Yaqub Sayma, Ananias Patricia, Shah Arpita, Luenam Kanita, Jose Arunima Mariya, Melo Joao Pedro, Turkistani Arifa, Mohammed Lubna
Internal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Public Health, University of Texas Health Science Center at Houston, Houston, USA.
Cureus. 2021 Sep 22;13(9):e18201. doi: 10.7759/cureus.18201. eCollection 2021 Sep.
Non-alcoholic fatty liver disease (NAFLD) is the most common hepatic manifestation of metabolic syndromes, and its roots are strongly associated with obesity and insulin resistance. The excess fat induces inflammatory pathways by tissue irritation and progresses to non-alcoholic steatohepatitis (NASH), fibrosis, and has emerged as the most frequent cause of hepatocellular cancer (HCC). This systematic review was structured per the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) guidelines. The evidence was obtained from 13 research articles published in PubMed, Google Scholar, and Science Direct databases, including cross-sectional, case-control, prospective cohort studies, meta-analysis, and systematic reviews. The inclusion/exclusion criteria of free articles, published in English involving humans of mid-age in the last five years were applied. This review highlights findings in 7781 individuals, including non-NAFLD, NAFLD, and NASH positive individuals based on anthropometric measurement, blood samples, FibroScan, flow cytometry, and liver biopsy. The results underscored that the onset of inflammation set on the background of NAFLD starts NASH; the understanding and control of inflammation will help us design definitive biomarkers and treatment modalities. The complex pathogenesis and comparatively slow advancement but high morbidity have led investigators to understand the nuts and bolts for early management and prevention. Lipotoxicity and dysbiosis stimulate the immune system to generate cytokines and chemokines and decline in adipokines. The role of proteinase3 (PR3) and antitrypsin (ATT) ratio and biliverdin reductase (BVR) compel the exploration for non-invasive tests for definitive therapy.
非酒精性脂肪性肝病（NAFLD）是代谢综合征最常见的肝脏表现，其根源与肥胖和胰岛素抵抗密切相关。过多的脂肪通过组织刺激引发炎症途径，并进展为非酒精性脂肪性肝炎（NASH）、肝纤维化，已成为肝细胞癌（HCC）最常见的病因。本系统评价按照系统评价和Meta分析的首选报告项目（PRISMA）指南进行构建。证据来源于在PubMed、谷歌学术和科学Direct数据库中发表的13篇研究文章，包括横断面研究、病例对照研究、前瞻性队列研究、Meta分析和系统评价。应用了过去五年发表的、涉及中年人的英文免费文章的纳入/排除标准。本综述重点介绍了7781名个体的研究结果，包括基于人体测量、血液样本、FibroScan、流式细胞术和肝活检的非NAFLD、NAFLD和NASH阳性个体。结果强调，在NAFLD背景下炎症的发生引发了NASH；对炎症的理解和控制将有助于我们设计明确生物标志物和治疗方式。复杂的发病机制以及相对缓慢的进展但高发病率促使研究人员了解早期管理和预防的基本要点。脂毒性和生态失调刺激免疫系统产生细胞因子和趋化因子，并导致脂肪因子减少。蛋白酶3（PR3）与抗胰蛋白酶（ATT）的比值以及胆绿素还原酶（BVR）的作用促使人们探索用于确定治疗的非侵入性检测方法。
