A new study finds that cancer incidence in individuals with cirrhosis is lower than originally believed—at most, about 4%.
In a population-based cohort study published in Alimentary Pharmacology and Therapeutics, researchers from the United Kingdom investigated the overall risk of developing hepatocellular carcinoma based on the different causes of cirrhosis.
Fibrosis, or the development of scar tissue, occurs as a result of the body trying to repair injured tissues. Likewise, liver fibrosis occurs after the body tries to restore the liver after it is injured due to infection. Cirrhosis develops when a patient’s liver becomes excessively scarred due to hepatitis, chronic alcoholism, or other liver conditions. As more scar tissues form on the liver, it becomes increasingly difficult for the liver to function properly. Unfortunately, damage to the liver as a result of cirrhosis is irreversible; however, if caught and treated early, additional damage to the liver may be preventable.
Cirrhosis has long been thought to be a major risk factor for hepatocellular carcinoma (HCC), the most common form of liver cancer. Cirrhosis also limits cancer treatments. But a new study has found that cancer incidence in patients with cirrhosis is lower than originally believed—at most, about 4%. Noting that there is little research that actually supports the cirrhosis-cancer link, researchers from The University of Nottingham set out to identify the cumulative incidence of HCC in individuals with cirrhosis.
Joe West, PhD, and colleagues gathered data on 3,107 patients with cirrhosis from the UK’s General Practice Research Database (1987 to 2006); HCC diagnoses were collected from linked national cancer registries (1971 to 2006). Using a Cox proportional hazards regression model, the researchers were able to estimate hazard ratios and predict 10-year cumulative incidence of HCC.
Just over half of the patients were male and between the ages of 18 and 65. The study subjects had various etiologies leading to cirrhosis, with the highest being alcohol at 56% (1,743 patients), followed by cryptogenic at 21% (647 patients), chronic viral hepatitis at 12% (374 patients), and autoimmune or metabolic disease at 11% (342 patients).
A total of 51 patients developed HCC within a decade (1.2% of patients with alcoholic cirrhosis and 1.1% of those with cirrhosis of unknown cause).
“This very low incidence of HCC occurrence in people with cirrhosis caused by alcohol or of unknown origin suggests that surveillance for HCC among these groups is likely to benefit patients little,” Dr. West, professor epidemiology at the university’s School of Medicine, said in a news release.
Study results showed that, “the adjusted relative risk of HCC was increased two-fold to three-fold among people with viral and autoimmune/metabolic etiologies, compared to those with alcohol-associated cirrhosis,” the authors wrote in the study.
Further findings indicated that 1.1% of patients with cryptogenic, 3.2% with autoimmune or metabolic disease, and 4% with chronic viral hepatitis developed HCC within 10 years.
Looking at the overall population—making up 12,977 person years—the HCC rate was 3.9 per 1,000 person years (0.4% annually).
“As surveillance incurs substantial cost, it is therefore unlikely to represent value for money for the NHS,” West concluded. “There may well be other ways of spending this money that would benefit patients far more.”