Hepatitis B virus infection after renal transplantation in the presence of antibody to hepatitis B surface antigen immunity

[Guest guest]

Journal of Gastroenterology and Hepatology

Volume 19 Issue 8 Page 847 - August 2004

doi:10.1111/j.1440-1746.2003.03303.x

HEPATOLOGY

Hepatitis B virus infection after renal transplantation in the presence of

antibody to hepatitis B surface antigen immunity

KYUN-HWAN KIM*, SANG HOON AHN*,, HYO YOUNG CHUNG, YONG HAN PAIK*,, KWAN SIK

Lee, YU SEUN KIM*,, CHAE YOON CHON, YOUNG MYOUNG MOON AND KWANG-HYUB HAN*,

Abstract

Background and Aim: Hepatitis B virus (HBV) infection has been known to be

hampered by immunity against hepatitis B surface antigen (HBsAg). However,

HBV with mutations within the common antigenic epitope of HBsAg, the 'a'

determinant region, can escape from humoral immunity. Moreover, HBV

infection by 'a' determinant mutants in chronic HBV patients has been

reported after renal transplantation. In the present study, the authors

investigated HBV infection after renal transplantation despite passive

immunization or resolved HBV infection.

Methods: A total of 1682 patients who underwent a renal transplant between

1979 and 1998 at the Severance Hospital, Yonsei University College of

Medicine, Korea, were enrolled. The sequence of the HBV genome was analyzed

from two patients with antibody to HBsAg (anti-HBs) immunity.

Results: Of 1682 patients who were HBsAg negative before transplantation, 21

patients were found to be HBsAg positive, with elevated aspartate

aminotransferase and alanine aminotransferase levels after transplantation.

Interestingly, six of 21 (28.6%) patients were anti-HBs positive before the

transplantation. Sequence analysis of the cloned HBV from two of six

patients with anti-HBs immunity showed no evidence of significant mutations

within the 'a' determinant region, suggesting a wild-type of HBV. Their

donors were not exposed to HBV before transplantation (all HBV markers were

negative). Seven deaths of 21 patients were ascribed to HBV-related

complications.

Conclusions: Regardless of anti-HBs immunity, HBV infection occurred in

immunosuppressed patients in a high endemic area. The molecular mechanism

and clinical impact of HBV infection after renal transplantation in patients

with anti-HBs immunity should be further reappraised.

© 2004 Blackwell Publishing Asia Pty Ltd

[Guest guest]

Journal of Gastroenterology and Hepatology

Volume 19 Issue 8 Page 847 - August 2004

doi:10.1111/j.1440-1746.2003.03303.x

HEPATOLOGY

Hepatitis B virus infection after renal transplantation in the presence of

antibody to hepatitis B surface antigen immunity

KYUN-HWAN KIM*, SANG HOON AHN*,, HYO YOUNG CHUNG, YONG HAN PAIK*,, KWAN SIK

Lee, YU SEUN KIM*,, CHAE YOON CHON, YOUNG MYOUNG MOON AND KWANG-HYUB HAN*,

Abstract

Background and Aim: Hepatitis B virus (HBV) infection has been known to be

hampered by immunity against hepatitis B surface antigen (HBsAg). However,

HBV with mutations within the common antigenic epitope of HBsAg, the 'a'

determinant region, can escape from humoral immunity. Moreover, HBV

infection by 'a' determinant mutants in chronic HBV patients has been

reported after renal transplantation. In the present study, the authors

investigated HBV infection after renal transplantation despite passive

immunization or resolved HBV infection.

Methods: A total of 1682 patients who underwent a renal transplant between

1979 and 1998 at the Severance Hospital, Yonsei University College of

Medicine, Korea, were enrolled. The sequence of the HBV genome was analyzed

from two patients with antibody to HBsAg (anti-HBs) immunity.

Results: Of 1682 patients who were HBsAg negative before transplantation, 21

patients were found to be HBsAg positive, with elevated aspartate

aminotransferase and alanine aminotransferase levels after transplantation.

Interestingly, six of 21 (28.6%) patients were anti-HBs positive before the

transplantation. Sequence analysis of the cloned HBV from two of six

patients with anti-HBs immunity showed no evidence of significant mutations

within the 'a' determinant region, suggesting a wild-type of HBV. Their

donors were not exposed to HBV before transplantation (all HBV markers were

negative). Seven deaths of 21 patients were ascribed to HBV-related

complications.

Conclusions: Regardless of anti-HBs immunity, HBV infection occurred in

immunosuppressed patients in a high endemic area. The molecular mechanism

and clinical impact of HBV infection after renal transplantation in patients

with anti-HBs immunity should be further reappraised.

© 2004 Blackwell Publishing Asia Pty Ltd

[Guest guest]

Journal of Gastroenterology and Hepatology

Volume 19 Issue 8 Page 847 - August 2004

doi:10.1111/j.1440-1746.2003.03303.x

HEPATOLOGY

Hepatitis B virus infection after renal transplantation in the presence of

antibody to hepatitis B surface antigen immunity

KYUN-HWAN KIM*, SANG HOON AHN*,, HYO YOUNG CHUNG, YONG HAN PAIK*,, KWAN SIK

Lee, YU SEUN KIM*,, CHAE YOON CHON, YOUNG MYOUNG MOON AND KWANG-HYUB HAN*,

Abstract

Background and Aim: Hepatitis B virus (HBV) infection has been known to be

hampered by immunity against hepatitis B surface antigen (HBsAg). However,

HBV with mutations within the common antigenic epitope of HBsAg, the 'a'

determinant region, can escape from humoral immunity. Moreover, HBV

infection by 'a' determinant mutants in chronic HBV patients has been

reported after renal transplantation. In the present study, the authors

investigated HBV infection after renal transplantation despite passive

immunization or resolved HBV infection.

Methods: A total of 1682 patients who underwent a renal transplant between

1979 and 1998 at the Severance Hospital, Yonsei University College of

Medicine, Korea, were enrolled. The sequence of the HBV genome was analyzed

from two patients with antibody to HBsAg (anti-HBs) immunity.

Results: Of 1682 patients who were HBsAg negative before transplantation, 21

patients were found to be HBsAg positive, with elevated aspartate

aminotransferase and alanine aminotransferase levels after transplantation.

Interestingly, six of 21 (28.6%) patients were anti-HBs positive before the

transplantation. Sequence analysis of the cloned HBV from two of six

patients with anti-HBs immunity showed no evidence of significant mutations

within the 'a' determinant region, suggesting a wild-type of HBV. Their

donors were not exposed to HBV before transplantation (all HBV markers were

negative). Seven deaths of 21 patients were ascribed to HBV-related

complications.

Conclusions: Regardless of anti-HBs immunity, HBV infection occurred in

immunosuppressed patients in a high endemic area. The molecular mechanism

and clinical impact of HBV infection after renal transplantation in patients

with anti-HBs immunity should be further reappraised.

© 2004 Blackwell Publishing Asia Pty Ltd

[Guest guest]

Journal of Gastroenterology and Hepatology

Volume 19 Issue 8 Page 847 - August 2004

doi:10.1111/j.1440-1746.2003.03303.x

HEPATOLOGY

Hepatitis B virus infection after renal transplantation in the presence of

antibody to hepatitis B surface antigen immunity

KYUN-HWAN KIM*, SANG HOON AHN*,, HYO YOUNG CHUNG, YONG HAN PAIK*,, KWAN SIK

Lee, YU SEUN KIM*,, CHAE YOON CHON, YOUNG MYOUNG MOON AND KWANG-HYUB HAN*,

Abstract

Background and Aim: Hepatitis B virus (HBV) infection has been known to be

hampered by immunity against hepatitis B surface antigen (HBsAg). However,

HBV with mutations within the common antigenic epitope of HBsAg, the 'a'

determinant region, can escape from humoral immunity. Moreover, HBV

infection by 'a' determinant mutants in chronic HBV patients has been

reported after renal transplantation. In the present study, the authors

investigated HBV infection after renal transplantation despite passive

immunization or resolved HBV infection.

Methods: A total of 1682 patients who underwent a renal transplant between

1979 and 1998 at the Severance Hospital, Yonsei University College of

Medicine, Korea, were enrolled. The sequence of the HBV genome was analyzed

from two patients with antibody to HBsAg (anti-HBs) immunity.

Results: Of 1682 patients who were HBsAg negative before transplantation, 21

patients were found to be HBsAg positive, with elevated aspartate

aminotransferase and alanine aminotransferase levels after transplantation.

Interestingly, six of 21 (28.6%) patients were anti-HBs positive before the

transplantation. Sequence analysis of the cloned HBV from two of six

patients with anti-HBs immunity showed no evidence of significant mutations

within the 'a' determinant region, suggesting a wild-type of HBV. Their

donors were not exposed to HBV before transplantation (all HBV markers were

negative). Seven deaths of 21 patients were ascribed to HBV-related

complications.

Conclusions: Regardless of anti-HBs immunity, HBV infection occurred in

immunosuppressed patients in a high endemic area. The molecular mechanism

and clinical impact of HBV infection after renal transplantation in patients

with anti-HBs immunity should be further reappraised.

© 2004 Blackwell Publishing Asia Pty Ltd