Analysis of HBV DNA level _data

HBV indicates that antigen-positive is the most important risk factor for HCC

Seropositivity for the hepatitis B surface antigen (HBsAg) are one of the most important risk factors for hepatocellular CA Rcinoma

HBV e antigen positive will increase the risk of HCC

In we previous study, seropositivity for the hepatitis B e antigen (HBeAg) is associated with a increased risk for HEPA Tocellular carcinoma.

The increased hepatocellular carcinoma risk in individuals seropositive for HBEAG remained significant regardless of serum Level of alanine aminotransferase (ALT) and status of Liver cirrhosis.8,9

Serum HBV DNA level was used as a criterion for antiviral treatment in patients with chronic hepatitis B. Effective Suppres Sion of Serum HBV DNA is a marker of efficacy for antiviral therapy

Multivariate regression analysis of risk predictors of hepatocellular carcinoma, increasing HBV DNA levels were the strongest independent predictors.

In multivariate Cox regression analyses
of risk factors predicting progression to liver cirrhosis,
Increasing HBV DNA level is the strongest independent
Predictor.

The degree of DNA replication does not mean that the actual damage to the liver, the degree of DNA replication is high, does not mean that the damage is serious.

Patients with HCC had higher
Serum HBV DNA levels at study entry than patients with
Cirrhosis who remained hcc-free during follow-up

The findings of cohort studies on the association between
Serum HBV DNA levels and HCC risk is summarized
In Table 3.

Decreased HBV DNA in the blood and improved liver significantly

More importantly, improvement in histological
Grade was strongly correlated with a decrease in serum
HBV DNA levels (R 0.96; P 0.001).

In four caseseries
Studies on the recurrence of HCC after surgical resection34,38,39
or transarterial chemolipidolization,37 patients
Serum HBV DNA levels at study entry had a
Significantly higher risk of HCC recurrence than those with
Low levels.

In multivariate Cox regression
Analyses of risk factors predicting progression to mortality,
Increasing HBV DNA level is the strongest
Independent predictor of death from chronic liver disease
and cirrhosis, and is second to cirrhosis in predicting
Death from HCC. There was no association between serum
HBV DNA levels and non–liver related mortality.

Recent unpublished data from this study, using
Data on serum HBV DNA and ALT levels at multiple
Time points and time-dependent regression modeling,
Confirm that elevated serum HBV DNA at multiple time
Points is indeed a very strong independent predictor of
HCC risk.44

http://www.ncbi.nlm.nih.gov/pubmed/23094699

HCC Risk Factors: Male, age increase, transaminase elevated, HBV e antigen positive, Hbv-dna high, HBV C-segment gene infection, core gene mutation

. In this community-based cohort study, male gender, older age, high serum alanine aminotransferase level, positive Hepatiti S B e antigen, higher Hbv-dna level, HBV genotype C infection, and core promoter mutation is independently associated wit H a higher risk of HCC.

While Hbv-dna level had better predictive accuracy than HBsAg level, when investigating the overall cohort in patients wit H Hbv-dna Level < iu/ml, HBsAg level≥1000 iu/ml is identified as a new independent risk factor for HCC

DNA refers to DNA, the replication of the virus is done by DNA replication, the higher the concentration of DNA, the more active replication of the virus. Together, Hbv-dna refers to the DNA of the hepatitis B virus. HBV DNA detection is a common means to judge the replication of HBV virus. In general, the value of more than 10 of 3 is positive, the 3-5 is considered to be low-volume replication, 5-7 Medium, greater than 7 times for a large number. Second liver two halves and can not accurately judge the virus replication situation, DNA make up for this insufficiency. However, due to the strict requirements of DNA testing technology, susceptible to interference, therefore, a result is not enough to explain the problem, met positive, you can change the hospital to check again.

DNA testing

Edit

Previous indications of antiviral treatment of hepatitis B patients are: Hepatitis B virus E antigen positive (big) patients Hbvdna value of 10 of the 5-copy/ml (20000U/ML), hepatitis B virus e antigen negative (applied) patients with hepatitis B virus DNA requirements to 10 4 copies/ ML (2000u/ml), but 10 of the 4-copy/ml below can not be considered to be no problem, the latest international Research data show: The liver disease progression associated with the virus DNA level domain value is unclear, even if the Hbvdna level continues to be less than 20000u/ml, May also be the hepatitis B virus is still further development, so the Hbvdna value should be lower the better, the current international recommended Hbvdna test should be:< 50u/ml 5, Other: HBV DNA test results to a certain extent can help to determine whether the hepatitis B virus produced a mutation, If in the course of the treatment of HBV DNA test results from negative to positive, it is suggested that the virus has undergone mutation, should be combined with specific conditions to re-select antiviral drugs.

participants with persistent elevation of serum HBV DNA level during follow-up had the highest hepatocellular carcinom A risk. Conclusion elevated serum HBV DNA level (≥10 copies/ml) is a strong risk predictor of hepatocellular CARC iNOMA independent of HBeAg, serum alanine aminotransferase level, and liver cirrhosis

Context Serum hepatitis B virus (HBV) DNA level was a marker of viral replication and efficacy of antiviral treatment in individual s with chronic hepatitis B.

Objective To evaluate the relationship between serum HBV DNA level and risk of hepatocellular carcinoma.

Design, Setting, and participants Prospective cohort Study of 3653 participants (aged 30-65 years), who were seropositive for the hepatitis B surface Antige N and seronegative for antibodies against the hepatitis C virus, recruited to a community-based cancer screening program I n Taiwan between 1991 and 1992.

Main outcome Measure Incidence of hepatocellular carcinoma during follow-up examination and by data linkage with the National Cancer Registry A nd the death certification systems.

ResultsThere were 164 incident cases of hepatocellular carcinoma and 346 deaths during a mean follow-up of 11.4 years and 41 779 Person-years of follow-up. The incidence of hepatocellular carcinoma increased with serum HBV DNA level at study entry in a dose-response Relationshi P ranging from 108 per person-years for a HBV DNA level of less than copies/ml to 1152 per Person-yea RS for a HBV DNA level of 1 million copies/ml or greater. The corresponding cumulative incidence rates of hepatocellular carcinoma were 1.3% and 14.9%, respectively. The biological gradient of hepatocellular carcinoma by serum HBV DNA levels remained significant (P<.001) after adjustment for sex, age, cigarette smoking, alcohol consumption, serostatus for the hepatitis B e antigen (HBeAg), serum alanine aminotransferase level, and liver cirrhosis at study entry. The dose-response relationship was, prominent for participants, were seronegative for HBeAg with normal serum Alani NE aminotransferase levels and no liver cirrhosis at study entry. Participants with persistent elevation of serum HBV DNA level during follow-up had the highest hepatocellular carcinoma ri Sk.

Conclusion Elevated serum HBV DNA level (≥10 copies/ml) is a strong risk predictor of hepatocellular carcinoma independent of HBe Ag, serum alanine aminotransferase level, and liver cirrhosis.

more than million persons in the world be infected with chronic hepatitis B-virus (HBV). 1 It is parti Cularly endemic in Taiwan, where the infection was usually acquired perinatally or in early Childhood.2 individuals with CH Ronic Hepatitis B infection is at an increased risk of developing liver cirrhosis, hepatic decompensation, and Hepatocell Ular carcinoma3; 15% to 40% of these individuals would develop these serious sequelae during their lifetime.3,4 hepatitis B virus is not dir Ectly Cytopathic, and the development of hepatocellular carcinoma in individuals with chronic hepatitis B is a multistage, Multifactorial process including the interaction between host and environmental factors.5 Risk factors for chronic hbv-re lated hepatocellular carcinoma include sex, age, cigarette smoking, alcohol consumption, chemical carcinogens, hormonal FA Ctors, and genetic susceptibility.6

seropositivity for the hepatitis B surface antigen (HBsAg) are one of the most important risk factors for H Epatocellular carcinoma.6 The risk of hepatocellular carcinoma associated with seropositivity for HBsAg ranges from 5-fold To 98-fold with a population-attributable risk of 8% to 94%.6 in we previous study, seropositivity for the hepatitis B E Antigen (HBEAG) was associated a increased risk for hepatocellular carcinoma.7 the adjusted hazard ratio (HR) of de Veloping hepatocellular carcinoma is 9.6 for individuals seropositive for HBsAg and 60.2 for those seropositive for both HBsAg and HBeAg compared with those seronegative for both HBsAg and HBeAg. The increased hepatocellular carcinoma risk in individuals seropositive for HBEAG remained significant regardless of serum Level of alanine aminotransferase (ALT) and status of liver cirrhosis.8,9

Highly sensitive testing methods based on polymerase chain reaction has become available for measuring serum level of HBV Dna. In current clinical Practice guidelines,10- 13 Serum HBV DNA level are used as a criterion for antiviral treatment in Patients with chronic hepatitis B. Effective suppression of serum HBV DNA is a marker of efficacy for antiviral therapy.14 Its implementation as the primary surrogate end point instead of liver histology in assessment of new antiviral therapies Remains to be validated.15 there is no long-term follow-up data on the relationship between serum HBV DNA level and risk of liver complications. In a small nested Case-control analysis,7 we reported a significant association between serum HBV DNA level at study entry and hepatocellular carcinoma risk among individuals seronegative for HBeAg. However, there were only a small number of hepatocellular carcinoma cases and controls included in this study. Neither hepatocellular carcinoma incidence nor CHAnge in serum HBV DNA level over time is studied.

In this population-based, long-term prospective study, we followed up a total of 3653 individuals who were seropositive fo R HBsAg and seronegative for antibodies against hepatitis C virus (ANTI-HCV) at study entry. The goals of this study were to assess the biological gradient of hepatocellular carcinoma risk by (1) Serum HBV DNA level S at study entry and adjusted for other risk factors including age, sex, cigarette smoking, alcohol consumption, seroposit Ivity for HBeAg, elevated serum ALT level, and presence of liver cirrhosis at study entry; and (2) persistent elevation of serum HBV DNA level at both study entry and follow-up examinations.

J Gastroenterol hepatol jan;28 (1): 10-7. doi:10.1111/jgh.12010.Risk stratification for hepatitis B virus related hepatocellular carcinoma. Lin CL1, Kao JH.Author InformationAbstract

Hepatitis B virus (HBV) infection is the major cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC) W Orldwide, especially in the Asia-pacific region. Several hepatitis B Viral factors predictive of clinical outcomes in HBV carriers has been identified. The Risk Evaluation of viral Load elevation and associated liver DISEASE/CANCER-HBV (REVEAL-HBV) study from Taiwan Illustr Ated the strong association between HBV-DNA level at study entry and risk of HCC over time. In this community-based cohort study, male gender, older age, high serum alanine aminotransferase level, positive Hepatiti S B e antigen, higher Hbv-dna level, HBV genotype C infection, and core promoter mutation is independently associated wit H a higher risk of HCC. Another large hospital-based elucidation of Risk factors for Disease Control or advancement in Taiwanese hepatitis B Carri ERS cohort of Taiwanese patients further validated the findings of REVEAL-HBV. The risk of HCC started to increase when HBv-dna level is higher than iu/ml. Both Hbv-dna and HBsAg levels were shown to being associated with HCC development. While Hbv-dna level had better predictive accuracy than HBsAg level, when investigating the overall cohort in patients wit H Hbv-dna Level < iu/ml, HBsAg level≥1000 iu/ml is identified as a new independent risk factor for HCC. With the results from REVEAL-HBV, a risk calculation for predicting HCC in non-cirrhotic patients have been developed and V Alidated by independent cohorts (Risk estimation for hepatocellular carcinoma in chronic hepatitis B). Taken together, ample evidence indicates, HBsAg level can complement Hbv-dna level in predicting HCC development, ESPE Cially in HBV carriers with low viral load. In conclusion, HBV treatment guidelines should include the risk stratification of HCC to individualize the management of H BV carriers with different levels of HCC risk.

© Journal of Gastroenterology and Hepatology Foundation and Wiley publishing Asia Pty Ltd.

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Analysis of HBV DNA level _data