scholarly journals A STUDY TO DETERMINE FOLLOW-UP STRATEGY FOR DIFFERENTIATING A TRUE INACTIVE CARRIERS FROM CHRONIC HEPATITIS PATIENTS WITH HBEAG NEGATIVE BY THE HBV DNA CUTOFF VALUE

2020 ◽  
pp. 1-2
Author(s):  
Subhash Kumar Saw ◽  
MD. Mohammad Sohail ◽  
Jainendra Kumar
Keyword(s):  
Chronic Hepatitis ◽  
Hbv Dna ◽  
First Year ◽  
Hbv Reactivation ◽  
Significant Drop ◽  
Inactive Carrier ◽  
Cutoff Value ◽  
Normal Alt ◽  
Negative Chronic Hepatitis

Background & Objective: As compare to true inactive carrier a significantly different prognosis generally observed in Patients with HBeAg-negative chronic hepatitis B (CHB). To differentiate this two condition accurately there are no reliable strategy. To determine follow-up strategy for differentiating a true inactive carriers from chronic hepatitis patients with HBeAg negative by the HBV DNA cutoff value. Materials and Methods: We had enrolled potential inactive carriers who were consecutive untreated patients. This inactive carriers defined as HBV DNA < 2000 IU/mL, normal ALT levels, anti-HBe-positive and definitely HBeAg-negative. HBV DNA level to ≥ 2000 IU/mL was defined as the HBV reactivation. Patients whose HBV DNA levels remained at < 2000 IU/mL were classified as true inactive carriers and patients whose HBV DNA level to ≥ 2000 were classified as false inactive carriers during the first year. Results: Among 112 inactive carrier (age, 48.3 ± 13.1 years) who were initially selected, 75 were males. As identified, 23.2 ± 7.9 IU/L and 359 ± 478 IU/mL were serum ALT and HBV DNA levels, respectively. In 24 patients there were a significant drop in HBV reactivation during the first year. Between true and false inactive carriers there were a significantly different ALT and HBV DNA levels. In patients, whose baseline HBV DNA level was ≥ 200 IU/mL as compare to patients whose baseline HBV DNA level was < 200 IU/mL, HBV reactivation developed more often during a follow-up of 354 ± 175 days. Conclusion: From true inactive carriers to differentiate patients with HBeAg-negative CHB, HBV DNA level was useful tool. As per HBV DNA level of inactive carriers applied follow-up strategies need to vary.

scholarly journals Large spontaneous HBV DNA fluctuations and potential usefulness of a single point measurement of combined HBV DNA and quantitative HBsAg for the exclusion of HBeAg negative chronic hepatitis B:  A prospective Tunisian cohort  study

2022 ◽  
Author(s):  
Amel Chtourou ◽  
Saba Gargouri ◽  
Emna Elleuch ◽  
Lamia Fki-Berrajah ◽  
Fahmi ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Liver Biopsy ◽  
Chronic Hepatitis B ◽  
Hbv Dna ◽  
Short Term ◽  
Tunisian Patients ◽  
Chronic Hbv ◽  
Negative Chronic Hepatitis

Abstract Background/Aims: We aimed to describe spontaneous short-term hepatitis B Virus (HBV) DNA level fluctuations and to assess the usefulness of quantitative HBsAg (qHBsAg) in Tunisian patients with HBeAg-negative chronic HBV infection.Patients and methods: We included 174 treatment-naïve patients with chronic HBeAg-negative HBV. A one-year prospective follow-up was carried out with serial determinations of HBV DNA, alanine aminotransferase levels and qHBsAg. Patients were classified into three groups: inactive carriers (G1), patients with HBeAg negative chronic hepatitis B (CHB) (G2) and patients with indeterminate state (G3). For this latter group, a liver biopsy was indicated.Results: Only genotype D was detected. During the follow-up, 21.6% and 19.5% of patients with low initial (<2000 IU/mL) and intermediate viral load (2000-20000 IU/mL), experienced a subsequent increase in their HBV DNA levels above 2000 and 20000 IU/mL, respectively. Significant variations of HBV DNA levels (≥0.5 log10 IU/mL) were observed in 61.1% of patients at 6 months-interval. Among the 174 patients, 89 (51.1%) belonged to G1, 33 (19%) to G2 and 52 (29.9%) to G3. Fourteen patients have undergone liver biopsy, among whom 7 (50%) showed moderate to severe liver disease. Combination of HBV DNA <2000 IU/mL and qHBsAg <832 IU/mL excluded CHB in 98.4% of cases.Conclusions: This study highlights the large short-term HBV DNA fluctuations in Tunisian patients with HBeAg negative chronic HBV of genotype D. HBV DNA < 2000 IU/mL along with qHBsAg < 832 IU/mL excluded CHB in 98.4% of cases. Significant proportion of patients with indeterminate state within genotype D would have HBeAg negative CHB.

Add-on peg-interferon leads to loss of HBsAg in patients with HBeAg-negative chronic hepatitis and HBV DNA fully suppressed by long-term nucleotide analogs

2013 ◽  
Vol 58 (4) ◽  
pp. 713-717 ◽  
Author(s):  
Denis Ouzan ◽  
Guillaume Pénaranda ◽  
Hélène Joly ◽  
Hacène Khiri ◽  
Antonnella Pironti ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hbv Dna ◽  
Nucleotide Analogs ◽  
Negative Chronic Hepatitis

scholarly journals Evaluation of a Hepatitis B Virus Reactivation Prevention Program in Lymphoma Patients Receiving Immunochemotherapy

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 1801-1801
Author(s):  
Blanca Sanchez-Gonzalez ◽  
Montserrat Garcia-Retortillo ◽  
Teresa Murcia ◽  
Mariana Ferraro ◽  
Francesc Garcia-Pallarols ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hbv Dna ◽  
Hbv Reactivation ◽  
Antiviral Prophylaxis ◽  
B Virus ◽  
Group A ◽  
Chronic Hbv ◽  
Group B

Abstract INTRODUCTION Chemotherapy-induced hepatitis B virus (HBV) reactivation is a well-recognized complication and is a potentially life-threatening condition in cancer patients with chronic HBV (hepatitis B surface antigen [HBsAg]-positive). Rituximab has been associated with an increase in HBV reactivation in chronic HBV patients (45%) and even in patients with resolved infection (HBsAg negative and hepatitis B core antibody [anti-HBc]-positive (22%); however, the reported frequency varies among different studies. Current guidelines for management of chronic HBV recommend routine antiviral HBV prophylaxis with lymphoma before starting chemotherapy. In contrast, there is little evidence-based consensus regarding patients with resolved HBV infection. Aim: To analyze the incidence of HBV reactivation and the role of antiviral HBV prophylaxis in lymphoma patients with chronic HBV or resolved HBV treated with chemotherapy, immunotherapy or immunochemotherapy managed according to our institutional HBV guidelines. Secondary endpoints were to analyze the incidence of HBV in this population and HBV guidelines adherence. PATIENTS AND METHODS Lymphoma patients with chronic HBV or resolved HBV in a single center. HBV viral status definitions: Active Chronic HBV infection: HBsAg positive, anti-HBc positive and HBV DNA >2000 IU/mL; Inactive Carriers: HBsAg positive, Anti-HBc positive, HBV DNA undetectable or <2000 IU/mL with normal transaminases; Resolved HBV: HBsAg negative, anti-HBc positive, HBV DNA undetectable. HBV reactivation was defined as increased serum HBV DNA (≥1 log10), regardless of liver biochemistry or HBsAg status. Institutional HBV guidelines: serum samples were collected at baseline for HBsAg and anti-HBc testing in all lymphoma patients. Patients were evaluated by a hepatologist if any of them fulfilled HBV viral status definition. Baseline at screening and monitoring every 3 months during therapy and up to 24 months after completing therapy (assessment of liver biochemistry, serum HBV DNA, HBsAg and anti-HBs levels). Specific prophylaxis strategies according to HBV status: Group A (Active chronic HBV): treatment for HBV; Group B (Inactive carriers): antiviral HBV prophylaxis; Group C (Resolved HBV): antiviral HBV prophylaxis if rituximab containing-therapy or follow-up only if rituximab-free therapy. HBV antiviral prophylaxis was started before therapy and finished 12 months after completing therapy. RESULTS From January 2012 to January 2015, 227 lymphoma patients received chemotherapy or immunochemotherapy. 142 (63%) patients received rituximab-containing therapy. 43 (19%) patients were anti-HBc positive. Group A: 2 (1%) patients; Group B: 2 (1%) patients; Group C: 39 (17%) patients. 14 (6%) patients have coinfection with hepatitis C virus and 12 (5%) patients co-infection with human immunodeficiency virus (HIV). Adherence to HBV guidelines was 90%. Patients in Group A (n=2) and B (n=2) received antiviral treatment/prophylaxis before starting therapy. In the Group C, 16 (41%) patients underwent only follow-up and 23 (59%) patients received HBV antiviral prophylaxis (lamivudine in 4, entecavir in 8 and tenofovir in 11). Median duration of HBV prophylaxis was 18 months (95% CI: 16-19 months). After a median follow-up of 21 months, 2 patients developed HBV reactivation during lymphoma treatment: 1 from group B (reactivation rate of 50%) and 1 from group C (reactivation rate of 3%). Both patients had received rituximab-containing treatment and both developed HBV reactivation (without hepatitis flare) within the first 6 months after finishing antiviral HBV prophylaxis (delayed HBV reactivation). Outcome was favorable in both patients. Characteristics of HBV reactivation patients are shown in table I. Cumulative incidence of HBV reactivation at 12 and 24 months were 0% and 8%, respectively. CONCLUSION Our strategy of close monitoring patients with chronic HBV or resolved HBV that receive chemotherapy and adding antiviral HBV prophylaxis only in selected patients clearly decrease HBV reactivation. Nevertheless, this strategy may not fully protect patients from late HBV reactivations. Larger validation studies are needed to confirm our data and to establish the best cost-effective strategy in this lymphoma population, especially in the new era of inmunomodulatory drugs of their real involvement in HBV reactivation is unknown. Table 1 Table 1. Disclosures No relevant conflicts of interest to declare.

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