Rao B Harshavardhan, Nair Priya, Koshy Anoop K, Krishnapriya S, Greeshma C R, Venu Rama P
Department of Gastroenterology, Amrita Institute of Medical Sciences, Kochi, Kerala 682041, India.
Healthcare Research Analyst, Department of Gastroenterology, Amrita Institute of Medical Sciences, Kochi, Kerala 682041, India.
Int J Hepatol. 2021 Dec 24;2021:1795851. doi: 10.1155/2021/1795851. eCollection 2021.
Systemic inflammation triggered by bacterial products like lipopolysaccharides (LPS) in the circulation is an important factor leading to decompensation in patients with chronic liver disease (CLD). High-density lipoprotein cholesterol (HDL-C) has a significant role in innate immune response to LPS in the circulation and could therefore increase the risk for decompensation in patients with CLD. In this study, we have explored the role of HDL-C as a prognostic marker for decompensation.
This was a prospective, observational, cohort study where consecutive patients with CLD were included. Patients with cholestatic liver disease and hepatocellular carcinoma were excluded. Fasting lipids were measured in all patients at the time of recruitment. Each patient was carefully followed up for development of decompensation events such as new-onset/worsening ascites, hepatic encephalopathy, or variceal bleed during follow-up.
A total of 170 patients were included (mean age 60 ± 11.5 years, M : F = 6 : 1). At the end of follow-up, 97/170 patients (57%) had decompensation events. Mean HDL-C levels were significantly lower among patients with decompensation (27.5 ± 15 mg/dL vs. 43.5 ± 13.9 mg/dL; value 0.004). Using ROC analysis, cut-off for HDL-C of 36.4 mg/dL was identified. On multivariate analysis, HDL-C (OR = 6.072; 95% CI 2.39-15.39) was found to have an independent association with risk of decompensation.
HDL-C level (<36.4 mg/dL) is a reliable marker for risk of decompensation and can be a useful addition to existing prognostic scoring systems in CLD. It can be a valuable tool to streamline treatment protocols and prioritise liver transplantation.
循环系统中由脂多糖（LPS）等细菌产物引发的全身炎症是导致慢性肝病（CLD）患者失代偿的重要因素。高密度脂蛋白胆固醇（HDL-C）在循环系统中对LPS的固有免疫反应中起重要作用，因此可能增加CLD患者失代偿的风险。在本研究中，我们探讨了HDL-C作为失代偿预后标志物的作用。
这是一项前瞻性、观察性队列研究，纳入了连续的CLD患者。排除胆汁淤积性肝病和肝细胞癌患者。在招募时测量所有患者的空腹血脂。对每位患者进行仔细随访，观察随访期间失代偿事件的发生情况，如新发/加重腹水、肝性脑病或静脉曲张出血。
共纳入170例患者（平均年龄60±11.5岁，男∶女 = 6∶1）。随访结束时，97/170例患者（57%）发生了失代偿事件。失代偿患者的平均HDL-C水平显著较低（27.5±15mg/dL vs. 43.5±13.9mg/dL；P值0.004）。通过ROC分析，确定HDL-C的截断值为36.4mg/dL。多因素分析发现，HDL-C（OR = 6.072；95%CI 2.39 - 15.39）与失代偿风险独立相关。
HDL-C水平（<36.4mg/dL）是失代偿风险的可靠标志物，可作为CLD现有预后评分系统的有益补充。它可以成为简化治疗方案和确定肝移植优先级的有价值工具。
