Publication: The Relation of Serum Nesfatin-1 Levels With Disease Severity and Complications in Patients With Liver Cirrhosis
Loading...
Date
Journal Title
Journal ISSN
Volume Title
Abstract
Objective: Nesfatin-1 is an anorectic polypeptide that plays important roles in regulating appetite and energy intake. Cachexia and malnutrition are common in individuals with cirrhosis. We examined the relationship between serum nesfatin-1 levels and stage of cirrhosis, with the hypothesis that an increase in nesfatin-1 levels in patients with cirrhosis may be related to this catabolic process. Material and Method: The study includes 51 patients with cirrhosis and 30 healthy volunteers. Nesfatin-1 levels in serum samples were compared using the enzyme-linked immunosorbent assay (ELISA). We calculated the Child-Pugh stages and Model for End-Stage Liver Disease (MELD) scores of patients with cirrhosis and examined their relationship with nesfatin-1. We've also investigated the relationship between cirrhosis complications and nesfatin-1. Results: We found nesfatin-1 levels to be significantly higher in the cirrhosis patient group compared to the control group (p=0.001). The patient group was divided into those with compensated and those with decompensated liver cirrhosis and compared with the control group. Nesfatin-1 levels were found to be significantly higher in the compensated liver cirrhosis group (p=0.01). When classifying the patients with cirrhosis based on their Child-Pugh stages and MELD scores, no significant relationship was detected between these groups and their nesfatin-1 levels. Conclusion: Nesfatin-1 may have antioxidant, anti-inflammatory, and anti-apoptotic effects in maintaining the state of patients with compensated liver cirrhosis. Low levels of nesfatin-1 in decompensated liver cirrhosis may result from defense mechanisms and inadequate production.
Description
Keywords
Citation
WoS Q
Scopus Q
Q4
Source
Journal of Istanbul Faculty of Medicine-Istanbul Tip Fakultesi Dergisi
Volume
87
Issue
3
Start Page
209
End Page
214
