JOURNAL OF CLINICAL AND EXPERIMENTAL HEPATOLOGY
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Conclusion: Telbivudine achieved a decline in mean HBsAg levels at week 4 in HBeAg positive as well as in cirrhotic patients. The HBV-DNA levels showed a rapid and statistically significant reduction at week 4.
S Balasubramanian, AS Velusamy, R Sigamani, RV Arcot, J Venkatraman Department of Medical Gastroenterology, Stanley Medical College, Chennai Background: Telbivudine (LdT) is approved for the treatment of chronic hepatitis B virus (CHB) infection. Aim: To assess the early response of telbivudine to hepatitis B surface antigen (HBsAg) and HBV-deoxyribonucleic acid (HBV-DNA) levels in CHB infection. Method: Forty patients with CHB were treated with Telbivudine (600 mg OD). The HBsAg levels were obtained at baseline, 4 weeks and 12 weeks while HBV-DNA levels at baseline and 4 weeks. Statistical analysis was done by using paired sample t-test. Result: In Group I (HBeAg positive: 17), the HBsAg levels showed a reduction from 4.24 + 1.32 log10 IU/mL to 0.47 log IU/mL and 0.57 log IU/mL at 4 weeks and 12 weeks, respectively. The baseline HBV-DNA levels (7.93 ± 1.16 log10 copies/mL) dropped to 2.38 log copies/mL at 4 weeks. None of them showed polymerase chain reaction (PCR) negativity. In Group II (HBeAg negative: 14), baseline HBsAg (3.93 + 0.61 log10 IU/mL), increased by 0.05 log IU/mL at 4 weeks with a subsequent decline of 0.03 log IU/mL at 12 weeks. The HBV-DNA levels (5.43 ± 1.01 log10 copies/mL) reduced to 2.23 log copies/mL at 4 weeks. Forty-three percent showed PCR negativity. In Group III (cirrhosis liver: 9), baseline HBsAg levels showed a reduction from 3.06 + 0.62 log10 IU/mL to 0.13 log IU/mL at 4 weeks and further to 0.09 log IU/mL at 12 weeks. The HBV-DNA levels (4.2 ± 2.62 log10 copies/mL) reduced to 1.21 log copies/mL. Thirty-four percent achieved polymerase chain reaction (PCR) negativity (Table 1).
13 OCCULT HEPATITIS B VIRAL INFECTION IN COASTAL ODISHA SP Singh1, S Kar1, SK Singh2, S Das2, R Panigrahi3, A Biswas2, R Chakravarty3 1 Department of Gastroenterology, SCB Medical College, Cuttack, 2Department of Zoology, Utkal University, Bhubaneswar, 3ICMR Virus Unit, ID and BG Hospital Campus, Kolkata, India Background and Aim: Occult hepatitis B virus (HBV) infection might transmit viremic units into the public blood supply if only hepatitis B surface antigen (HBsAg) testing is used for donor screening. The aim of our study was to evaluate the prevalence of occult HBV infection among the general population. Method: A total of 173 apparently healthy persons were included in this study. Assay for HBsAg and anti-HBc by enzyme-linked immunosorbent assay (ELISA) was performed in all the samples. All anti-HBc positive samples were amplified by in-house nucleic acid test (NAT) for detection of occult HBV infection, and genotyping and subgenotyping were performed after direct sequencing. Result: Out of 173, a total of 15 were anti-HBc positive. Of them, 9 were HBV-DNA positive by NAT. Thus, the HBV-DNA positivity among the general population was 8.67% and among anti-HBc positive group was 60%. Genotyping was done after sequencing of the surface gene, and it was found that all the samples were HBV/D genotype. The mutations identified in the major hydrophillic region were T127P, Q129R with Q129R as an escape mutant.
Table 1 The effect of telbivudine treatment on hepatitis B virus-deoxyribonucleic acid and hepatitis B e-antigen levels. HBeAg positive group HBV-DNA (quantitative) IU/mL Mean N
SD
HBsAg (quantitative) IU/mL P value
68,785,786.6
81,603,398.4
4 weeks
573,325.6
1,214,072.2
245,228.4
653,393.4
22,271.3
41,106.8
0.358
34,078.8
50,307.6
0.308
9 0.0000
12 weeks Reduction at 4 weeks
SD
17
Baseline
P value
Mean
68,212,461.03
Reduction at 12 weeks
222,957.1 211,149.6
HBeAg: hepatitis B e-antigen; HBsAg: hepatitis B surface antigen; HBV-DNA: hepatitis B virus-deoxyribonucleic acid; SD: standard deviation.
Journal of Clinical and Experimental Hepatology | March 2012 | Vol. 2 | Suppl 1 | S6–S39
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Abstracts
EARLY RESPONSE TO TELBIVUDINE IN TREATMENT-NAIVE PATIENTS WITH CHRONIC HEPATITIS B INFECTION