Serial HBV DNA levels in patients with persistently normal transaminase over 10 years following spontaneous HBeAg seroconversion

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2893.2011.01450.x/abstract

Serial HBV DNA levels in patients with persistently normal transaminase over 10

years following spontaneous HBeAg seroconversion

Y.-C. Chen1, S.-F. Huang2, C.-M. Chu1, Y.-F. Liaw1

Article first published online: 14 MAR 2011

DOI: 10.1111/j.1365-2893.2011.01450.x

© 2011 Blackwell Publishing Ltd

Issue

Journal of Viral Hepatitis

Early View (Articles online in advance of print)

Summary.  Earlier studies addressing the hepatitis B virus (HBV) DNA cut-off

level for inactive chronic HBV infection largely involved patients with normal

alanine aminotransferase (ALT) for only 1–2 years and based on a single time

HBV DNA assay. This study was conducted to address this issue using serial HBV

DNA assays in patients with persistently normal ALT (PNALT) over 10 years

following spontaneous hepatitis B e antigen (HBeAg) seroconversion. Serial serum

specimens (mean 9 samples per patient) of 62 patients with PNALT and no disease

progression over 10 years (median 18.1 years) after spontaneous HBeAg

seroconversion were assayed for HBV DNA. Excluding assays within 1 year after

HBeAg seroconversion, 21% and 82.3% of the patients with PNALT had HBV DNA

levels persistently lower than 4 log10 and 5 log10 copies/mL, respectively, and

only 8% had a level ≥5 log10 copies/mL in at least two assays. Of the 27

patients with PNALT defined by ALT <30 U/L for male and <19 U/L for female, only

33% had serum HBV DNA level persistently <4 log10 copies/mL. There was no

significant difference in the serial HBV DNA changes among patients with

different gender, HBV genotype or age at HBeAg seroconversion. Liver biopsy in

nine patients invariably showed minimal necroinflammation and one showed Ishak

fibrosis score 4. These results suggest that 5 log10 copies/mL (20 000 IU/mL) is

a more appropriate cut-off HBV DNA level for inactive chronic HBV infection in

the setting of PNALT.

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2893.2011.01450.x/abstract

Serial HBV DNA levels in patients with persistently normal transaminase over 10

years following spontaneous HBeAg seroconversion

Y.-C. Chen1, S.-F. Huang2, C.-M. Chu1, Y.-F. Liaw1

Article first published online: 14 MAR 2011

DOI: 10.1111/j.1365-2893.2011.01450.x

© 2011 Blackwell Publishing Ltd

Issue

Journal of Viral Hepatitis

Early View (Articles online in advance of print)

Summary.  Earlier studies addressing the hepatitis B virus (HBV) DNA cut-off

level for inactive chronic HBV infection largely involved patients with normal

alanine aminotransferase (ALT) for only 1–2 years and based on a single time

HBV DNA assay. This study was conducted to address this issue using serial HBV

DNA assays in patients with persistently normal ALT (PNALT) over 10 years

following spontaneous hepatitis B e antigen (HBeAg) seroconversion. Serial serum

specimens (mean 9 samples per patient) of 62 patients with PNALT and no disease

progression over 10 years (median 18.1 years) after spontaneous HBeAg

seroconversion were assayed for HBV DNA. Excluding assays within 1 year after

HBeAg seroconversion, 21% and 82.3% of the patients with PNALT had HBV DNA

levels persistently lower than 4 log10 and 5 log10 copies/mL, respectively, and

only 8% had a level ≥5 log10 copies/mL in at least two assays. Of the 27

patients with PNALT defined by ALT <30 U/L for male and <19 U/L for female, only

33% had serum HBV DNA level persistently <4 log10 copies/mL. There was no

significant difference in the serial HBV DNA changes among patients with

different gender, HBV genotype or age at HBeAg seroconversion. Liver biopsy in

nine patients invariably showed minimal necroinflammation and one showed Ishak

fibrosis score 4. These results suggest that 5 log10 copies/mL (20 000 IU/mL) is

a more appropriate cut-off HBV DNA level for inactive chronic HBV infection in

the setting of PNALT.