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REPLY
Sequelae and Serologic Outcome in Persons with Hepatitis B Virus Infection
Brian J. McMahon, MD, and
Lisa Bulkow, MS
1 October 2002 | Volume 137 Issue 7 | Page 619
IN RESPONSE:
Drs. Cainelli and Vento correctly point out that information regarding HBV DNA levels in HBsAg-positive persons would be important in understanding the natural history of HBV. Knowledge of HBV genotype, presence or absence of precore variant, and liver aminotransferase levels could also be helpful in selecting patients for treatment (1, 2). When our study began in 1982, HBV DNA levels were not readily obtainable. In addition, HBV DNA levels alone are not sufficient to determine whether progressive liver damage is present. Aminotransferase levels, the more important indicator, along with HBV DNA levels above 100 000 copies/mL, correlate with ongoing clinical hepatitis on biopsy (3).
We were unable to determine aminotransferase levels in our patients because before 2000 most villages did not have centrifuges, and aminotransferase levels are not stable unless blood specimens are separated immediately. A recent practice guideline from the American Association for the Study of Liver Diseases does not recommend that HBV DNA levels be obtained in persons with inactive HBV (those who are positive for anti-HBe but have normal aminotransferase levels) (4). In 1992, we tested alanine aminotransferase levels within 36 hours of sampling in 192 carriers, 115 males and 77 females, who were from 17 villages and were between 10 and 70 years of age. Levels were normal in 131 of 162 anti-HBe–positive carriers (80.9%) but elevated in 18 of 30 of HBeAg–positive carriers (60%) (P > 0.01). This finding suggests that most Alaska natives with chronic HBV infection who seroconvert from HBeAg to anti-HBe do not have active hepatitis.
We have embarked on a 4-year prospective study to examine HBV DNA levels, genotypes, and precore mutants in persons in our population with chronic HBV infection. We hope that information gained from this study will address the important issue that Drs. Cainelli and Vento have raised, namely identifying which carriers could be targeted for antiviral therapy.
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Author and Article Information
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Alaska Native Medical Center; Arctic Investigation Program; Centers for Disease Control and Prevention Anchorage, AK 99508-5902 (McMahon, Bulkow)
1. Kao JH, Chen PJ, Lai MY, Chen DS. Hepatitis B genotypes correlate with clinical outcomes in patients with chronic hepatitis B Gastroenterology. 2000;118:554-9. [PMID: 10702206].[Medline]
2. Rodriguez-Frias F, Buti M, Jardi R, Cotrina M, Viladomiu L, Esteban R, et al. Hepatitis B virus infection: precore mutants and its relation to viral genotypes and core mutations Hepatology. 1995;22:1641-7. [PMID: 7489968].[Medline]
3. Lindh M, Horal P, Dhillon AP, Norkrans G. Hepatitis B virus DNA levels, precore mutations, genotypes and histological activity in chronic hepatitis B J Viral Hepat. 2000;7:258-67. [PMID: 10886534].[Medline]
4. Lok AS, McMahon BJ. Chronic hepatitis B Hepatology. 2001;34:1225-41. [PMID: 11732013].[Medline]
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