Increased hepatocellular carcinoma risk in chronic hepatitis B patients with persistently elevated serum total bile acid: a retrospective cohort study

Wang, Haoliang; Shang, Xiaoyun; Wan, Xing; Xiang, Xiaomei; Mao, Qing; Deng, Guohong; Wu, Yuzhang

doi:10.1038/srep38180

Cited by 20 publications

(15 citation statements)

References 32 publications

(40 reference statements)

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“…After adjustment, TBA and PIVKA-II were two variables that significantly influence the incidence of HCC for the most at-risk population and the hazard ratios were 1.918 (95% CI: 1.111–3.310, P = 0.019) and 0.433(95% CI: 0.277–0.678, P < 0.001). This was consistent with our previous study that constant high level of TBA increased the risk of HCC [ 25 ].…”

Section: Resultssupporting

confidence: 94%

Effectiveness of PIVKA-II in the detection of hepatocellular carcinoma based on real-world clinical data

Tan

Xiang

et al. 2017

BMC Cancer

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BackgroundProtein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II) is an efficient biomarker specific for hepatocellular carcinoma (HCC). Some researchers have proved that levels of PIVKA-II reflect HCC oncogenesis and progression. However, the effectiveness of PIVKA-II based on real-world clnical data has barely been studied.MethodsA total of 14,861 samples were tested in Southwest Hospital in over 2 years’ time. Among them, 4073 samples were PIVKA-II positive. Finally, a total of 2070 patients with at least two image examinations were enrolled in this study. Levels of AFP and PIVKA-II were measured by chemiluminescence enzyme immunoassay (CLEIA) and chemiluminescent microparticle Immunoassay (CMIA), respectively.ResultsA total of 1016 patients with HCC were detected by PIVKA-II in a real-world application. In all these cases, 88.7% cases primarily occurred and patients with advanced HCC covered 61.3%. Levels of PIVKA-II were significantly higher in advanced group (4650.0 mAU/ml, 667.0–33,438.0 mAU/ml) than early-stage group (104.5 mAU/ml, 61.0–348.8 mAU/ml; P < 0.001). Levels of PIVKA-II elevated significantly in recurrence and residual group than recovery group (P < 0.001). A total of 1054 PIVKA-II positive patients were non-HCC cases. Among them, cirrhosis took the largest part (46.3%), followed by hepatitis (20.6%) and benign nodules (15.3%). High-levels of PIVKA-II in at-risk patients is an indicator of HCC development in two-year time.ConclusionsOur data showed that PIVKA-II effectively increases the detection rate of HCC was a valid complement to AFP and image examination in HCC surveillance.

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Section: Resultssupporting

confidence: 94%

Effectiveness of PIVKA-II in the detection of hepatocellular carcinoma based on real-world clinical data

Tan

Xiang

et al. 2017

BMC Cancer

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“…2b 27 p : vaccination protection rate per year;0.85 (0.75−0.95) 20, 21, 27, 40 ε : perinatal infection rate per year;0.06 (0.03−0.09) 34–37 w : proportion of HBsAg positive mothers in the total prevalence of HBsAg aged 15–49 years;0.8491 (Calculated according to survey data in 1992) 15 q p :proportion of acute HBV infections that became chronic during delivery period;0.90 1, 34, 36 m a : age-specific mortality rate of HBV-related diseases per year;See Fig. 2c 21, 29–33 d a ( t ): age-specific total death rate in year t ;See Fig. 2d 22–26 1990 ≤ t ≤ 1995 d a ( t ) = d a (1990),1996 ≤ t ≤ 2002 d a ( t ) = d a (2000),2003 ≤ t ≤ 2007 d a ( t ) = d a (2005),2008 ≤ t ≤ 2014 d a ( t ) = d a (2010). μ a ( t ): age-specific death rate of non-HBV related diseases in year t ; μ a ( t ) = ( d a ( t ) N a ( t ) − m a C a ( t ))/ N a ( t ) 21–26, 29–33 θ a ( t ): catch-up vaccination coverage rate for adolescents in year t ;0.95 (For population aged 8–15 years in 2009–2011). 28 q a : age-specific proportion of acute HBV infections that became chronic per year; 1, 34, 36 0 ≤ a < 1 year0.301 ≤ a ≤ 4 years0.255 ≤ a ≤ 15 years0.0616 ≤ a ≤ 100 years0.03 β a (1992): age-specific transmission rate of HBV in 1992.See Fig.…”

Section: Methodsmentioning

confidence: 99%

“…2c 21, 29–33 d a ( t ): age-specific total death rate in year t ;See Fig. 2d 22–26 1990 ≤ t ≤ 1995 d a ( t ) = d a (1990),1996 ≤ t ≤ 2002 d a ( t ) = d a (2000),2003 ≤ t ≤ 2007 d a ( t ) = d a (2005),2008 ≤ t ≤ 2014 d a ( t ) = d a (2010). μ a ( t ): age-specific death rate of non-HBV related diseases in year t ; μ a ( t ) = ( d a ( t ) N a ( t ) − m a C a ( t ))/ N a ( t ) 21–26, 29–33 θ a ( t ): catch-up vaccination coverage rate for adolescents in year t ;0.95 (For population aged 8–15 years in 2009–2011). 28 q a : age-specific proportion of acute HBV infections that became chronic per year; 1, 34, 36 0 ≤ a < 1 year0.301 ≤ a ≤ 4 years0.255 ≤ a ≤ 15 years0.0616 ≤ a ≤ 100 years0.03 β a (1992): age-specific transmission rate of HBV in 1992.See Fig. 2e 15, 40

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Section: Methodsmentioning

confidence: 99%

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Estimating age-related incidence of HBsAg seroclearance in chronic hepatitis B virus infections of China by using a dynamic compartmental model

Zhuang

Liang

et al. 2017

Sci Rep

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The age-specific seroclearance pattern of hepatitis B surface antigen (HBsAg) in chronic hepatitis B virus (HBV) infections of China remains unclear. In this study, based on three national serosurvey data of hepatitis B in China, we propose an age- and time-dependent discrete model and use the method of non-linear least squares to estimate the age-specific annual rate of HBsAg seroclearance. We found that the HBsAg seroclearance in chronic HBV infections of China aged 1–59 years occurred at an average annual rate of 1.80% (95% CI, 1.54–2.06%) from 1993 to 2006. The HBsAg seroclearance occurred predominantly in the early childhood, 20–24 and 35–39 year age groups. Moreover, our model estimated that HBsAg seroclearance resulted in 23.38% of the decrease of total HBsAg prevalence for population aged 1–59 years in 2006. It also prevented 9.30% of new HBV infections (about 7.43 million people) and 9.95% of HBV-related deaths (about 0.25 million people) from 1993 to 2006. This study develops a new and efficient method to estimate the age-specific incidence of HBsAg seroclearance at a population-level and evaluate its effect.

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“…Factors including the gut microbiota (5), bile salt transporters (6) and nuclear receptor farnesoid-X-receptor (FXR) (7), participate in the regulation of BA homeostasis. Chronic cholestasis leads to fibrosis, cirrhosis, and eventually liver failure and hepatocellular/cholangiocellular carcinomas (7,8). Recent studies have shown that alterations in BA homeostasis occur in liver diseases.…”

Section: Introductionmentioning

confidence: 99%

Role of bile acids in the diagnosis and progression of liver cirrhosis: A prospective observational study

Liu

Jiao

et al. 2019

Exp Ther Med

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The accumulation of toxic bile acids (BAs) is closely related to liver injury, inflammation and tumorigenesis. The aim of the present study was to determine the role of the serum BA spectrum in the diagnosis and progression of liver cirrhosis. This was a prospective observational study involving patients with chronic hepatitis (n=23), liver cirrhosis (n=101), and cirrhosis complicated with hepatocellular carcinoma (CC-HCC; n=56). The 6-month survival of cirrhotic patients was recorded after blood collection. Comparisons of serum total BAs and individual BAs between different groups were performed using the Mann-Whitney U or Kruskal-Wallis tests. Correlation analysis was conducted by Spearman's correlation. Diagnosis and prediction analyses were performed using receiver operating characteristic curves. Survival was analyzed using the Kaplan-Meier method and multivariable Cox regression analysis. The concentrations of total BAs, glycocholic acid (GCA), glycochenodeoxycholic acid (GCDCA), taurocholic acid (TCA), taurochenoxycholic acid and tauroursodeoxycholic acid (TUDCA) were increased significantly in patients with early cirrhosis compared to patients with chronic hepatitis (P<0.05) and were associated with the diagnosis of cirrhosis (P=0.049, 0.004, 0.002, 0.003, 0.010 and 0.009, respectively). The levels of total BAs, primary conjugated BAs, and TUDCA increased as liver cirrhosis progressed (P<0.05). Serum total BAs, GCA, GCDCA, and TCA predicted the 6-month survival of patients with liver cirrhosis (P=0.0003, 0.005, 0.002, and 0.010 respectively). Based on multivariate Cox regression analysis, the level of total BAs was an independent predictor of mortality in cirrhotic patients (hazard ratios, 4.046; 95% CI, 1.620–10.108; P=0.003). In the early-stage cirrhosis group, the concentrations of total BAs and primary conjugated BAs were significantly elevated in patients with CC-HCC compared with patients with cirrhosis alone. In conclusion, total and individual BAs, especially primary conjugated BAs, are effective non-invasive markers in the diagnosis and prognosis of liver cirrhosis, and may be potential indicators in the occurrence of hepatocellular carcinoma in patients with early cirrhosis.

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Increased hepatocellular carcinoma risk in chronic hepatitis B patients with persistently elevated serum total bile acid: a retrospective cohort study

Cited by 20 publications

References 32 publications

Effectiveness of PIVKA-II in the detection of hepatocellular carcinoma based on real-world clinical data

Effectiveness of PIVKA-II in the detection of hepatocellular carcinoma based on real-world clinical data

Estimating age-related incidence of HBsAg seroclearance in chronic hepatitis B virus infections of China by using a dynamic compartmental model

Role of bile acids in the diagnosis and progression of liver cirrhosis: A prospective observational study

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