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Individual and combined effects of hepatitis B surface antigen level and viral load on liver cancer risk.

ABSTRACT: BACKGROUND:Hepatitis B surface antigen (HBsAg) and viral load are both hallmarks of hepatitis B virus (HBV) infection and have potential to stratify liver cancer risk. METHODS:We carried out a nested case-control study including 211 liver cancer cases and 221 controls who were seropositive for HBsAg within two population-based cohorts in Shanghai. Logistic regression was performed to estimate the odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS:Risk of liver cancer was positively related to increasing levels of HBV-DNA and HBsAg in dose-response manners. Compared with subjects with HBV-DNA < 2000 IU/ml, the adjusted ORs increased from 2.11 (95%CI: 0.99-4.50) to 10.47 (95%CI: 5.06-21.68) for those with HBV-DNA level at 2000-19 999 to ? 20 000 IU/ml. Compared with subjects at a low level of HBsAg (0.05-99 IU/ml), the adjusted ORs increased from 1.82 (95%CI: 0.90-3.68) to 2.21 (95%CI: 1.10-4.43) for those with HBsAg level at 100-999 to ? 1000 IU/ml. Compared with subjects with HBV-DNA < 2000 IU/ml and HBsAg < 100 IU/ml, the adjusted ORs were increased from 2.20 (95%CI: 1.07-4.49) for those with HBV-DNA < 2000 and HBsAg ? 100 IU/ml to 6.94 (95%CI: 3.39-14.23) for those with HBV-DNA ? 2000 IU/ml and HBsAg < 1000 IU/ml, and 16.15 (95%CI: 7.60-34.32) for those with HBV-DNA ? 2000 IU/ml and HBsAg ? 1000 IU/ml. CONCLUSION:Elevated levels of HBV-DNA and HBsAg are associated with increased risks of liver cancer. Chronic HBsAg carriers may be suggested to simultaneously lower the viral load to < 2000 IU/ml and HBsAg level to < 100 IU/ml to lower their liver cancer risk.

SUBMITTER: Yang Y

PROVIDER: S-EPMC5902426 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature

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Individual and combined effects of hepatitis B surface antigen level and viral load on liver cancer risk.

Yang Yang Y Gao Jing J Tan Yu-Ting YT Li Hong-Lan HL Wang Jing J Ma Xiao X Zheng Wei W Shu Xiao-Ou XO Xiang Yong-Bing YB

Journal of gastroenterology and hepatology 20180205 5

<h4>Background</h4>Hepatitis B surface antigen (HBsAg) and viral load are both hallmarks of hepatitis B virus (HBV) infection and have potential to stratify liver cancer risk.<h4>Methods</h4>We carried out a nested case-control study including 211 liver cancer cases and 221 controls who were seropositive for HBsAg within two population-based cohorts in Shanghai. Logistic regression was performed to estimate the odds ratios (ORs) and 95% confidence intervals (CIs).<h4>Results</h4>Risk of liver ca ...[more]

PMID: 29065440

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Project description:BackgroundHepatocellular carcinoma (HCC) causes over 800,000 deaths worldwide annually, mainly in low income countries, and incidence is rising rapidly in the developed world with the spread of hepatitis B (HBV) and C (HCV) viruses. Natural Killer (NK) cells protect against viral infections and tumours by killing abnormal cells recognised by Killer-cell Immunoglobulin-like Receptors (KIR). Thus genes and haplotypes encoding these receptors may be important in determining both outcome of initial hepatitis infection and subsequent chronic liver disease and tumour formation. HBV is highly prevalent in The Gambia and the commonest cause of liver disease. The Gambia Liver Cancer Study was a matched case-control study conducted between September 1997 and January 2001 where cases with liver disease were identified in three tertiary referral hospitals and matched with out-patient controls with no clinical evidence of liver disease.MethodsWe typed 15 KIR genes using the polymerase chain reaction with sequence specific primers (PCR-SSP) in 279 adult Gambians, 136 with liver disease (HCC or Cirrhosis) and 143 matched controls. We investigated effects of KIR genotypes and haplotypes on HBV infection and associations with cirrhosis and HCC.ResultsHomozygosity for KIR group A gene-content haplotype was associated with HBsAg carriage (OR 3.7, 95% CI 1.4-10.0) whilst telomeric A genotype (t-AA) was associated with reduced risk of e antigenaemia (OR 0.2, 95% CI 0.0-0.6) and lower viral loads (mean log viral load 5.2 vs. 6.9, pc = 0.022). One novel telomeric B genotype (t-ABx2) containing KIR3DS1 (which is rare in West Africa) was also linked to e antigenaemia (OR 8.8, 95% CI 1.3-60.5). There were no associations with cirrhosis or HCC.ConclusionCertain KIR profiles may promote clearance of hepatitis B surface antigen whilst others predispose to e antigen carriage and high viral load. Larger studies are necessary to quantify the effects of individual KIR genes, haplotypes and KIR/HLA combinations on long-term viral carriage and risk of liver cancer. KIR status could potentially inform antiviral therapy and identify those at increased risk of complications for enhanced surveillance.

Project description:BackgroundSerum hepatitis B virus (HBV) RNA may reflect intrahepatic HBV replication. Novel anti-viral drugs have shown potent HBV RNA decline without concomitant hepatitis B surface antigen (HBsAg) decrease. How this relates to off-treatment response is yet unclear.AimTo study the degree of on-treatment viral antigen decline among patients with pronounced HBV RNA decrease in relation to off-treatment sustained response and HBsAg loss.MethodsHBV RNA, HBsAg and hepatitis B core-related antigen (HBcrAg) were quantified in patients with chronic hepatitis B who participated in two randomised controlled trials of peginterferon-based therapy. Sustained response (HBV DNA <2000 IU/mL) and/or HBsAg loss were assessed in patients with and without on-treatment HBV RNA response (either >2 log HBV RNA decline or >1 log decline resulting in an undetectable value at on-treatment week 24), stratified by concomitant HBsAg decline (<0.5/0.5-1/>1 log).ResultsWe enrolled 279 patients; 176 were hepatitis B e antigen (HBeAg)-positive, and 103 were HBeAg-negative. Sustained response was achieved in 20.4% of patients. At on-treatment week 24, HBV RNA response was associated with higher sustained response rates (27.4% vs 13.0% in non-responders, P = 0.004). However, among patients with an HBV RNA response (n = 135), 56.4% did not experience >0.5 log HBsAg decline. Among HBV RNA responders, sustained response was achieved in 47.6% of those with >1 log HBsAg decline (n = 20/42), vs 16.0% with <0.5 log decline (n = 12/75, P = 0.001). Similar results were obtained with HBcrAg and when response was defined as HBsAg loss.ConclusionsIn this cohort, many patients with HBV RNA response during peginterferon-based treatment did not experience HBsAg and/or HBcrAg decline. The absence of concomitant decline in these viral antigens was associated with low rates of treatment response and HBsAg loss. Future trials should therefore consider kinetics of combined biomarkers to assess anti-viral efficacy. Trial registration, ClinicalTrials.gov: NCT00114361, NCT00146705.

Project description:Liver steatosis may occur concomitantly in patients with chronic hepatitis B infection (CHB) and is implicated in increased morbidity and mortality. Hepatitis B virus (HBV) viral load is a marker for disease progression and long-term outcomes in CHB. We investigated the association between liver steatosis and HBV viral load and their individual effects on all-cause mortality and the development of cancer in patients with CHB and liver steatosis.MethodsThis retrospective study included 524 treatment-naïve patients with CHB, with a mean follow-up of 6 years. Liver biopsy was available for 170 patients and liver steatosis was validated by at least 3 ultrasonographic examinations.ResultsA total of 241/524 (46%) patients with CHB had liver steatosis, with a strong correlation between the degree of liver steatosis as assessed by ultrasonography or by liver biopsy (r = 0.9, p < 0.001). Although liver steatosis was not significantly associated with advanced fibrosis, a multivariate analysis showed that liver steatosis was associated with a 4-fold increased risk of all-cause mortality and cancer (hazard ratio 4.35; 95% CI 1.69-8.99; p < 0.001), irrespective of other major metabolic factors. However, baseline HBV viral load was not significantly associated with this composite outcome (hazard ratio 1.65; p = 0.29). In addition, liver steatosis was inversely associated with HBV viral load.ConclusionPatients with CHB and liver steatosis have an increased risk of all-cause mortality and cancer development compared to patients with CHB without liver steatosis, regardless of their baseline HBV viral load. Although tending to have a lower baseline viral load, patients with CHB and liver steatosis should be closely monitored irrespective of viral load.Lay summaryPatients with chronic hepatitis B infection (CHB) may have liver steatosis at the same time. Here we show that in patients with CHB, liver steatosis is significantly associated with all-cause mortality and cancer, irrespective of other major metabolic factors, and the effect of liver steatosis on mortality and cancer is stronger than the effect of hepatitis B viral load on these outcomes. Thus, patients with CHB and liver steatosis should be closely monitored, irrespective of their viral load.

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Individual and combined effects of hepatitis B surface antigen level and viral load on liver cancer risk.

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Individual and combined effects of hepatitis B surface antigen level and viral load on liver cancer risk.

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