title: Response to interferon-alpha 2a in patients with e antigen-negative chronic hepatitis B.
abstract: Sixty-eight consecutive patients with chronic hepatitis B received 702 million units of recombinant interferon-alpha 2a. Of the 24 patients negative for hepatitis B e antigen (HBeAg) in serum, the normalization of serum transaminase occurred in 14 (58%) at the completion of interferon therapy and in 13 (54%) at 12 months thereafter; it was normalized in 17 (39%) and 13 (30%), respectively, of the 44 HBeAg-positive patients. Of the HBeAg-negative patients, hepatitis B virus DNA was cleared from serum in six (25%) at the completion and in one (4%) at 12 months thereafter, in contrast to only one (2%, p < 0.05) and none of the HBeAg-positive patients, respectively. The 1896th nucleotide of G (G1896) for codon 28 for tryptophan or A (A1896) for the stop codon 28 in the precore region was determined by restriction fragment length polymorphism. The ten HBeAg-negative patients with A1896 only in the precore region had lower pretreatment levels of viral markers, which decreased more rapidly and extensively after interferon than in the 14 HBeAg-negative patients with a mixture of G1896 and A1896 or in the 44 HBeAg-positive patients. These results indicate that patients with HBeAg-negative chronic hepatitis B may respond better to interferon than HBeAg-positive patients, and that the precore mutant with the stop codon 28 may be sensitive to interferon.
authors.affiliation: Fourth Department of Internal Medicine, Teikyo University Hospital at Mizonokuchi, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Kako
authors.forename: K
authors.initials: K
authors.lastname: Kanai
authors.forename: T
authors.initials: T
authors.lastname: Aikawa
authors.forename: S
authors.initials: S
authors.lastname: Iwabuchi
authors.forename: Y
authors.initials: Y
authors.lastname: Takehira
authors.forename: T
authors.initials: T
authors.lastname: Kawasaki
authors.forename: H
authors.initials: H
authors.lastname: Tsubouchi
authors.forename: K
authors.initials: K
authors.lastname: Hino
authors.forename: F
authors.initials: F
authors.lastname: Tsuda
authors.forename: H
authors.initials: H
authors.lastname: Okamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Miyakawa
authors.forename: M
authors.initials: M
authors.lastname: Mayumi
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000998:Antiviral Agents / Q000627:therapeutic use*; D004279:DNA, Viral / Q000032:analysis* / Q000097:blood; D005260:Female; D006513:Hepatitis B e Antigens / Q000097:blood*; D006515:Hepatitis B virus / Q000302:isolation & purification*; D019694:Hepatitis B, Chronic / Q000097:blood / Q000188:drug therapy*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D011994:Recombinant Proteins
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D006513:Hepatitis B e Antigens; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D000410:Alanine Transaminase