New research suggests that statins may have liver benefits beyond cholesterol control.
- In terms of death risk, liver cancer is one of the leading types of
cancer linked to high mortality.
- Experts have been trying to find ways to help people who are most at
risk for liver cancer.
- One study explored the use of statins, a class of medications
typically used to lower LDL cholesterol levels to reduce the risk of
stroke and heart disease.
- Researchers found that statin use decreased the risk for
hepatocellular carcinoma and hepatic decompensation, which is an advanced
stage of liver disease.
According to the
National Cancer Institute, liver cancer ranks sixth in causing death from cancer in the U.S. A
recent study published in JAMA Internal
Medicine examined how statin use affected liver cancer
risk in participants who had chronic liver disease.
The authors found that
statin use appeared to decrease the “10-year-cumulative incidence” of liver
cancer and hepatic decompensation, or decompensated cirrhosis. Hepatic
decompensation is when a person may be reaching end stage liver failure and
experiences complications such as ascites and jaundice as liver function
continues to decrease.
Participants in this study who used lipophilic
(fat-soluble) statins like atorvastatin and simvastatin had the greatest
outcomes for liver cancer, and participants with longer exposure to statins had
the best outcomes for liver cancer and hepatic decompensation.
Participants on statins
also had better outcomes for liver
fibrosis, which is a buildup of scar tissue that can make it hard
for the liver to function.
How do
statins affect liver cancer risk?
Chronic liver
disease has to do with a slow decrease in the liver’s ability
to do its job. Statins typically help lower cholesterol levels,
particularly the “bad” cholesterol.
Researchers examined how
statin use affected hepatocellular carcinoma and liver decompensation. Hepatocellular
carcinoma accounts for most liver cancer that begins in the
liver. Hepatic decompensation has to do with troubles in liver
function. For this study, researchers defined hepatic decompensation as the
presence of certain conditions like hepatic
encephalopathy and hepatorenal
syndrome.
This historical cohort
study included 16,501 participants. Of this, 3,610 were statin users. Data was
from hospitals that were part of the Mass General Brigham health care system.
The average age of
participants was just under age 60. All participants were over 40 years of age
and had chronic liver disease. Participants had received their chronic liver
disease diagnoses between July 2000 and June 2023. They excluded participants
based on factors like previous liver transplant or hepatocellular carcinoma.
Regarding fibrosis, they excluded participants with a Fibrosis-4 score lower
than 1.3. This blood test indicates the degree of fibrosis in the liver,
with a higher number indicating worse fibrosis.
Lipophilic vs. hydrophilic statins
Participants were not
taking statins for the first 180 days after diagnosis of chronic liver disease.
Five statins participants took were lipophilic statins, and two were
hydrophilic statins. Participants were considered nonstatin users if their cumulative
defined daily dose was less than 30.
“Statins, which are
generally used to help lower cholesterol levels and mitigate the risk of MACE
(major adverse cardiac events) in patients, can also play other roles in the
body and thus their use may be considered in other conditions. This study,
which is a cohort study including over 16,000 patients, theorizes that statins,
specifically lipophilic statins may help to slow down the progression of
fibrosis, thus in a subset of patients may then help to mitigate the risk of
hepatocellular carcinoma,” explained Jossef
Amirian, MD, board certified cardiologist with Manhattan Cardiology
in NYC, who was not involved in the study, to Medical News Today.
During the study, there
were 755 incident cases of hepatocellular carcinoma and 2,011 cases of hepatic
decompensation.
The results of the study
showed better outcomes for participants who used statins.
The 10-year cumulative
incidence of hepatocellular carcinoma was lower for statin users. While 8% of
nonusers developed hepatocellular carcinoma, only 3.8% of statin users did.
After the multivariable adjustment, researchers
found that statin users’ risk for hepatocellular carcinoma was 33% lower than
for participants who did not use statins.
The 10-year cumulative
incidence of hepatic decompensation was also better for statin users. While
19.5% of nonusers developed hepatic decompensation, only 10.6% of statin users
did. After the multivariable adjustment, statin users had a 22% lower risk for
hepatic decompensation.
When looking at the duration of use, those with the
longest duration saw the most minimal 10-year cumulative incidence rate of
hepatocellular carcinoma and hepatic decompensation. However, those with less
time of statin use still had better outcomes in these areas compared to
nonusers.
Does statin
type impact outcome?
Researchers also
analyzed if statin type impacted the outcomes.
The lipophilic statin
group had slightly better outcomes than the hydrophilic statin group for
hepatocellular carcinoma. For the hydrophilic statin group, the 10-year
cumulative incidence was 4.1%, while it was 3.7% for the lipophilic statin
group.
In contrast, the hydrophilic statin group had better
outcomes for hepatic decompensation. The hydrophilic statin group had a 7.9%
10-year cumulative incidence, while the lipophilic statin group was 11.2%.
Subgroup analyses also
showed the benefits of statin use. For example, among participants with
dyslipidemia, i.e. those who had blood lipid levels that were too high or low,
using statins helped to decrease the risk for hepatocellular carcinoma by 57%.
Statin-using
participants with cirrhosis saw a lower 10-year incidence of hepatocellular
carcinoma and hepatic decompensation. Statin-using participants with metabolic
dysfunction-associated steatotic liver disease and those without, with other
causes of chronic liver disease, and participants taking metformin and aspirin
also saw risk reduction for hepatocellular carcinoma.
Additionally,
researchers examined a subset of about 7,000 participants to see if statin use
affected the transition to various stages of liver fibrosis.
The authors note that
people with low liver fibrosis also have low incidences of hepatocellular
carcinoma. Fewer statin participants transitioned from an intermediate to a
high fibrosis score. More statin users moved from the high fibrosis score group
to the intermediate group than non-statin users. More statin users also moved
from the intermediate group to the low group.
With participants who
developed hepatocellular carcinoma, there were worse fibrosis outcomes than for
participants who did not develop hepatocellular carcinoma.
Researchers note that the findings “underscore the
potential of statins as chemopreventive agents against HCC [hepatocellular
carcinoma] through their role in mitigating fibrosis progression.”
Study
limitations
The research does have
certain limitations. First, it focused on one region and users of one
particular healthcare system; about 79% of participants were white. It also
focused on hospital-based participants who met inclusion criteria. Thus, the
results cannot be generalized to everyone.
Second, researchers were
able to adjust for several confounders, but others, like socioeconomic status
or healthcare access, could have influenced the findings. Third, researchers
could not account for possible treatments participants received postindex and
had to assume that all participants received the standard of care appropriate
for their type of chronic liver disease.
Finally, they only used the Fibrosis-4 score method to
look at fibrosis indirectly, and liver biopsies would have been more direct.
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