Hepatology Oct 2000 A1570|
Decompensated hepatitis C cirrhotic patients can be safely treated
with titrated doses of interferon and ribavirin; they have a highly
significant HCV-RNA response to treatment
Bennet Cecil MD and Tami Hill MD, Hepatitis C Treatment Centers, INC
Mary Lavelle ARNP Louisville VAMC
Introduction: Decompensated hepatitis C cirrhosis is a lethal illness killing 8,000-10,000 US patients each year. In addition, many of the 14,500 patients dying from liver cancer each year have hepatitis C as the etiology. Effective antiviral therapy can prevent unnecessary deaths, but most physicians are unwilling to treat patients with decompensated hepatitis C cirrhosis with interferon. They fear causing liver failure as seen in interferon treatment of hepatitis B cirrhosis. Instead, the current practice is to avoid antiviral treatment of decompensated hepatitis C. Patients are simply placed on an ever-lengthening list for liver transplantation. Many die because there is a shortage of donor livers. We report safe and successful treatment of decompensated hepatitis C cirrhotics using titrated doses of interferon and ribavirin. This strategy can allow some patients to at least partially reverse their cirrhosis. Transplantation may be avoided, or if still needed, prevention of reinfection of the donor liver.
Methods: Since January 1999, we have offered patients with decompensated hepatitis C cirrhosis (ascites, bleeding esophageal varices or encephalopathy) individualized titrated antiviral treatment. Patients were referred for concurrent liver transplantation evaluation and for endoscopy. Those with large varices received beta-blockers or had prophylactic esophageal band ligation. Patients were generally started on 480,000 units of Roferon® or Intron A® daily and 0-600mg of ribavirin daily. Ribavirin induced hemolysis produces jaundice in cirrhotic patients so ribavirin was usually added after several weeks of interferon. Patients were followed weekly, then biweekly and later monthly. The absolute neutrophil count was kept above 500, and the platelet count above 20,000. The HCV-RNA was measured before treatment, 4 weeks later and periodically thereafter. Medication changes were made slowly and gradually as indicated by the patient’s response. The goal of therapy was to reach an HCV-RNA <100 copies/ml and to continue treatment for at least an additional 20 weeks.
Results: Nine patients with decompensated hepatitis C cirrhosis have been treated. The mean log of the pretreatment HCV was 5.045, stand dev 0.885, range, 3.744-6.518. The mean log of HCV-RNA during treatment fell to 3.307; stand dev 1.197, range, 1.740-5.484. The log of HCV-RNA fell significantly with Rx by paired-t test P=0.0004, StatView for Windows SAS Institute Inc. v. 5.0.1. There were no deaths in treated patients. No episodes of serious bleeding occurred in spite of platelet counts less than 30,000.
Conclusion: Decompensated hepatitis C cirrhosis is a lethal illness. Unlike patients with decompensated hepatitis B cirrhosis, patients with decompensated hepatitis C cirrhosis can be safely treated using individualized, titrated doses of inteferon. Ribavirin can be added later to improve the likelihood of success. We have demonstrated a significant fall in the log HCV RNA (P=0.004) with antiviral treatment. A substantial proportion of patients responds to treatment and sustained viral responders are anticipated. Esophageal varices are the major risk of serious bleeding in advanced hepatitis C cirrhosis-not thrombocytopenia from interferon. Experienced physicians should offer carefully titrated antiviral therapy to their patients with decompensated hepatitis C cirrhosis. This strategy can reduce the death rate from hepatitis C and hopefully the need for liver transplantation in some patients.