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Long-Term Remission of Chronic Hepatitis B after Alpha-Interferon Therapy

Julia Korenman, MD; Bennie Baker, MD, PhD; Jeanne Waggoner, BA; James E. Everhart, MD; Adrian M. Di Bisceglie, MD; and Jay H. Hoofnagle, MD
[+] Article, Author, and Disclosure Information

Requests for Reprints: Jay H. Hoofnagle, MD, Division of Digestive Diseases and Nutrition, Building 31, Room 9A23, National Institutes of Health, Bethesda, MD 20892.

Current Author Addresses: Dr. Korenman: 1401 Blairmill Road #1703, Silver Springs, MD 20910.

Drs. Baker and Di Bisceglie and Ms. Waggoner: Liver Disease Section, National Institutes of Health, Building 10, Room 4D52, Bethesda, MD 20892.

Dr. Everhart: Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Disease, National Institutes of Health, Federal Building, Room 106, Bethesda, MD 20892.

Dr. Hoofnagle: Division of Digestive Diseases and Nutrition, National Institutes of Health, Building 31, Room 9A23, Bethesda, MD 20892.

Ann Intern Med. 1991;114(8):629-634. doi:10.7326/0003-4819-114-8-629
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Objective: To evaluate whether remissions of chronic hepatitis B induced by alpha-interferon therapy are of long duration.

Design: Cohort study.

Setting: Clinical Center of the National Institutes of Health, a tertiary referral center.

Patients: Sixty-four patients with chronic hepatitis B were treated with alpha-interferon between 1984 and 1986.

Main Outcome Measures: Patients were followed with frequent examinations and determinations of serum liver biochemical tests and hepatitis B virus (HBV) markers including hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), and HBV DNA using blot hybridization and polymerase chain reaction.

Results: Among 64 patients with chronic hepatitis B who were treated with alpha-interferon, 23 (36%) responded to treatment with loss of HBeAg and improvement in serum aminotransferases. All 23 have been followed for 3 to 7 years (mean, 4.3 years). During follow-up, 3 of 23 patients relapsed, with reappearance of HBeAg and abnormal serum aminotransferases, all within 1 year of therapy. The remaining 20 patients continued to have no detectable HBeAg or HBV DNA (using blot hybridization) in serum and to be asymptomatic for liver disease, although 3 had minimal elevations in serum aminotransferases. Thirteen patients (65%) became negative for HBsAg between 0.2 and 6 years (mean, 3 years) after loss of HBeAg. Although no patient had HBV DNA that was detectable by blot hybridization, the 7 patients who remained HBsAg positive all had HBV DNA in serum detected by polymerase chain reaction, but only 2 of 13 HBsAg-negative patients had viral genome using this method. Testing sequential samples indicated that HBV DNA detected by polymerase chain reaction usually disappeared at or around the time that test results for HBsAg became negative.

Conclusions: Remissions in chronic hepatitis B induced by alphainterferon are of long duration and are followed, in most patients, by the loss of HBsAg and all evidence of residual virus replication.





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