Statins linked to reduced liver cancer risk in major cohort study

Harvard Medical School researchers have found that statin use significantly reduces the risk of hepatocellular carcinoma (HCC) and hepatic decompensation among patients with chronic liver disease (CLD). Statins, particularly lipophilic statins like atorvastatin and simvastatin, were associated with a substantial decrease in the likelihood of liver cancer and complications. Longer duration of statin use further increases this protective effect.

The study is published in the journal JAMA Internal Medicine.

Hepatocellular carcinoma remains a leading cause of cancer-related death worldwide, with chronic liver disease identified as a primary risk factor. Historically, viral hepatitis was the predominant cause of HCC; yet, advances in antiviral treatments have reduced cases due to this cause. Currently, metabolic and alcohol-related liver diseases are more common, elevating the importance of strategies to prevent HCC in these populations.

Previous experimental studies have indicated that statins, widely prescribed for cholesterol reduction, possess properties such as anti-inflammatory, antifibrotic, and antioxidant effects. Observational studies have supported an association between statin use and reduced liver disease progression, though earlier research often focused narrowly on specific CLD causes or lacked assessment of fibrosis progression.

In the study titled “Statin Use and Risk of Hepatocellular Carcinoma and Liver Fibrosis in Chronic Liver Disease,” researchers conducted a historical cohort analysis of data from the Research Patient Data Registry, clinical data from hospitals within the Mass General Brigham health care system, covering the years 2000 to 2023.

Participants included 16,501 adult patients aged 40 or older diagnosed with CLD and a baseline Fibrosis-4 (FIB-4) score of 1.3 or higher. Individuals were grouped into statin users and nonusers. Researchers evaluated the cumulative 10-year incidence of hepatocellular carcinoma and hepatic decompensation, as well as changes in liver fibrosis severity based on the FIB-4 score. Adjustments were made for confounding factors through inverse probability of treatment weighting.

Statin use correlated with significantly lower incidences of HCC, reducing the 10-year cumulative incidence from 8.0% among nonusers to 3.8% among statin users. This corresponds to an absolute risk difference of −4.2% (95% CI, −5.3% to −3.1%) and a 33% lower adjusted hazard ratio (aSHR 0.67). Similarly, hepatic decompensation risk decreased from 19.5% in nonusers to 10.6% in statin users, with an absolute risk difference of −9.0% (95% CI, −10.6% to −7.3%) and an aSHR of 0.78 (22% lower risk).

Lipophilic statins had stronger protective associations, lowering HCC risk by 36% (aSHR 0.64), compared with a 21% risk reduction observed with hydrophilic statins such as rosuvastatin and pravastatin (aSHR 0.79). Longer-term statin use further improved these outcomes. Patients prescribed at least 600 cumulative daily doses had a 40% reduction in HCC risk (aSHR 0.60) and a 36% reduction in hepatic decompensation (aSHR 0.64).

In evaluating fibrosis progression among a subgroup of 7,038 patients with serial FIB-4 measurements, statin users showed better outcomes, with fewer progressing to higher-risk fibrosis categories and more transitioning from high-risk to intermediate- or low-risk categories.

Findings indicate that statin use is associated with significant reductions in hepatocellular carcinoma risk and hepatic decompensation among CLD patients. Lipophilic statins, particularly with prolonged usage, demonstrated the strongest protective effects, supporting their consideration as preventive treatments for hepatocellular carcinoma in chronic liver disease patients.

© 2025 Science X Network

Harvard Medical School researchers have found that statin use significantly reduces the risk of hepatocellular carcinoma (HCC) and hepatic decompensation among patients with chronic liver disease (CLD). Statins, particularly lipophilic statins like atorvastatin and simvastatin, were associated with a substantial decrease in the likelihood of liver cancer and complications. Longer duration of statin use further increases this protective effect.

The study is published in the journal JAMA Internal Medicine.

Hepatocellular carcinoma remains a leading cause of cancer-related death worldwide, with chronic liver disease identified as a primary risk factor. Historically, viral hepatitis was the predominant cause of HCC; yet, advances in antiviral treatments have reduced cases due to this cause. Currently, metabolic and alcohol-related liver diseases are more common, elevating the importance of strategies to prevent HCC in these populations.

Previous experimental studies have indicated that statins, widely prescribed for cholesterol reduction, possess properties such as anti-inflammatory, antifibrotic, and antioxidant effects. Observational studies have supported an association between statin use and reduced liver disease progression, though earlier research often focused narrowly on specific CLD causes or lacked assessment of fibrosis progression.

In the study titled “Statin Use and Risk of Hepatocellular Carcinoma and Liver Fibrosis in Chronic Liver Disease,” researchers conducted a historical cohort analysis of data from the Research Patient Data Registry, clinical data from hospitals within the Mass General Brigham health care system, covering the years 2000 to 2023.

Participants included 16,501 adult patients aged 40 or older diagnosed with CLD and a baseline Fibrosis-4 (FIB-4) score of 1.3 or higher. Individuals were grouped into statin users and nonusers. Researchers evaluated the cumulative 10-year incidence of hepatocellular carcinoma and hepatic decompensation, as well as changes in liver fibrosis severity based on the FIB-4 score. Adjustments were made for confounding factors through inverse probability of treatment weighting.

Statin use correlated with significantly lower incidences of HCC, reducing the 10-year cumulative incidence from 8.0% among nonusers to 3.8% among statin users. This corresponds to an absolute risk difference of −4.2% (95% CI, −5.3% to −3.1%) and a 33% lower adjusted hazard ratio (aSHR 0.67). Similarly, hepatic decompensation risk decreased from 19.5% in nonusers to 10.6% in statin users, with an absolute risk difference of −9.0% (95% CI, −10.6% to −7.3%) and an aSHR of 0.78 (22% lower risk).

Lipophilic statins had stronger protective associations, lowering HCC risk by 36% (aSHR 0.64), compared with a 21% risk reduction observed with hydrophilic statins such as rosuvastatin and pravastatin (aSHR 0.79). Longer-term statin use further improved these outcomes. Patients prescribed at least 600 cumulative daily doses had a 40% reduction in HCC risk (aSHR 0.60) and a 36% reduction in hepatic decompensation (aSHR 0.64).

In evaluating fibrosis progression among a subgroup of 7,038 patients with serial FIB-4 measurements, statin users showed better outcomes, with fewer progressing to higher-risk fibrosis categories and more transitioning from high-risk to intermediate- or low-risk categories.

Findings indicate that statin use is associated with significant reductions in hepatocellular carcinoma risk and hepatic decompensation among CLD patients. Lipophilic statins, particularly with prolonged usage, demonstrated the strongest protective effects, supporting their consideration as preventive treatments for hepatocellular carcinoma in chronic liver disease patients.

© 2025 Science X Network