May 6, 2014

Provided by HPCLive

By Marcia Frellick | May 05, 2014

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New research from the Hepatitis C Antiviral Long-term Treatment Against Cirrhosis (HALT-C) trial cohort indicates that continuous statin use can significantly reduce liver fibrosis progression in patients with advanced chronic hepatitis C infection.

Study results, released Sunday at Digestive Disease Week 2014 in Chicago, IL, add to evidence demonstrating that statins have anti-proliferative, anti-angiogenic, and anti-inflammatory effects on hepatic cells.
Although animal models have demonstrated that statins, or 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, effectively prevent the progression of liver fibrosis, little human data was available.

Tracey G. Simon, MD, an internist in the Gastrointestinal Unit at Massachusetts General Hospital, and Brigham and Women's Hospital in Boston, MA, and colleagues studied 547 non-cirrhotic patients with chronic hepatitis C who previously had not responded to standard interferon therapy.
The patients had Ishak Fibrosis Staging scores ≥ 3 and underwent serial liver biopsies at baseline, 1.5 years, and 3.5 years after the trial began. Inflammation was graded on an 18-point histology activity index.

Patients reported statin use as part of the comprehensive medical history taken prior to enrollment and at each follow-up visit over the length of the study. Statin users were more likely to be African American, to have lower baseline alanine transferase (ALT) levels, and to be diabetic when compared to patient who reported no statin use.

The mean change in Ishak score over the study period for those who used statins was -0.34 during 3.5 years of observation, while the mean change in the Ishak score among those in the non-statin group was +0.42 [(SE 0.07), p= 0.006] after adjustment for baseline fibrosis score.

Continuous statin use was linked with a significant decrease in time to histological progression even after adjusting for known predictors of histological outcome, including diabetes, body mass index, platelets, and hepatic steatosis (HR 0.31, 95% CI 0.10 - 0.97).

Therapies to reduce the progression of liver scarring are critical as the damage keeps the liver from performing essential functions. Slowing the progression can slow hepatic decompensation and help patients live longer. However, some clinicians have been reluctant to initiate statin therapy along with treatment for hepatitis C without more evidence that they are safe and effective for this purpose.

The HALT-C researchers said further prospective studies with a large proportion of statin users are needed to define the optimal timing for starting statins, the ideal length of therapy, and the impact on those with less severe fibrosis or other etiologies of liver disease.

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