A Comparative Observational Study on the Effect of Leptin in Regulating Interleukin-6 (IL-6) and Tumor Necrosis Factor-Alpha (TNF-α) in Patients with Alcoholic Hepatitis in a Tertiary Healthcare Setting

一项比较观察性研究,探讨瘦素在三级医疗机构中对酒精性肝炎患者白细胞介素-6 (IL-6) 和肿瘤坏死因子-α (TNF-α) 的调节作用

阅读:2

Abstract

BACKGROUND: Alcoholic hepatitis is a chronic liver disease characterized by jaundice and hepatomegaly, influenced by excessive alcohol consumption, elevated pro-inflammatory cytokines, and decreased leptin levels. AIM AND OBJECTIVES: This study aimed to assess leptin's role in regulating IL-6 and TNF-α in alcoholic hepatitis patients, evaluate serum levels of these hormones, and investigate their interrelationship. METHODOLOGY: A total of 160 venous blood samples were collected, comprising 80 samples from nonalcoholic individuals (controls) and 80 from alcoholic patients (cases). The samples were centrifuged, and serum was collected in Eppendorf tubes. Approximately 1.5-2 mL of serum was required to perform enzyme-linked immunosorbent assay (ELISA) tests for leptin, IL-6, and TNF-α. RESULTS: In a cohort of 80 alcoholic patients, decreased leptin levels were found in 82.5%, particularly prevalent in the 40-50 years age group with alcoholic hepatitis (88.9%). Elevated IL-6 and TNF-α levels were each observed in 53.8% of participants, showing significant correlations with reduced leptin (93.0% and 95.3%, respectively; P < 0.05). Notably, all patients with elevated bilirubin had both decreased leptin and increased TNF-α, while among those with normal bilirubin, reduced leptin (71.4%) and TNF-α (75.5%) were still common. CONCLUSION: The study reveals a significant link between leptin, IL-6, and TNF-α levels and liver dysfunction indicators like total bilirubin, indicating leptin's potential as a biomarker for hepatic inflammation in alcoholic liver disease, emphasizing systemic inflammatory pathways' role in its pathophysiology.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。