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Featured researches published by Tai-Chung Tseng.


Clinical Infectious Diseases | 2008

Pegylated Interferon-α-2a plus Ribavirin for Treatment-Naive Asian Patients with Hepatitis C Virus Genotype 1 Infection: A Multicenter, Randomized Controlled Trial

Chen-Hua Liu; Chun-Jen Liu; Chih-Lin Lin; Cheng-Chao Liang; Shih-Jer Hsu; Sheng-Shun Yang; Ching-Sheng Hsu; Tai-Chung Tseng; Chia-Chi Wang; Ming-Yang Lai; Jun-Herng Chen; Pei-Jer Chen; Ding-Shinn Chen; Jia-Horng Kao

BACKGROUND Comparable sustained virologic response (SVR) rates have been documented between Asian patients who received 24 weeks of pegylated interferon (IFN) plus ribavirin and white patients who received 48 weeks of combination therapy for hepatitis C virus genotype 1 (HCV-1) infection. Whether a 48-week course of combination therapy shows a better SVR rate than a 24-week course of such therapy among Asian patients with HCV-1 infection has not been confirmed in multicenter, randomized studies. METHODS In this multicenter, randomized trial, 308 treatment-naive HCV-1-infected Asian patients were randomly assigned to receive either 24 or 48 weeks of pegylated IFN-alpha-2a (180 microg per week) plus ribavirin (1000-1200 mg/day) therapy. The primary end point was SVR, defined as an undetectable serum HCV RNA level 24 weeks after discontinuation of therapy. In addition, rapid virologic response (RVR) was defined as an undetectable serum HCV RNA level at week 4 of therapy, and complete early virologic response was defined as an undetectable serum HCV RNA level at 12 weeks of therapy in the absence of RVR. RESULTS By intention-to-treat analysis, patients who received 48 weeks of therapy had a significantly higher SVR rate than did those who received 24 weeks of therapy (76% vs. 56%; P < .001). Among patients with a baseline serum HCV RNA level <800,000 IU/mL and RVR, SVR rates were comparable between 24- and 48-week courses of therapy (94% vs. 100%; P = .13). In contrast, 48 weeks of therapy was associated with a significantly higher SVR rate than was 24 weeks of therapy among patients without RVR (39% vs.16%; P = .01) and among those who achieved a complete early virologic response (44% vs. 20%; P = .02). CONCLUSIONS In treatment-naive Asian patients with HCV-1 infection, 48 weeks of pegylated IFN-alpha-2a plus ribavirin therapy is associated with a higher SVR rate, compared with 24 weeks of such therapy. Patients with a baseline serum HCV RNA level <800,000 IU/mL and who have achieved an RVR can receive a 24-week course of therapy without compromising the SVR rates; however, those who have not achieved an RVR but who have achieved a complete early virologic response should receive a 48-week course of therapy.


Hepatology | 2013

Serum hepatitis B surface antigen levels help predict disease progression in patients with low hepatitis B virus loads

Tai-Chung Tseng; Chun-Jen Liu; Hung-Chih Yang; Tung-Hung Su; Chia-Chi Wang; Chi-Ling Chen; Cheng-An Hsu; Stephanie Fang-Tzu Kuo; Chen-Hua Liu; Pei-Jer Chen; Ding-Shinn Chen; Jia-Horng Kao

Chronic hepatitis B patients with high viral loads are at increased risk of cirrhosis and hepatocellular carcinoma (HCC). In patients with low viral loads, higher hepatitis B surface antigen (HBsAg) levels have been shown to predict HCC development. However, little is known about the difference in risk for other hepatitis B virus (HBV)‐related adverse outcomes with varying HBsAg levels. A total of 1,068 Taiwanese hepatitis B e antigen (HBeAg)‐negative HBV carriers with serum HBV DNA level <2,000 IU/mL at baseline were followed for a mean duration of 13.0 years. Patients were categorized based on their HBsAg levels, and the relationships between HBsAg level and development of HBeAg‐negative hepatitis, hepatitis flare, and cirrhosis were investigated. Of the 1068 patients with low viral loads, 280 developed HBeAg‐negative hepatitis, with an annual incidence rate of 2.0%. HBsAg level, but not HBV DNA level, was found to be a risk factor for HBeAg‐negative hepatitis. Multivariate analysis showed that the adjusted hazard ratio in patients with an HBsAg level ≥1,000 versus <1000 IU/mL was 1.5 (95% confidence interval, 1.2–1.9). The positive correlation was present when evaluating other endpoints, including hepatitis flare and cirrhosis, and remained consistent when the study population was restricted to those with normal alanine aminotransferase (ALT) level at baseline. The annual incidence rate of HBeAg‐negative hepatitis was lowered to 1.1% in patients with low levels of HBV DNA, HBsAg, and ALT. Conclusion: In HBeAg‐negative patients with low viral loads and genotype B or C virus infection, a higher HBsAg level can predict disease progression. HBsAg <1,000 IU/mL in combination with low levels of HBV DNA and ALT help define minimal‐risk HBV carriers. (HEPATOLOGY 2013)


Hepatology | 2012

Determinants of spontaneous surface antigen loss in hepatitis B e antigen-negative patients with a low viral load.

Tai-Chung Tseng; Chun-Jen Liu; Hung-Chih Yang; Tung-Hung Su; Chia-Chi Wang; Chi-Ling Chen; Stephanie Fang-Tzu Kuo; Chen-Hua Liu; Pei-Jer Chen; Ding-Shinn Chen; Jia-Horng Kao

Loss of hepatitis B surface antigen (HBsAg) usually indicates the cure of hepatitis B virus (HBV) infection. In spontaneous hepatitis B e antigen (HBeAg) seroconverters, lower serum HBsAg and HBV DNA levels have been shown to be associated with HBsAg loss over time. However, little is known about their impacts on HBsAg loss in HBeAg‐negative patients with limited viral replication. A total of 688 HBeAg‐negative patients with baseline serum HBV DNA levels <2000 IU/mL were enrolled in Taiwan. The relationships of HBsAg and HBV DNA levels with subsequent HBsAg loss were investigated. In a mean follow‐up of 11.6 years, the average annual rate of HBsAg loss was 1.6%. Baseline HBsAg and HBV DNA levels were inversely associated with subsequent HBsAg loss. When compared to patients who had HBsAg levels >1000 IU/mL, the rates of HBsAg loss were significantly higher in patients with HBsAg levels of 100‐999, 10‐99, and <10 IU/mL, with hazard ratios of 2.5 (95% confidence interval [CI], 1.6‐4.0), 2.8 (95% CI, 1.6‐5.0), and 13.2 (95% CI, 8.1‐21.5), respectively. Multivariate analysis showed that HBsAg level, but not HBV DNA, remained as an independent factor. The adjusted hazard ratio of HBsAg loss was 13.2 (95% CI, 7.8‐22.1) for HBsAg level <10 versus ≥1000 IU/mL. When compared to HBV DNA level by receiver operating characteristic curve analysis, HBsAg level served as a better predictor of both 5‐year and 10‐year HBsAg loss. Conclusion: In HBeAg‐negative patients with HBV genotype B or C infection who have HBV DNA level <2000 IU/mL, HBsAg level <10 IU/mL is the strongest predictor of HBsAg loss. (HEPATOLOGY 2012;55:68–76)


Antiviral Therapy | 2010

Serum hepatitis B surface antigen concentration correlates with HBV DNA level in patients with chronic hepatitis B

Tung-Hung Su; Ching-Sheng Hsu; Chi-Ling Chen; Chen-Hua Liu; Yi-Wen Huang; Tai-Chung Tseng; Chun-Jen Liu; Pei-Jer Chen; Ming-Yang Lai; Ding-Shinn Chen; Jia-Horng Kao

BACKGROUND Serum HBV DNA level is crucial in the management of chronic hepatitis B (CHB); however, the assay is expensive and cannot be used widely. Therefore, we explored the possibility of hepatitis B surface antigen (HBsAg) quantification as a surrogate marker for HBV DNA level in CHB patients. METHODS A total of 289 CHB patients were enrolled, 251 were evaluated at baseline and 75 of them were also evaluated during anti-HBV treatment. Another 38 on-treatment patients were used for validation. Serum HBsAg titre was quantified by an immunoassay and HBV DNA level by a PCR-based method. Baseline and on-treatment data were analysed. RESULTS In parallel to log(10) HBV DNA, the log(10) HBsAg was high in both immune tolerance and immune clearance phases, and significantly decreased in the inactive carrier state and was again increased in the reactivation phase of the CHB infection. There was a positive correlation between log(10) HBsAg and log(10) HBV DNA, which was greater in patients with chronic hepatitis, hepatitis B e antigen-positivity, greater alanine aminotransferase or HBsAg levels at baseline and during pegylated interferon treatment. Log(10) HBsAg could predict log(10) HBV DNA independently. An HBsAg titre of >900 IU/ml at baseline or >1,500 IU/ml within the first year of treatment could predict an HBV DNA level of >20,000 IU/ml, especially in subgroups of chronic hepatitis with alanine aminotransferase levels >40 IU/l. The dynamics of HBsAg might also predict serial HBV DNA changes. In the validation group, 64% of patients with on-treatment HBV DNA levels >20,000 IU/ml could be correctly predicted. CONCLUSIONS Serum HBsAg concentration might serve as a surrogate marker of HBV DNA level in CHB patients.


Antiviral Therapy | 2011

Effect of host and viral factors on hepatitis B e antigen-positive chronic hepatitis B patients receiving pegylated interferon-α-2a therapy.

Tai-Chung Tseng; Ming-Lung Yu; Chun-Jen Liu; Chih-Lin Lin; Yi-Wen Huang; Ching-Sheng Hsu; Chen-Hua Liu; Stephanie Fang-Tzu Kuo; Corinna Jen-Hui Pan; Sheng-Shun Yang; Chien-Wei Su; Pei-Jer Chen; Ding-Shinn Chen; Jia-Horng Kao

BACKGROUND Pegylated interferon (PEG-IFN)-α-2a improves the hepatitis B e antigen (HBeAg) seroconversion rate in HBeAg-positive chronic hepatitis B patients. However, baseline factors predicting favourable responses to PEG-IFN-α-2a remain largely unknown. METHODS A total of 115 HBeAg-positive chronic hepatitis B patients who had a pre-therapy serum alanine aminotransferase (ALT) level over two times the upper limit of normal and received PEG-IFN-α-2a for 6-12 months were consecutively enrolled according to the local reimbursed guidelines. HBeAg seroconversion and combined response defined as HBeAg seroconversion, HBV-DNA level <20,000 IU/ml as well as ALT normalization at 6 months off therapy were primary and secondary therapeutic end points, respectively. Baseline viral factors, including viral load, genotype and major sequences of precore stop codon/basal core promoter (BCP), and host factors, including three single nucleotide polymorphisms among the HLA-DPA1, HLA-DPB1 and IL28B regions, were determined to correlate with therapeutic end points. RESULTS HBeAg seroconversion and combined response rates were 26.1% and 18.3%, respectively. By multivariate analysis, BCP mutation (OR 8.04, 95% CI 2.00-32.28) and rs3077 G/G genotype (OR 3.49, 95% CI 1.12-10.84) were associated with a higher HBeAg seroconversion rate; BCP mutation (OR 9.28, 95% CI 1.92-44.99) and baseline viral load <2 × 10(6) IU/ml (OR 4.78, 95% CI 1.37-16.69) were associated with a higher combined response rate. CONCLUSIONS BCP mutation is associated with higher HBeAg seroconversion and combined response rates at 6 months off therapy in HBeAg-positive chronic hepatitis B patients treated with PEG-IFN-α-2a. Genetic variants in the HLA-DPA1 region may also affect treatment-induced HBeAg seroconversion.


Gut | 2015

Higher proportion of viral basal core promoter mutant increases the risk of liver cirrhosis in hepatitis B carriers

Tai-Chung Tseng; Chun-Jen Liu; Hung-Chih Yang; Chi-Ling Chen; Wan-Ting Yang; Cheng-Shiue Tsai; Stephanie Fang-Tzu Kuo; Femke Carolien Verbree; Tung-Hung Su; Chia-Chi Wang; Chen-Hua Liu; Pei-Jer Chen; Ding-Shinn Chen; Jia-Horng Kao

Background and objective Precore (PC) variant (G1896A) and basal core promoter (BCP) variant (A1762T/G1764A) of HBV are associated with risk of hepatocellular carcinoma in HBV carriers. However, little is known about their impact on the adverse outcomes of hepatitis B e antigen (HBeAg)-negative hepatitis and liver cirrhosis. Methods 251 spontaneous HBeAg seroconverters who had genotype B or C infection and received a long-term follow-up were enrolled. PC and BCP mutants were determined qualitatively and quantitatively to correlate with these adverse outcomes. The findings were validated by an independent case–control study, which included 184 patients with biopsy-proven liver fibrosis stages. Results In the longitudinal cohort study, BCP mutant and possibly PC wild type were associated with cirrhosis development, but not HBeAg-negative hepatitis. Multivariable analysis showed that only BCP mutant was an independent risk factor for cirrhosis development. Using quantitative analysis of BCP mutant, a higher proportion of BCP mutant, defined as a continuous variable, a dichotomous variable or an ordinal variable, was associated with a higher risk of cirrhosis. If we chose 45% of BCP mutant as the cut-off, the risk of cirrhosis was higher in patients with BCP mutant ≥45% compared to <45% in the longitudinal cohort; this finding was validated by the case–control study (adjusted OR: 2.81, 95% CI 1.40 to 5.67). Conclusions A higher proportion of BCP mutant increases the risk of liver cirrhosis development in HBV carriers with genotype B or C infection.


Proceedings of the National Academy of Sciences of the United States of America | 2011

Association of IL28B gene variations with mathematical modeling of viral kinetics in chronic hepatitis C patients with IFN plus ribavirin therapy

Ching-Sheng Hsu; Shih-Jer Hsu; Hung-Chia Chen; Tai-Chung Tseng; Chen-Hua Liu; Wei-Fang Niu; Jenher Jeng; Chun-Jen Liu; Ming-Yang Lai; Pei-Jer Chen; Jia-Horng Kao; Ding-Shinn Chen

Asian patients with chronic hepatitis C (CHC) are known to have better virological responses to pegylated (Peg) IFN-based therapy than Western patients. Although IL28B gene polymorphisms may contribute to this difference, whether favorable hepatitis C virus (HCV) kinetics during treatment plays a role remains unclear. We enrolled 145 consecutive Taiwanese patients with CHC receiving Peg-IFN α-2a plus ribavirin for the study. Blood samples were taken more frequently at defined intervals in the first 3 d. Peg-IFN was administered at week 1. It was then administered weekly in combination with daily ribavirin for 24 or 48 wk. A mathematical model fitted to the observed HCV kinetics was constructed, which could interpret the transient HCV titer elevation after Peg-IFN treatment. The results demonstrated a comparable viral clearance rate (c = 3.45 ± 3.73) (day−1, mean ± SD) but lower daily viral production rate (P = 106–1012) in our patients than those reported previously in Western patients. Of 110 patients with a sustained virological response (SVR), 47 (43%) had a transient elevation of viral titer within 12 h (proportion of 12 h/3 d: 44% in non-SVR vs. 70% in SVR; P = 0.029). Among 91 patients with available rs8099917 data, patients with the TT genotype had an early surge of viral titer after therapy and a higher SVR and viral clearance rate than those with the GT genotype. In conclusion, Taiwanese patients with CHC receiving Peg-IFN plus ribavirin therapy have a lower daily viral production rate than Western patients, and the rs8099917 TT genotype may contribute to the increased viral clearance rate and better virological responses in these patients.


Proceedings of the National Academy of Sciences of the United States of America | 2013

Serum microRNA-122 level correlates with virologic responses to pegylated interferon therapy in chronic hepatitis C

Tung-Hung Su; Chen-Hua Liu; Chun-Jen Liu; Chi-Ling Chen; Te-Tien Ting; Tai-Chung Tseng; Pei-Jer Chen; Jia-Horng Kao; Ding-Shinn Chen

MicroRNA-122 (miR-122) facilitates hepatitis C virus replication in vitro. Serum miR-122 has been implicated as a biomarker for various liver diseases; however, its role in chronic hepatitis C remains unclear. To address this issue, 126 patients with chronic hepatitis C who completed pegylated IFN plus ribavirin therapy with sustained virologic response (SVR) or nonresponse (NR) were retrospectively included, and their pretreatment clinical profiles and treatment responses were collected. Serum miR-122 was quantified before and during treatment. Another 51 patients in SVR and NR groups were prospectively enrolled for validation. Serum miR-122 was found to be a surrogate for hepatic miR-122 and positively correlated with hepatic necroinflammation. Patients who showed complete early virologic response and SVR had significantly higher pretreatment serum miR-122 levels than those with NR (P = 0.001 and P = 0.008, respectively), especially in subgroups of patients with hepatitis C virus genotype 2 and IL-28B rs8099917 TT genotype. Patients with IL-28B TT genotype had significantly better treatment responses and higher pretreatment serum miR-122 level than those with GT or GG genotypes. Univariate analysis showed that pretreatment body mass index, γ-glutamyl transpeptidase, triglyceride, IL-28B TT genotype, and serum miR-122 are predictors for SVR. Multivariate analysis specifically in IL-28B TT genotype demonstrated that pretreatment serum miR-122 independently predicted SVR. The validation cohort confirmed a significantly greater pretreatment serum miR-122 level in patients with SVR compared with NR (P = 0.025). In conclusion, serum miR-122 may serve as a surrogate of hepatic miR-122, and a higher pretreatment serum miR-122 level can help predict virologic responses to pegylated IFN plus ribavirin therapy.


The Journal of Infectious Diseases | 2012

Serum Hepatitis B Virus-DNA Levels Correlate With Long-term Adverse Outcomes in Spontaneous Hepatitis B e Antigen Seroconverters

Tai-Chung Tseng; Chun-Jen Liu; Chi-Ling Chen; Chia-Chi Wang; Tung-Hung Su; Stephanie Fang-Tzu Kuo; Pei-Jer Chen; Ding-Shinn Chen; Jia-Horng Kao

BACKGROUND Hepatitis B e antigen (HBeAg) status and serum hepatitis B virus (HBV) DNA levels are major factors affecting the prognosis of adult HBV carriers; however, the impact of viral load on long-term outcomes after spontaneous HBeAg seroconversion remains unclear. METHODS A total of 390 spontaneous HBeAg seroconverters with a long-term follow-up were enrolled. Serum HBV-DNA levels at 1 year after HBeAg seroconversion were determined, and their correlation with long-term adverse outcomes was explored. RESULTS In a mean follow-up of 6.8 years, the average annual incidence rates were 4.4% and 1.9% for HBeAg-negative hepatitis and hepatitis flare, respectively. Compared with patients with HBV-DNA levels <200 IU/mL, the adjusted hazard ratios of HBeAg-negative hepatitis were 2.4 (95% confidence interval, 1.3-4.4), 3.6 (1.8-7.2), and 5.3 (2.8-10.0), respectively, for serum HBV-DNA level of 2000 -2 × 10(4), 2 × 10(4) -2 × 10(5), and ≥2 × 10(5) IU/mL. In addition, serum HBV-DNA levels were independently associated with HBeAg-negative hepatitis flare, which confirmed their impact on the immune active hepatitis after HBeAg seroconversion. CONCLUSIONS HBeAg seroconversion may not always confer favorable outcomes. Serum HBV-DNA levels ≥2000 IU/mL at 1 year post HBeAg seroconversion correlate with increased risk of HBeAg-negative hepatitis and hepatitis flare.


Antiviral Therapy | 2011

Interleukin 28B genetic polymorphisms and viral factors help identify HCV genotype-1 patients who benefit from 24-week pegylated interferon plus ribavirin therapy.

Chen-Hua Liu; Cheng-Chao Liang; Chun-Jen Liu; Tai-Chung Tseng; Chih-Lin Lin; Sheng-Shun Yang; Tung-Hung Su; Shih-Jer Hsu; Jou-Wei Lin; Jun-Herng Chen; Pei-Jer Chen; Ding-Shinn Chen; Jia-Horng Kao

BACKGROUND Interleukin 28B (IL28B) single nucleotide polymorphism (SNP) genotypes and viral factors can predict sustained virological response (SVR) in HCV genotype-1 (HCV-1) patients receiving 48 weeks of pegylated interferon and ribavirin. Whether these factors would identify those patients who can benefit from a shorter duration of therapy remains unclear. METHODS Treatment-naive HCV-1 patients (n=662) receiving 24 or 48 weeks of combination therapy were enrolled. Baseline demographic data, HCV viral load, IL28B SNP genotypes (rs8099917), duration of therapy and rapid virological response (RVR) were evaluated to predict SVR. The SVR rates were further stratified by the independent factors and compared. RESULTS The IL28B rs8099917 TT genotype, low baseline viral load (HCV RNA≤600,000 IU/ml), RVR and 48-week therapy independently predicted SVR. In RVR patients with the IL28B rs8099917 TT genotype, the SVR rate of 24-week therapy was comparable to 48-week therapy (95% versus 99%; P=0.21) at low baseline viral load, but was inferior to 48-week therapy (70% versus 97%; P<0.001) at high baseline viral load. In non-RVR patients, the SVR rate of 24-week therapy was inferior to 48-week therapy for those with the IL28B rs8099917 TT genotype but high baseline viral load (23% versus 62%; P<0.001), and those with the IL28B rs8099917 GT/GG genotype but low baseline viral load (0% versus 33%; P=0.02). CONCLUSIONS HCV-1 patients simultaneously bearing the IL28B rs8099917 TT genotype, low baseline viral load and RVR can benefit from a shorter duration of combination therapy.

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Jia-Horng Kao

National Taiwan University

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Ding-Shinn Chen

National Taiwan University

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Pei-Jer Chen

National Taiwan University

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Chun-Jen Liu

National Taiwan University

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Chen-Hua Liu

National Taiwan University

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Tung-Hung Su

National Taiwan University

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Hung-Chih Yang

National Taiwan University

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Chi-Ling Chen

National Taiwan University

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