title: Interferon treatment for chronic hepatitis C infection in hemophiliacs--influence of virus load, genotype, and liver pathology on response.
abstract: In this study, we assessed the effectiveness of interferon treatment in 31 hemophiliacs with chronic hepatitis C virus (HCV) infection. Interferon alfa-2a (3 MU three times weekly) was administered for 6 months. Response was assessed by both serial alanine transaminase (ALT) and HCV RNA levels measured by a sensitive semiquantitative polymerase chain reaction (PCR) method. HCV genotype was determined by restriction fragment length polymorphism (RFLP), and evidence of changing genotypes during interferon therapy was sought. Severity of liver disease was assessed by both noninvasive and invasive methods, including laparoscopic liver inspection and biopsy. Sustained normalization of ALT levels occurred in eight patients (28%), and seven (24%) became nonviremic as assessed by PCR (<80 HCV/mL). Responders universally cleared HCV RNA within 2 months of starting interferon. Genotype 3a was associated with a favorable response to interferon. No evidence was found for a change in circulating genotype in patients who failed to respond to interferon or who relapsed. This study confirms that response rates to interferon are low in hemophiliacs as compared with other groups with chronic HCV infection. We have also demonstrated that virus load measurement over the first 8 to 12 weeks of treatment is an extremely useful method to identify responders at an early stage.
authors.affiliation: Department of Haematology, Royal Infirmary of Edinburgh, Scotland.
authors.forename: J P
authors.initials: JP
authors.lastname: Hanley
authors.forename: L M
authors.initials: LM
authors.lastname: Jarvis
authors.forename: J
authors.initials: J
authors.lastname: Andrew
authors.forename: R
authors.initials: R
authors.lastname: Dennis
authors.forename: P C
authors.initials: PC
authors.lastname: Hayes
authors.forename: J
authors.initials: J
authors.lastname: Piris
authors.forename: R
authors.initials: R
authors.lastname: Lee
authors.forename: P
authors.initials: P
authors.lastname: Simmonds
authors.forename: C A
authors.initials: CA
authors.lastname: Ludlam
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D015415:Biomarkers; D001706:Biopsy; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D015658:HIV Infections / Q000150:complications; D016174:Hepacivirus / Q000145:classification / Q000235:genetics / Q000302:isolation & purification; D006526:Hepatitis C / Q000150:complications / Q000201:enzymology / Q000473:pathology / Q000628:therapy* / Q000821:virology; D006521:Hepatitis, Chronic / Q000150:complications / Q000201:enzymology / Q000473:pathology / Q000628:therapy*; D006801:Humans; D007155:Immunologic Factors / Q000627:therapeutic use*; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008099:Liver / Q000201:enzymology / Q000473:pathology / Q000821:virology; D008103:Liver Cirrhosis / Q000209:etiology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood*; D011994:Recombinant Proteins; D012008:Recurrence; D017211:Treatment Failure; D014766:Viremia / Q000150:complications / Q000201:enzymology / Q000628:therapy*
chemical_list: D015415:Biomarkers; D007155:Immunologic Factors; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D000410:Alanine Transaminase