■非酒精性脂肪性肝病(NAFLD)表现为过度的肝内脂肪积累而没有大量的酒精摄入。据报道涉及多因素发病机制。溶酶体酸性脂肪酶(LAL)活性降低被认为是新的致病机制之一。这篇综述总结了LAL活性在NAFLD发病机制中作用的现有证据。
■四个数据库,即PubMed/Medline,科学直接,科克伦图书馆,搜索和Google学者以确定相关的观察记录,评估LAL活性在NAFLD发病机制中的作用。通过使用纽卡斯尔-渥太华量表或JoannaBriggs研究所关键评估工具进行队列和横断面研究,对所有研究进行了质量评估。分别。LAL活性和其他临床结果的估计表示为平均值(SD)和数量(%),如主要研究中所示。
■共有9项质量良好的研究,其中包括来自不同组的1711名NAFLD患者和877名对照(健康志愿者,酗酒者,隐源性肝硬化,和HCV阳性)被包括在内。NAFLD组的人,59.55%为男性,研究之间的总体平均年龄从儿科的12.6±8.5个月到成人的58.90±13.82岁。在NAFLD组中,研究之间的LAL活性在0.53±0.08至1.3±0.70(nmol/spot/hr)之间变化,低于所有对照组,除了隐源性肝硬化患者(0.5±0.15nmol/spot/hr)。在其他感兴趣的结果中,ALT,AST,总胆固醇,甘油三酯,NAFLD患者的LDL胆固醇水平高于对照组。
■目前的证据表明,根据其严重程度,LAL活性降低与NAFLD发病机制的潜在相关性。建议进行大规模研究,更重要的是在没有代谢或遗传参与的NAFLD患者中。此外,LAL可以作为一种新的非侵入性诊断生物标志物来识别特定的NAFLD亚群。
UNASSIGNED: Non-alcoholic fatty liver disease (NAFLD) presents with the accumulation of excessive intra-hepatic fat without significant alcohol intake. Multifactorial pathogenesis is reported to be involved. Reduced lysosomal acid lipase (LAL) activity is suggested as one of the novel-involved pathogenic mechanisms. This
review summarizes the available evidence on the role of LAL activity in NAFLD pathogenesis.
UNASSIGNED: Four databases namely, PubMed/Medline, Science direct, Cochrane Library, and Google scholar were searched to identify relevant observational records evaluating the role of LAL activity in the pathogenesis of NAFLD. All studies were assessed for their quality by using Newcastle-Ottawa Scale or The Joanna Briggs Institute Critical Appraisal tools for cohort and cross-sectional studies, respectively. The estimates of LAL activity and other clinical outcomes were expressed as mean (SD) and number (%) as presented in the primary studies.
UNASSIGNED: A total of nine good quality studies with 1711 patients with NAFLD and 877 controls from different groups (healthy volunteers, alcoholics, cryptogenic cirrhosis, and HCV-positive) were included. From the NAFLD group, 59.55% were males and the overall mean age ranged between the studies from 12.6 ± 8.5 months in pediatrics to 58.90 ± 13.82 years in adults. In the NAFLD group, the LAL activity varied from 0.53 ± 0.08 to 1.3 ± 0.70 (nmol/spot/hr) between the studies which was less than all control groups except cryptogenic cirrhosis patients (0.5 ± 0.15 nmol/spot/hr). Of the other outcomes of interest, ALT, AST, total cholesterol, triglyceride, and LDL cholesterol were found elevated in NAFLD patients than in controls.
UNASSIGNED: The current evidence suggests a potential correlation of reduced LAL activity with NAFLD pathogenesis according to its severity. Large-scale studies are recommended, more importantly in patients with NAFLD having no metabolic or genetic involvement. Further LAL can act as a new non-invasive diagnostic biomarker to identify that specific NAFLD subgroup.