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Published on: October 12, 2017
Role of High-Density Lipoprotein Cholesterol (HDL-C) as a Clinical Predictor of Decompensation in Patients with
Harshavardhan Rao B1, Priya Nair1, Anoop K Koshy1
1Department of Gastroenterology, Amrita Institute of Medical Sciences, Kochi, Kerala 682041, India.
Insights
Low high-density lipoprotein cholesterol (HDL-C) levels predict decompensation in chronic liver disease (CLD) patients. Measuring HDL-C can help identify patients at higher risk for liver decompensation, aiding treatment decisions.
Area of Science:
- Hepatology
- Cardiovascular Medicine
- Immunology
Background:
- Systemic inflammation from bacterial products like lipopolysaccharides (LPS) contributes to chronic liver disease (CLD) decompensation.
- High-density lipoprotein cholesterol (HDL-C) plays a role in the innate immune response to LPS.
- This study investigates HDL-C as a prognostic marker for decompensation in CLD patients.
Purpose of the Study:
- To explore the role of HDL-C as a prognostic marker for decompensation in patients with chronic liver disease.
- To determine if HDL-C levels can predict the risk of decompensation events in CLD.
Main Methods:
- Prospective, observational cohort study design.
- Inclusion of consecutive patients with CLD, excluding cholestatic liver disease and hepatocellular carcinoma.
- Measurement of fasting lipids and follow-up for decompensation events (ascites, hepatic encephalopathy, variceal bleed).
Main Results:
- 170 CLD patients included; 57% experienced decompensation.
- Mean HDL-C was significantly lower in patients with decompensation (27.5 mg/dL) compared to those without (43.5 mg/dL).
- An HDL-C cutoff of 36.4 mg/dL predicted decompensation risk, with lower levels independently associated (OR = 6.072).
Conclusions:
- HDL-C levels below 36.4 mg/dL are a reliable risk marker for decompensation in CLD.
- HDL-C can enhance existing prognostic scoring systems for CLD.
- This marker can aid in streamlining treatment and prioritizing liver transplantation.
Introduction:
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.
Methods:
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.
Results:
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; p 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.
Conclusions:
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.
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