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Low Levels of Blood Lipids Are Associated with Etiology and Lethal Outcome in Acute Liver Failure
Authors:Paul Manka  Verena Olliges  Lars P Bechmann  Martin Schlattjan  Christoph Jochum  Jürgen W Treckmann  Fuat H Saner  Guido Gerken  Wing-Kin Syn  Ali Canbay
Institution:1. Department of Gastroenterology and Hepatology, University Hospital, University Duisburg-Essen, Essen, Germany.; 2. Department of General, Visceral and Transplantation Surgery, University Hospital, University Duisburg-Essen, Essen, Germany.; 3. Liver Regeneration and Repair, The Institute of Hepatology, Foundation for Liver Research, London, United Kingdom.; 4. Department of Hepatology, Barts Health NHS Trust, London, United Kingdom.; UMR Inserm U1052/CNRS 5286, France,
Abstract:

Background/Aims

Emerging data links different aspects of lipid metabolism to liver regeneration. In patients with acute liver failure (ALF), low levels of lipids may correlate with disease severity. Thus, we determined whether there is an etiology-specific link between lipid levels in patients suffering from ALF and aimed to investigate an effect of lipid levels on the prognosis of ALF.

Methods

In this retrospective single center study, we reviewed 89 consecutive ALF patients, who met the criteria of the “Acute Liver Failure Study Group”. Patient characteristics, clinical data and laboratory parameters were individually analyzed at admission and correlated with the patients'' outcome after a four week follow up. Possible endpoints were either discharge, or death or liver transplantation.

Results

High-density lipoprotein (HDL), cholesterol and triglyceride levels were significantly lower in patients who died or required a liver transplant. HDL levels were significantly higher in patients with ALF caused by acetaminophen intoxication, compared to fulminant HBV infection or drug induced liver injury. HDL levels correlated with hepatic injury by ALT levels, and Albumin, and inversely correlated with the MELD score, INR, and bilirubin.

Conclusion

In our cohort of patients with ALF, we could show that HDL and cholesterol are suppressed. In addition novel etiology specific patterns between acteminophen and non-acteminophen induced liver failure were detected for serum lipid components. Further studies are needed to address the role of cholesterol and lipid metabolism and the according pathways in different etiologies of ALF.
Keywords:
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