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Natural History of Hepatitis B Virus Infection in Renal Transplant Recipients–A Fifteen‐Year Follow‐Up
Author(s) -
Dusheiko Geoffrey,
Song Ernest,
Bowyer Sheila,
Whitcutt Michael,
Maier Gunthild,
Meyers Anthony,
Kew Mlchael C.
Publication year - 2007
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840030309
Subject(s) - hbeag , hbsag , medicine , hepatitis b virus , immunosuppression , transplantation , virology , hepatitis b , immunology , liver transplantation , hbcag , hepadnaviridae , hepatitis , kidney transplantation , virus , gastroenterology
Hepatitis B virus (HBV) markers were measured in 83 immunosuppressed renal transplant patients who were followed for periods of 2 to 15 years. Sixty‐nine patients were negative for HBsAg before transplantation, of whom 14 were positive for anti‐HBs. The remaining 14 patients were HBsAg positive prior to transplantation. Eighteen patients were identified as being HBsAg positive during the follow‐up period. Four patients acquired primary type B hepatitis; one died of submassive hepatic necrosis and the remaining three became chronic HBV carriers with positive HBeAg, DNA polymerase, and HBV DNA. Several patterns of HBV expression were observed in HBsAg‐positive patients. Four patients were HBsAg, HBeAg, DNA polymerase, and HBV DNA positive prior to transplantation, and these markers persisted. Reactivation of HBV replication occurred in eight patients, seven of whom were HBsAg positive and HBeAg and anti‐HBe negative originally; one patient was anti‐HBc positive. A single patient was HBsAg and anti‐HBe positive and remained so for 22 months. The remaining previously HBsAg‐positive patient is currently HBsAg negative. These serological data suggest that reactivation of HBV replication or continued hepatitis B virion replication occurs as commonly or more commonly than de novo infection in renal transplant recipients. The presence of HBeAg in serum predisposes to long‐term Dane particle expression in immunosuppressed patients, whereas anti‐HBe‐positive carriers may not always be susceptible to reactivation of HBV replication despite immunosuppression.