A study using the Taiwan National Health Insurance research database investigated the efficacy of statin use on preventing the development of liver decompensation in patients with different cirrhosis etiologies.
A study conducted by Ching-Liang Lu, MD, and colleagues and published in the Journal of Hepatology aimed to investigate the relationship between statin use and the risk of developing decompensation and hepatocellular carcinoma (HCC) in patients with liver cirrhosis.
Liver cirrhosis is often a complication of chronic infections with the Hepatitis C or B viruses, as well as chronic alcohol abuse. Cirrhosis is defined as scarring of the liver tissue, which can impact liver function as the cirrhosis progresses. Cirrhosis can be classified as compensated or decompensated, with prognosis for patients with compensated cirrhosis being significantly better. Patients with decompensated cirrhosis display symptoms stemming from hepatic insufficiency, such as jaundice, as well as those caused by portal hypertension, such as the presence of ascites.
Recent studies have shown that statins, drugs typically administered to lower cholesterol, have the potential to treat portal hypertension. However, these studies had major limitations in being small scale studies with limited non-cirrhotic patient populations. As a result, there is a need to investigate the effect statins have in patients with liver cirrhosis, whether it’s due to infection with viral hepatitis or alcohol consumption.
Dr. Lu and colleagues utilized the Taiwan National Health Insurance research database (NHIRD), which includes information on patient medical status, prescriptions, as well as hospital visits. Adult patients, aged 20 years and older, were included in the study and patients were classified into three cirrhosis etiology groups: HCV, HBV, and alcohol-related cirrhosis. Patients with HIV coinfection were excluded from the study. These were further broken down into groups based on statin use.
In comparison to non-statin users, who had a 29% chance of developing decompensation, patients receiving statins only had a 14% chance. In addition, those receiving statins had a lower rate of mortality (9% vs 18%) and a lower rate of developing HCC than their non-statin user counterparts (6% vs 10%). The study authors noted that the statins showed a dose-dependent response in lowering the risk for decompensation. However, when analyzing statin efficacy in those with alcohol-related cirrhosis, the authors found that use of statin in these patients did not have as much of an effect on the risk of decompensation as it did in others. The authors suspect that this finding could be due to either poor adherence to the statin regimen or continued alcohol consumption in patients alcohol-related cirrhosis. More work is needed to better explain the effect observed in this study in regards to statin use in alcoholic cirrhotics.
Understanding the molecular mechanism underlying the effect statins have in reducing the risk of cirrhotic patients developing decompensation is important, and the authors pose a few potential mechanisms to address this question. First, the statins could be increasing nitric oxide (NO) availability, which would lead to vasodilation and to reduced portal hypertension, as well as to increased liver function. Conversely, the statins could be causing an anti-inflammatory effect through the reduction of a particular product of hepatocytes that has been shown to lead to poor prognosis in patients with liver cirrhosis.
Overall, this study is the first to demonstrate the protective effect of statins on patients with liver cirrhosis specifically.
Samar Mahmoud graduated from Drew University in 2011 with a BA in Biochemistry and Molecular Biology. After two years of working in industry as a Quality Control Technician for a blood bank, she went back to school and graduated from Montclair State University in 2016 with an MS in Pharmaceutical Biochemistry. She is currently pursuing her PhD in Molecular and Cellular Biology at the University of Massachusetts at Amherst.