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Yu C.-W.,Chang Gung University | Juan L.-I.,Buddhist Tzu Chi General Hospital Taipei Branch | Hsu S.-C.,Chang Gung University | Chen C.-K.,Chang Gung University | And 4 more authors.
American Journal of Emergency Medicine | Year: 2013

Background Infective endocarditis (IE) is a diagnostic challenge. We aimed to systemically summarize the current evidence on the diagnostic value of procalcitonin (PCT) in identifying IE. Methods We searched EMBASE, MEDLINE, Cochrane database, and reference lists of relevant articles with no language restrictions through September 2012 and selected studies that reported the diagnostic performance of PCT alone or compare with other biomarkers to diagnose IE. We summarized test performance characteristics with the use of forest plots, hierarchical summary receiver operating characteristic curves, and bivariate random effects models. Results We found 6 qualifying studies that included 1006 episodes of suspected infection with 216 (21.5%) confirmed IE episodes from 5 countries. Bivariate pooled sensitivity, specificity, positive likelihood ratios, and negative likelihood ratios were 64% (95% confidence interval [CI], 52%-74%), 73% (95% CI 58%-84%), 2.35 (95% CI 1.40-3.95), and 0.50 (95% CI 0.35-0.70), respectively. Of the 5 studies examining C-reactive protein (CRP), the pooled sensitivity, specificity, positive likelihood ratios, and negative likelihood ratios were 75% (95% CI 62%-85%), 73% (95% CI 61%-82%), 2.81 (95% CI 1.70-4.65), and 0.34 (95% CI 0.19-0.60), respectively. The global measures of accuracy, area under the receiver operating characteristic curve (AUC) and diagnostic odds ratio (dOR), showed CRP (AUC 0.80, dOR 8.55) may have higher accuracy than PCT (AUC 0.71, dOR 4.67) in diagnosing IE. Conclusions Current evidence does not support the routine use of serum PCT or CRP to rule in or rule out IE in patients suspected to have IE. © 2013 Elsevier Inc. Source


Cheng H.-R.,National Taiwan University | Liu C.-J.,National Taiwan University | Liu C.-J.,National Taiwan University Hospital | Tseng T.-C.,Buddhist Tzu Chi General Hospital Taipei Branch | And 6 more authors.
PLoS ONE | Year: 2013

Spontaneous clearance of hepatitis B surface antigen (HBsAg) in chronic hepatitis B (CHB) patients usually indicates a remission of hepatitis activity and a favorable outcome. Two single nucleotide polymorphisms (SNP), rs3077 near HLA-DPA1 region and rs9277535 near HLA-DPB1 region, have been shown to be associated with HBV persistence after acute HBV infection. However, little is known about the impact of these 2 SNPs on spontaneous HBsAg clearance in CHB patients. In this case-control study, a total of 100 male HBeAg-negative chronic HBV carriers who cleared HBsAg spontaneously (case group) and 100 age-matched HBeAg-negative male patients with persistent HBsAg positivity (control group) were enrolled. We investigated the relationship between these 2 SNPs and HBsAg clearance. There was a higher frequency of rs9277535 non-GG genotype in the case group (57% vs. 42%). Patients with rs9277535 non-GG genotype had a higher chance to clear HBsAg [Odds ratio (OR): 1.83, 95% confidence interval (CI): 1.04~3.21, P = 0.034]. Compared to GG haplotype of rs3077 and rs9277535, GA haplotype had a higher chance of achieving spontaneous HBsAg loss (OR: 2.17, 95% CI: 1.14~4.16, P = 0.030). In conclusion, rs9277535 non-GG genotype is associated with a higher likelihood of spontaneous HBsAg seroclearance in CHB patients. © 2013 Cheng et al. Source


Tseng T.-C.,Buddhist Tzu Chi General Hospital Taipei Branch | Liu C.-J.,National Taiwan University Hospital | Kao J.-H.,National Taiwan University Hospital
Current Pharmacogenomics and Personalized Medicine | Year: 2010

Infection due to hepatitis B virus (HBV) is a global public health issue. With effective treatment, it is possible to prevent disease progression to cirrhosis and hepatocellular carcinoma in chronic hepatitis B patients. Several viral factors have been documented to be associated with disease progression and treatment response, including HBV genotype and several naturally occurring HBV mutants, such as precore stop codon mutation (G1896A) and basal core promoter mutation (A1762T/G1764A). Recent studies suggested that responses to standard interferon or peginterferon are more favourable in patients infected with the HBV virus of genotype A or B than the genotype C or D infection. In contrast, therapeutic responses to nucleos(t)ide analogues are generally comparable between HBV genotypes. In addition to the viral genotype, BCP mutation (A1762T/G1764A) is likely to be associated with a higher sustained viral response in HBeAg-positive patients receiving interferon or peginterferon treatment. In conclusion, therapeutic differences seem to exist among HBV genotypes and genetic variations. However, the definite contribution of each viral factor still remains unclear. Since the majority of current studies included small numbers of patients and were not powered to answer such critical questions, the role of viral genetic variation for treatment outcomes awaits further studies before personalized treatment strategies can be planned. © 2010 Bentham Science Publishers Ltd. Source


Tseng T.-C.,Buddhist Tzu Chi General Hospital Taipei Branch | Tseng T.-C.,National Taiwan University Hospital | Tseng T.-C.,Tzu Chi University | Liu C.-J.,National Taiwan University Hospital | And 10 more authors.
Hepatology | Year: 2012

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. © 2011 American Association for the Study of Liver Diseases. Source


Tseng T.-C.,Buddhist Tzu Chi General Hospital Taipei Branch | Tseng T.-C.,National Taiwan University Hospital | Tseng T.-C.,Tzu Chi University | Liu C.-J.,National Taiwan University Hospital | And 10 more authors.
Gastroenterology | Year: 2012

Background & Aims: Patients with chronic hepatitis B virus (HBV) infection have a high risk for developing hepatocellular carcinoma (HCC). Patients with lower levels of hepatitis B surface antigen (HBsAg) have higher chances of losing HBsAg than those with high levels. However, little is known about whether higher levels of HBsAg increase risk for HCC. Methods: We followed 2688 Taiwanese HBsAg-positive patients without evidence of cirrhosis for a mean time period of 14.7 years. In addition to the known risk factors of HCC, we investigated the association between levels of HBsAg and development of HCC. Results: Of the patients followed, 191 developed HCC, with an average annual incidence rate of 0.5%. Baseline levels of HBsAg and HBV were associated with development of HCC, and risk increased with level. Compared to HBsAg level, by receiver operating characteristic curve analysis, HBV DNA level better predicted the development of HCC during 10-year and 15-year periods (both, P <.001). However, when we evaluated hepatitis B e antigen-negative patients with levels of HBV DNA <2000 IU/mL, factors that determined HCC risk included sex, age, and levels of alanine aminotransferase and HBsAg (<1000 IU/mL), but not level of HBV DNA. Multivariate analysis showed that the adjusted hazard ratio for HCC in patients with levels of HBsAg <1000 IU/mL versus <1000 IU/mL was 13.7 (95% confidence interval: 4.8-39.3). Conclusions: Among patients infected with HBV genotype B or C, determinants of HCC risk include their sex, age, hepatitis B e antigen status, HBV genotype, and levels of alanine aminotransferase and HBV DNA, but not level of HBsAg. Among hepatitis B e antigen-negative patients with low viral loads, HCC risk is determined by levels of HBsAg and alanine aminotransferase and age, but not HBV DNA. © 2012 AGA Institute. Source

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