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. 2011 Oct 1;11(10):835–842. doi: 10.5812/kowsar.1735143X.775

Table 1. Demographic Data and Clinical Features of Patients in Each Study Group.

aAdd-on Strategy, (n = 88) Switch Strategy, (n = 106)
Male, No. (%) 66 (75) 70 (66)
Age, median y (range) 45 (13–68) 38 (16–61)
HBeAg positive, No. (%) 30 (34) 36 (33.9)
ALT b, median U/L (range) 68 (16–537) 84 (12–1082)
AST b, median U/L (range) 61 (14–709) 55 (13–579)
HBV DNA, median log10 IU/mL (range) 4.4 (2.0–6.0) 3.8 (2.0–6.1)
HBV subgenotype D, No. (%)
D1 74 (84) 82 (77)
D2 12 (14) 12 (11)
D3 2 (2) 10 (10)
D4 0 (0) 2 (2)
History of chronic hepatitis B infection
Patients in the immune-tolerant phase 24 22
Patients in the immune-reactive phase 6 14
HBeAg-negative patients 58 70
Biopsy status
Patients with Knodell fibrosis scores 40 72
Patients without biopsy 48 34
Therapy status c
LAM b to LAM + ADV b 74 -
ADV to ADV + ETV b 14 -
LAM to ADV + ETV - 12
LAM to ADV + TDF b - 10
LAM to ETV - 24
ADV to ETV - 30
Treatment duration, median mon (range)
LAM 28.7 (3–60) 24.8 (2–126)
LAM + ADV 23.3 (6–48) -
ADV - 13.1 (3–36)
ADV + ETV 16 (6–22) -
ETV - 11.4 (6–24)

a Serological markers of all patients were found to be negative for hepatitis C virus and hepatitis D virus.

b Abbreviations: ADV, adefovir dipivoxil; ALT, alanine aminotransferase; AST, aspartate aminotransferase; ETV, entecavir; LAM, lamivudine; TDF, tenofovir disoproxil fumarate.

c The combination of NUCs used was selected according to the emergence of drug resistance (primary or compensatory resistance) or clinical and/or virological breakthrough.