Reactivation of chronic hepatitis B virus infection by cancer chemotherapy

J. H. Hoofnagle, G. M. Dusheiko, D. F. Schafer, E. A. Jones, K. C. Micetich, R. C. Young, J. Costa

Research output: Contribution to journalArticle

347 Citations (Scopus)

Abstract

Two patients referred for cancer chemotherapy were found to be chronic, asymptomatic hepatitis B surface antigen (HBsAg) carriers. They had normal serum aminotransferase levels, but their sera were positive for HBsAg and antibody to hepatitis B e antigen. Both patients developed acute, icteric hepatitis within 3 months of starting cycled chemotherapy. In both cases, the disease seemed to be caused by a recurrence of type B hepatitis; it was accompanied by a marked increase in HBsAg titer and the appearance of hepatitis B virus DNA and DNA polymerase in the serum. One patient had a second episode of acute hepatitis after a second course of chemotherapy, but both patients ultimately recovered and became seronegative for HBsAg. Thus, it seems that cancer chemotherapeutic agents can reactivate type B hepatitis in asymptomatic HBsAg carriers. This reactivation is most likely due to an increase in hepatitis B virus synthesis followed by a rebound in host immune responses to hepatitis B virus infection when therapy is stopped. Such a phenomenon could have important implications for the therapy of chronic hepatitis B virus infection.

Original languageEnglish (US)
Pages (from-to)447-449
Number of pages3
JournalUnknown Journal
Volume96
Issue number4
DOIs
StatePublished - Jan 1 1982

Fingerprint

Chronic Hepatitis B
Virus Diseases
Hepatitis B Surface Antigens
Hepatitis B virus
Drug Therapy
Neoplasms
Hepatitis B
Hepatitis
Serum
Hepatitis B Antibodies
Hepatitis B e Antigens
DNA-Directed DNA Polymerase
Transaminases
Recurrence
DNA
Therapeutics

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Hoofnagle, J. H., Dusheiko, G. M., Schafer, D. F., Jones, E. A., Micetich, K. C., Young, R. C., & Costa, J. (1982). Reactivation of chronic hepatitis B virus infection by cancer chemotherapy. Unknown Journal, 96(4), 447-449. https://doi.org/10.7326/0003-4819-96-4-447

Reactivation of chronic hepatitis B virus infection by cancer chemotherapy. / Hoofnagle, J. H.; Dusheiko, G. M.; Schafer, D. F.; Jones, E. A.; Micetich, K. C.; Young, R. C.; Costa, J.

In: Unknown Journal, Vol. 96, No. 4, 01.01.1982, p. 447-449.

Research output: Contribution to journalArticle

Hoofnagle, JH, Dusheiko, GM, Schafer, DF, Jones, EA, Micetich, KC, Young, RC & Costa, J 1982, 'Reactivation of chronic hepatitis B virus infection by cancer chemotherapy', Unknown Journal, vol. 96, no. 4, pp. 447-449. https://doi.org/10.7326/0003-4819-96-4-447
Hoofnagle JH, Dusheiko GM, Schafer DF, Jones EA, Micetich KC, Young RC et al. Reactivation of chronic hepatitis B virus infection by cancer chemotherapy. Unknown Journal. 1982 Jan 1;96(4):447-449. https://doi.org/10.7326/0003-4819-96-4-447
Hoofnagle, J. H. ; Dusheiko, G. M. ; Schafer, D. F. ; Jones, E. A. ; Micetich, K. C. ; Young, R. C. ; Costa, J. / Reactivation of chronic hepatitis B virus infection by cancer chemotherapy. In: Unknown Journal. 1982 ; Vol. 96, No. 4. pp. 447-449.
@article{08a6d9845b9049db9fd92eeb06e447ef,
title = "Reactivation of chronic hepatitis B virus infection by cancer chemotherapy",
abstract = "Two patients referred for cancer chemotherapy were found to be chronic, asymptomatic hepatitis B surface antigen (HBsAg) carriers. They had normal serum aminotransferase levels, but their sera were positive for HBsAg and antibody to hepatitis B e antigen. Both patients developed acute, icteric hepatitis within 3 months of starting cycled chemotherapy. In both cases, the disease seemed to be caused by a recurrence of type B hepatitis; it was accompanied by a marked increase in HBsAg titer and the appearance of hepatitis B virus DNA and DNA polymerase in the serum. One patient had a second episode of acute hepatitis after a second course of chemotherapy, but both patients ultimately recovered and became seronegative for HBsAg. Thus, it seems that cancer chemotherapeutic agents can reactivate type B hepatitis in asymptomatic HBsAg carriers. This reactivation is most likely due to an increase in hepatitis B virus synthesis followed by a rebound in host immune responses to hepatitis B virus infection when therapy is stopped. Such a phenomenon could have important implications for the therapy of chronic hepatitis B virus infection.",
author = "Hoofnagle, {J. H.} and Dusheiko, {G. M.} and Schafer, {D. F.} and Jones, {E. A.} and Micetich, {K. C.} and Young, {R. C.} and J. Costa",
year = "1982",
month = "1",
day = "1",
doi = "10.7326/0003-4819-96-4-447",
language = "English (US)",
volume = "96",
pages = "447--449",
journal = "ImmunoMethods",
issn = "1046-2023",
publisher = "Academic Press Inc.",
number = "4",

}

TY - JOUR

T1 - Reactivation of chronic hepatitis B virus infection by cancer chemotherapy

AU - Hoofnagle, J. H.

AU - Dusheiko, G. M.

AU - Schafer, D. F.

AU - Jones, E. A.

AU - Micetich, K. C.

AU - Young, R. C.

AU - Costa, J.

PY - 1982/1/1

Y1 - 1982/1/1

N2 - Two patients referred for cancer chemotherapy were found to be chronic, asymptomatic hepatitis B surface antigen (HBsAg) carriers. They had normal serum aminotransferase levels, but their sera were positive for HBsAg and antibody to hepatitis B e antigen. Both patients developed acute, icteric hepatitis within 3 months of starting cycled chemotherapy. In both cases, the disease seemed to be caused by a recurrence of type B hepatitis; it was accompanied by a marked increase in HBsAg titer and the appearance of hepatitis B virus DNA and DNA polymerase in the serum. One patient had a second episode of acute hepatitis after a second course of chemotherapy, but both patients ultimately recovered and became seronegative for HBsAg. Thus, it seems that cancer chemotherapeutic agents can reactivate type B hepatitis in asymptomatic HBsAg carriers. This reactivation is most likely due to an increase in hepatitis B virus synthesis followed by a rebound in host immune responses to hepatitis B virus infection when therapy is stopped. Such a phenomenon could have important implications for the therapy of chronic hepatitis B virus infection.

AB - Two patients referred for cancer chemotherapy were found to be chronic, asymptomatic hepatitis B surface antigen (HBsAg) carriers. They had normal serum aminotransferase levels, but their sera were positive for HBsAg and antibody to hepatitis B e antigen. Both patients developed acute, icteric hepatitis within 3 months of starting cycled chemotherapy. In both cases, the disease seemed to be caused by a recurrence of type B hepatitis; it was accompanied by a marked increase in HBsAg titer and the appearance of hepatitis B virus DNA and DNA polymerase in the serum. One patient had a second episode of acute hepatitis after a second course of chemotherapy, but both patients ultimately recovered and became seronegative for HBsAg. Thus, it seems that cancer chemotherapeutic agents can reactivate type B hepatitis in asymptomatic HBsAg carriers. This reactivation is most likely due to an increase in hepatitis B virus synthesis followed by a rebound in host immune responses to hepatitis B virus infection when therapy is stopped. Such a phenomenon could have important implications for the therapy of chronic hepatitis B virus infection.

UR - http://www.scopus.com/inward/record.url?scp=0020079497&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020079497&partnerID=8YFLogxK

U2 - 10.7326/0003-4819-96-4-447

DO - 10.7326/0003-4819-96-4-447

M3 - Article

C2 - 7065560

AN - SCOPUS:0020079497

VL - 96

SP - 447

EP - 449

JO - ImmunoMethods

JF - ImmunoMethods

SN - 1046-2023

IS - 4

ER -