and urine increased with increasing degree of albuminuria, reaching higher levels in macroalbuminuric patients (P < 0.001). In multiple regression analysis, serum cystatin C was affected by C-reactive protein (CRP), sex, albumin-creatinine ratio (ACR) and eGFR. Urine cystatin C was affected by triglyceride, age, eGFR and ACR. In multivariate logistic analysis, cystatin C levels of serum and urine were identified as independent factors associated with eGFR < 60 mL/min/1.73 m2 estimated by MDRD equation in patients with normoalbuminuria. On the other hand, eGFR < 60 mL/min/1.73 m2 estimated by CKD-EPI equation was independently associated with low level of high-density lipoprotein in normoalbuminuric patients. The cystatin C levels of serum and urine could be useful markers for renal dysfunction in type 2 diabetic patients with normoalbuminuria
The Clinical Characteristics of Normoalbuminuric Renal Insufficiency in Korean Type 2 Diabetic Patients: A Possible Early Stage Renal Complication
It has been recently reported that a considerable portion of diabetic patients with renal insufficiency show normoalbuminuria. As little is known about normoalbuminuric renal insufficiency in the Asian population, we examined its prevalence and clinical characteristics in Korean type 2 diabetic patients. We studied 562 patients with type 2 diabetes from Seoul National University Hospital. The estimated glomerular filtration rate (eGFR) was calculated by the Modification of Diet in Renal Disease formula and the degree of albuminuria was evaluated by spot urine albumin-creatinine ratio. Of 562 patients, 151 (26.9%) patients had renal insufficiency (eGFR <60 mL/min/1.73m2). Among them, 44 (29.1%) patients had normoalbuminuria. After excluding the patients using renin-angiotensin system (RAS) inhibitors, the prevalence of normoalbuminuric renal insufficiency was 35.3% (18 of 51 patients). Compared with micro- and macroalbuminuric renal insufficiency, normoalbuminuric renal insufficiency was associated with the female predominance, shorter duration of diabetes, lower prevalence of diabetic retinopathy, and lower prevalence of using antihypertensive drugs except RAS inhibitors. The prevalence decreased progressively with an increase in the duration of diabetes and an increase in the severity of retinopathy. Normoalbuminuric renal insufficiency was prevalent in Korean type 2 diabetic patients. The association with a shorter duration of the diabetes and a lower prevalence of retinopathy suggests that it might be an early stage renal complication
EEG recordings as biomarkers of pain perception: where do we stand and where to go?
Introduction:
The universality and complexity of pain, which is highly prevalent, yield its significance to both patients and researchers. Developing a non-invasive tool that can objectively measure pain is of the utmost importance for clinical and research purposes. Traditionally electroencephalography (EEG) has been mostly used in epilepsy; however, over the recent years EEG has become an important non-invasive clinical tool that has helped increase our understanding of brain network complexities and for the identification of areas of dysfunction. This review aimed to investigate the role of EEG recordings as potential biomarkers of pain perception.
Methods:
A systematic search of the PubMed database led to the identification of 938 papers, of which 919 were excluded as a result of not meeting the eligibility criteria, and one article was identified through screening of the reference lists of the 19 eligible studies. Ultimately, 20 papers were included in this systematic review.
Results:
Changes of the cortical activation have potential, though the described changes are not always consistent. The most consistent finding is the increase in the delta and gamma power activity. Only a limited number of studies have looked into brain networks encoding pain perception.
Conclusion:
Although no robust EEG biomarkers of pain perception have been identified yet, EEG has potential and future research should be attempted. Designing strong research protocols, controlling for potential risk of biases, as well as investigating brain networks rather than isolated cortical changes will be crucial in this attempt
Estimating glomerular filtration rate in diabetes: a comparison of cystatin-C-and creatinine-based methods
Abstract Aims/hypothesis: We compared the predictive performance of a GFR based on serum cystatin C levels with commonly used creatinine-based methods in subjects with diabetes. Subjects, materials and methods: In a crosssectional study of 251 consecutive clinic patients, the mean reference (plasma clearance of 99m Tc-diethylene-triaminepenta-acetic acid) GFR (iGFR) was 88±2 ml min . A regression equation describing the relationship between iGFR and 1/cystatin C levels was derived from a test population (n=125) to allow for the estimation of GFR by cystatin C (eGFR-cystatin C). The predictive performance of eGFR-cystatin C, the Modification of Diet in Renal Disease 4 variable formula (MDRD-4) and Cockcroft-Gault (C-G) formulas were then compared in a validation population (n=126). Results: There was no difference in renal function (ml min −1 1.73 m −
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Acute exposure to diesel affects inflammation and vascular function.
BACKGROUND: Diesel exhaust fumes represent one of the most common toxic pollutants. The prolonged effects of acute exposure to this pollutant on inflammatory status and vascular properties are unknown. METHODS: During a 2-h session, 40 healthy subjects were exposed to diesel exhaust fumes and/or filtered air. Endothelial function was assessed with flow mediated dilation, arterial stiffness with pulse wave velocity and reflected waves with augmentation index. C-reactive protein, fibrinogen, protein C levels and protein S activity were also measured. Standard deviation of normal to normal R-R intervals (SDNN) was used to assess heart rate variability. Measurements were assessed before exposure and 2 and 24 h after diesel exposure. RESULTS: Compared with filtered air, exposure to diesel exhaust fumes decreased flow mediated dilation and increased pulse wave velocity and augmentation index up to 24 h after the exposure (p < 0.001 for all). Similarly, compared with filtered air, diesel exhaust exposure impaired SDNN during the 24-h study period (p = 0.007). C-reactive protein and fibrinogen levels were significantly increased after diesel exhaust exposure while protein C levels and protein S activity decreased (p < 0.01 for all). Exposure to diesel exhaust fumes resulted in higher C-reactive protein concentration in smokers compared with non-smokers (p < 0.001). CONCLUSION: Short-term exposure to diesel exhaust fumes has a prolonged adverse impact on endothelial function and vascular wall properties, along with impaired heart rate variability, abnormal fibrinolytic activity and increased markers of inflammation. These findings give insights into the mechanisms underlining the increased cardiovascular risk of subjects regularly exposed to diesel exhaust fumes
THE IMPACT OF DIFFERENT TYPES OF AEROBIC EXERCISE ON ENDOTHELIAL FUNCTION AND ARTERIAL STIFFNESS
Microangiopathic complications in type 1 diabetes mellitus: differences in severity when isolated or associated with autoimmune polyendocrinopathies
Μελέτη της επίπτωσης πολυμορφισμών στο γονίδιο της ιντερλευκίνης-6 και στο γονίδιο του ινωδογόνου, καθώς και της επίδρασης αυτών στη φλεγμονή, στην ενδοθηλιακή λειτουργία και στους αιμοστατικούς παράγοντες σε ασθενείς με ασταθή στηθάγχη
Εισαγωγή-Σκοπός: Η ασταθής στηθάγχη χαρακτηρίζεται από μυοκαρδιακή ισχαιμία που προκαλείται από ανισορροπία μεταξύ παροχής και ανάγκης οξυγόνου, χωρίς βλάβη των μυοκαρδιακών κυττάρων. Η στένωση των επικαρδιακών αρτηριών και η μικροαγγειακή δυσλειτουργία μπορεί να εμπλέκονται στην εμφάνιση ασταθούς στηθάγχης. Μεταξύ άλλων παραγόντων, η συστηματική φλεγμονή είναι ένας πιθανός συνδετικός κρίκος μεταξύ μικροαγγειακής δυσλειτουργίας και επιταχυνόμενης αθηροσκλήρωσης. Γενετικοί πολυμορφισμοί όπως ο 174G/C (rs1800795) στον υποκινητή του γονιδίου της ιντερλευκίνης-6 (IL-6) και ο 455G/A (rs180070) στον υποκινητή του γονιδίου της β-αλυσίδας του ινωδογόνου εμπλέκονται στην έκφραση των γονιδίων της IL-6 και του ινωδογόνου. Επίσης, έχουν συσχετιστεί με τη ενεργοποίηση της φλεγμονής και της θρόμβωσης σε άτομα με στεφανιαία νόσο. Συνεπώς, σε αυτή τη μελέτη, εξετάζουμε το ρόλο των γενετικών αυτών πολυμορφισμών σε άτομα με ασταθή στηθάγχη.
Μέθοδος: Μελετήσαμε 272 ασθενείς με ασταθή στηθάγχη και 250 άτομα χωρίς στεφανιαία νόσο. Συλλέξαμε δείγματα αίματος από όλους τους συμμετέχοντες και μετρήθηκαν τα επίπεδα IL-6 και ινωδογόνου. Επιπροσθέτως, διενεργήθηκε αλυσιδωτή αντίδραση πολυμεράσης (Polymerase chain reaction, Restriction Fragment Length Polymorphism) για τον εντοπισμό των πολυμορφισμών και χρησιμοποιήθηκαν κατάλληλα περιοριστικά ένζυμα για την αναγνώριση των γονοτύπων. Τέλος, μελετήθηκε η ενδοθηλιακή λειτουργία των συμμετεχόντων με την μέτρηση της προκαλούμενης από τη ροή αγγειοδιαστολής (FMD) στη βραχιόνιο αρτηρία.
Αποτελέσματα: Τα άτομα με ασταθή στηθάγχη ήταν πιο συχνά άνδρες μεγαλύτερης ηλικίας συγκριτικά με την ομάδα ελέγχου (p=0.001). Ο επιπολασμός των παραγόντων καρδιαγγειακού κινδύνου (αρτηριακή υπέρταση, σακχαρώδης διαβήτης, δυσλιπιδαιμία) ήταν σημαντικά μεγαλύτερος στην ομάδα των ασθενών με ασταθή στηθάγχη. Τα άτομα με ασταθή στηθάγχη είχαν υψηλότερα επίπεδα IL-6 (p=0.001) και ινωδογόνου (p=0.001), καθώς και επηρεασμένο FMD (p=0.001) συγκριτικά με την ομάδα ελέγχου. Αναφορικά με τους γενετικούς πολυμορφισμούς, δεν παρατηρήθηκαν διαφορές στην κατανομή των γονοτύπων μεταξύ των δύο εξεταζόμενων ομάδων. Σε ασθενείς με ασταθή στηθάγχη διαπιστώσαμε σημαντικά υψηλότερα επίπεδα IL-6 σε ομοζυγώτες 174CC συγκριτικά με τους φορείς του G αλληλίου. Με βάση την ανάλυση λογιστικής παλινδρόμησης, τα άτομα με ασταθή στηθάγχη που έφεραν το G αλλήλιο είχαν χαμηλότερα επίπεδα IL-6 κατά 0.621 pg/ml συγκριτικά με τους ομοζυγώτες 174CC (p=0.05). Επιπροσθέτως, παρατηρήθηκε μια τάση για επηρεασμένη ενδοθηλιακή λειτουργία (FMD) σε ομοζυγώτες 174CC (p=0.09). Δεν ανευρέθησαν διαφορές στα επίπεδα του ινωδογόνου με βάση τους γονοτύπους του πολυμορφισμού της IL-6. Τα επίπεδα IL-6, ινωδογόνου, καθώς και το FMD δεν επηρεάζονταν από τους διάφορους γονοτύπους του G455A του υποκινητή του γονιδίου της β-αλυσίδας του ινωδογόνου.
Συμπέρασμα: Οι συγκεκριμένοι γενετικοί πολυμορφισμοί της IL-6 και του ινωδογόνου δεν σχετίζονται με αυξημένη επίπτωση ασταθούς στηθάγχης. Ωστόσο, ο πολυμορφισμός 174G/C της IL-6 επηρεάζει σημαντικά τα επίπεδα IL-6 σε 174CC ομοζυγώτες, συγκριτικά με τους φορείς του G αλληλίου. Μελλοντικές μελέτες είναι απαραίτητες για να διερευνηθεί περαιτέρω η σημασία του γενετικού πολυμορφισμού 174G/C της IL-6 στην εκδήλωση καi την εξέλιξη της στεφανιαίας νόσου.Background: Unstable angina (UA) is characterized by myocardial ischemia caused by oxygen supply and demand imbalance, without myocardial cell damage. Narrowing of the major epicardial arteries and/or microvascular dysfunction may be implicated in the presentation of unstable angina. Among other factors, systemic inflammation may be a link between microvascular dysfunction and accelerated atherosclerosis. Genetic variants such as the -174G/C (rs1800795) single nucleotide polymorphism of interleukin-6 (IL-6) gene promoter and the -455G/A (rs180070) single nucleotide polymorphism of the b-chain fibrinogens’ gene promoter are implicated in IL-6 and fibrinogen genes expression, and they have been connected to the systemic inflammation and prothrombotic activation in patients with coronary artery disease. Therefore, in this study we evaluate the role of inflammation and thrombosis genetic polymorphisms implicated in the endothelial dysfunction and UA.
Methods: We studied 272 patients with unstable angina that were admitted to the Coronary Care Unit and 250 control subjects. Blood samples were collected from all participants and fibrinogen and IL-6 were measured. Furthermore, Polymerase chain reaction - Restriction Fragment Length Polymorphism was performed for detection of polymorphisms and restriction enzymes were used for identification of genotypes. Finally, subjects’ endothelial function was assessed by measuring flow-mediated dilation (FMD) with ultrasound.
Results: In the studied population, subjects with UA were older compared to control subjects (p<0.001), incidence of male sex was higher in the UA population compared to control group (p<0.001), as well as the prevalence of other cardiovascular risk factors such as hypertension, diabetes mellitus, and dyslipidemia. Subjects with UA were found to have higher levels of IL-6 (p<0.001) and fibrinogen (p=0.001), as well as impaired FMD (p<0.001) compared to controls. Regarding the single nucleotide polymorphisms, there was no difference in the distribution of the genotypes in the two studied groups (control vs. UA). In subjects with UA, we found significantly increased serum IL-6 levels in CC homozygotes for the examined IL-6 gene promoter single nucleotide polymorphism, compared to carriers of the G allele according to a recessive/dominant model. According to a logistic regression analysis, UA subjects carrying the G allele had 0.621 pg/ml lower levels of IL-6 compared to CC homozygotes (p=0.05). Moreover, there was a trend towards impaired FMD in the CC homozygotes (p=0.09). No differences in fibrinogen levels were observed. Serum IL-6, fibrinogen, and FMD were not affected by G455A genotype.
Conclusion: Genetic variants of IL-6 and fibrinogen do not affect the incidence of UA. However, the 174G/C IL-6 gene promoter significantly affects IL-6 levels in CC homozygotes compared to the carries of the G allele, indicating that when coronary atherosclerosis progresses to a rapidly accelerated and unstable phase, this genetic variant, under epigenetic modifications, may have a predisposing role in the progression to acute coronary syndromes. Additional, adequately designed studies are required to elucidate the importance of the 174G/C IL-6 single nucleotide polymorphism in coronary artery disease
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