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Prospective Study on Lamivudine‐Resistant Hepatitis B in Renal Allograft Recipients
Author(s) -
Chan Tak Mao,
Tse Kai Chung,
Tang Colin S. O.,
Lai Kar Neng,
Ho Stephen K. N.
Publication year - 2004
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2004.00467.x
Subject(s) - lamivudine , medicine , gastroenterology , hbsag , hepatitis b virus , hepatitis b , decompensation , exacerbation , virology , virus
The natural history of lamivudine‐resistant hepatitis B virus (HBV) infection in renal transplant recipients (RTx) is unclear, despite its increasing incidence. Twenty‐nine HBsAg‐positive RTx with rising HBV DNA received lamivudine therapy. The course of lamivudine‐resistant HBV infection was studied prospectively. During 68.7 ± 12.5 months of follow‐up, 14 (48.3%) patients developed lamivudine resistance, at 10–35 months (mean 16.9 ± 7.0). All showed mutant sequences at codons 552 and 528 of the YMDD motif, while 13 patients demonstrated wild‐type sequence at codon 555. Lamivudine resistance was unrelated to patient demographics, HBeAg status/sero‐conversion, or genotype. Following resistance, HBV DNA and alanine aminotransferase showed an initial increase followed by spontaneous gradual reduction. The subsequent peak HBV DNA was lower (1.26 ± 1.09 × 10 9 vs. 6.26 ± 12.23 × 10 9 copies/mL, p = 0.011), while that of alanine aminotransferase was higher (196 ± 117 vs. 77 ± 47 iμ/l, p = 0.005), compared with pretreatment levels. Post‐resistance hepatitic flare occurred in 11 (78.6%) patients. This was transient in four (36.4%), but became chronic in six (54.5%) patients. Decompensation was noted in one patient during this flare, but all survived. We conclude that drug resistance is prevalent in lamivudine‐treated RTx. Despite a lower ensuing peak viremia compared with baseline, hepatitic flare is common. While most patients have spontaneous resolution, a minority may develop potentially fatal decompensation during the preceding exacerbation.