WASHINGTON -- Satins may improve liver function in patients with chronic hepatitis C, according to a small pilot study that challenges the widely accepted belief that the agents are hepatotoxic.
WASHINGTON, May 20 -- Satins may improve liver function in patients with chronic hepatitis C virus infection (HCV), according to a small pilot study that challenges the widely accepted belief that the agents are hepatotoxic.
Patients who had abnormal alanine aminotransferase (ALT) levels at baseline had significant improvement after 14 days of fluvastatin (Lescol) -- even at doses four times higher than the one approved by the FDA, said Ted Bader, M.D., of the University of Oklahoma and the VA Medical Center in Oklahoma City.
Moreover, HCV patients who had normal baseline ALT values "had no worsening of ALT with statin therapy," Dr. Bader said at Digestive Disease Week here.
And data from the VA's HCV database hint that when statins are given to patients who are receiving standard HCV therapy with peginterferon and ribavirin, "statins appear to improve the [sustained viral response rate]. In our retrospective analysis the 'cure' rate improved form 37% to 63%."
John M. Vierling, M.D., of Baylor College of Medicine in Houston, commented that although Dr. Bader's findings are preliminary, they add to the "accumulating data that suggest that statins do not damage the liver so that patients with liver disease should not be denied the benefits of these drugs."
Television advertisements for statins routinely add the tag line that the drugs are not recommended for pregnant women or patients with liver disease, but Dr. Bader said that, too, might be changing. He said the FDA has quietly approved label changes for three statins -- simvastatin (Zocor), pravastatin (Pravachol), and lovastatin (Mevacor) -- eliminating the recommendation for regular liver function tests.
The prospective study tested four fluvastatin doses -- 80 mg, which is the FDA approved dose, 160 mg, 240 mg, and 320 mg.
The three patients with elevated ALT at baseline were randomized to three different dose groups.
A patient who had a baseline ALT of 81 IU/mL had an ALT of 68 IU/mL after 14 days of fluvastin at 80 mg/day (normal ALT < 64 IU/ml), and a patient who had the same baseline ALT dropped to 66 IU/ml after 14 days of fluvastain dosed at 160 mg/day. Seven days after statin therapy was stopped, the first patient had an ALT of 64 IU/ml, and the second patient had an ALT of 83 IU/mL.
A third patient who started the study with an ALT of 113 IU/mlL dropped to 90 IU/mL after 14 days at the 240 mg/day dose. Seven days after statin treatment was stopped, the patient's ALT was 104 IU/mL.
At all doses, there was no worsening of ALT values among patients with normal baseline ALT. That finding, Dr. Bader said, prompted him to examine retrospectively the effect of statin use on patients with chronic HCV.
He analyzed data from 60 HCV patients who were using statins and identified 13 who had elevated ALT values when they started statin therapy.
"Eleven of those 13 had improved ALT values since initiating statin therapy," he said. "The two who didn't have improvements had other risk factors -- alcohol use -- that may have contributed to the elevated ALT."
In a second retrospective study, he identified 104 patients who were undergoing standard peginterferon and ribavirin and compared their sustained viral response rate with the rate in patients who were using statins concurrently with peginterferon/ribavirin therapy.
Twenty-five patients were using simvastatin, two were taking lovastatin and two used atrovastatin (Lipitor). One patient used fluvastatin.
Dr. Bader's trials were funded by the VA.