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Meeting Ieee 519-1992 Harmonic Limits

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7. Wright TL, Mamish D, Combs C, et al. Hepatitis B virus and apparent fulminant non-A, non-B hepatitis. Lancet 1992; 339: 952. 8. Omata M, Ehata T, Yokosuka O, et al. Mutations in the precore region of hepatitis B virus DNA in patients with fulminant and severe hepatitis. N Engl J Med 1991; 324:1699. 9. Liang TJ, Hasegawa K, Rimon N, et al. A hepatitis B virus mutant associated with an epidemic of fulminant hepatitis. N Engl J Med 1991; 324:1705. 10. Ritt DJ, Whelan G, Werner DJ, et al. Acute hepatic necrosis with stupor and coma.

Liver disease is inactive in these patients as documented by normal ALT levels and resolution of inflammation on liver biopsies. There may also be regression of fibrosis in some patients who have sustained HBeAg seroconversion. HBV DNA is usually undetectable by hybridization assays but positive with PCR assays except in those individuals who lose HBsAg (60). 0% per year (61, 62). Because of the presence of small amounts of virus in the liver, institution of immunosuppres- 20 Figure 6 Hussain and Lok Natural history of adult acquired chronic HBV infection.

Akarca US, Lok ASF. Naturally occuring hepatitis B virus core gene mutations. Hepatology 1995; 22:50. 71. Brunetto MR, Giarin M, Saracco G, et al. Hepatitis B virus unable to secrete e antigen and response to interferon in chronic hepatitis B. Gastroenterology 1993; 105:845. 72. Chan HL, Hussain M, Lok AS. Different hepatitis B virus genotypes are associated with different mutations in the core promoter and precore regions during hepatitis B e antigen seroconversion. Hepatology 1999; 29(3):976.

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