Scientific Sessions 2015: Hepatitis b&c and treatment options
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This document discusses hepatitis B and hepatitis C infections. It covers transmission risks, testing and diagnosis, disease progression, complications, global prevalence, and treatment approaches. Treatment goals include preventing disease progression, achieving sustained virologic response, and promoting compliance. Treatment options discussed include various antiviral medications and consideration of host and viral factors in determining appropriate therapy. Vaccination strategies are outlined for pre-exposure, post-exposure, and acute or chronic hepatitis B infection. Eligibility criteria and standard/newer treatment regimens are also summarized.
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Scientific Sessions 2015: Hepatitis b&c and treatment options
- 1. Dr Upali Weragama MBBS(Pera), MD(Col), MRCP(UK), MAGA(USA) Consultant Physician Sri Lanka Police Hospital Colombo
- 2. High risk of transmission Other STIs Alcohol & other substance abuse Treatment & compliance Reinfection & anti-viral drug resistance Complications & prognosis
- 3. Progressive necro-inflammation leading to fibrosis cirrhosis Liver failure Hepatocellular carcinoma (HCC) Extra-hepatic manifestations
- 4. •More than 400 million people have chronic HBV infection •Estimated 170 million people infected with HCV •About 1.4 million die each year from causes related to these two infections
- 6. High risk sexual behaviour - unprotected receptive anal intercourse with ejaculation - - anal fisting -group sex Associated other STIs & HIV Abuse of alcohol & other substances
- 8. Antigens Hepatitis B surface Antigen Hepatitis B e antigen Hepatitis B core antigen – not seen in blood Antibody Hepatitis B surface antibody Hepatitis B e antibody Hepatitis B core antibody (IgM and total)
- 9. Molecular assays Hepatitis B DNA Qualitative or quantitative correlates with circulating viral particles either measured as copies / ml or IU / ml treatment if HBV DNA - > 20,000 IU / ml Genotypes ( upto 10; A-J,) & many subgenotypes
- 10. •HCV antibody (positive 1-6 months after infection) •All anti-HCV positive patients HCV RNA for confirmation Viral load assay Genotyping ( 6 genotypes & more than 50 subtypes) •Liver biopsy is not mandatory before treatment but may be helpful
- 13. Prevent / reduce progression of the disease, particularly to cirrhosis liver failure hepatocellular carcinoma (HCC) extra-hepatic manifestations Acheive SVR Promote compliance / counseling
- 14. Host Non-Modifiable older age at time of infection male sex Modifiable alcohol consumption Nonalcoholic fatty liver disease obesity / insulin resistance Viral Genotype Coinfection with hepatisis B / C virus or HIV
- 17. Pre exposure ( vaccination) Immediate post exposure Acute Hep B infection Chronic Hep B infection
- 18. Given before exposure to high risk groups Three doses at 0, 1, 6 months Transient HBsAg positivity after vaccination Anti HBs 1 – 2 months after the 3rd dose Effective ~ 90% Last about 20 years No routine boosters are recommended If no antibodies , can repeat vaccination schedule
- 19. Given within 48 hours, (up to a week) following known / possible exposure vaccination & antibody status of the recipient HBV serology status ( eg e antigen) of the source dose - depending on body weight different site from vaccine – antero-lateral thigh
- 20. Antiviral therapy is generally not necessary because 95% of immunocompetent adults recover spontaneously Severe or fulminant acute hepatitis B Lamivudine or telbivudine
- 21. HBe status Age of the patient & comrbidities Presence of significant fibrosis / cirrhosis ALT level HBV DNA level
- 25. Antiviral therapy is generally not necessary -will spontaneously clear in 20% to 50% of patients -in two-thirds of patients, this will occur within 6 months -regular laboratory monitoring is recommended HCV RNA (eg, every 4 -8 weeks) for 12 months Severe or fulminant acute hepatitis C infection
- 27. •Elevated serum alanine aminotransferase (ALT) levels •Fibrosis •Age greater than 18 years •Positive HCV antibody and serum HCV RNA test results •Compensated liver disease (eg, no hepatic encephalopathy or ascites) •Acceptable hematologic and biochemical indices (hemoglobin, neutrophil count, serum creatinine •Willingness to be treated and to adhere to treatment requirements
- 28. Standard therapy is a combination of peginterferon and ribavirin Newer drugs shorter treatment duration well tolerated increased SVR rates
- 29. Boceprevir - first protease inhibitor Telaprevir Simeprevir Sofosbuvir - NS5B polymerase inhibitor
Editor's Notes
- Men who have Sex with Men Certain high risk sexual behaviour In particular, safer sex strategies should be emphasized given the high rates of reinfection after SVR, which may approach 30% over 2 years, in HIV-infected MSM with acute HCV infection.
- Glomerularnephritis, PAN Cryoglobulinemia: Idiopathic thrombocytopenic purpura Lichen planus Keratoconjunctivitis sicca Raynaud syndrome Sjögren syndrome Porphyria cutanea tarda Necrotizing cutaneous vasculitis Non-Hodgkin lymphoma Mixed essential cryoglobulinaemia
- 7.3 billion 6%, 2.6% Death HBV 800,000 & HCV 500,000
- overall sero-prevalence of HBV (<2%) and HCV ( <1%) A sero-surveillance study of 407 children aged 1 to 5 Years in Kalutara district tested negative for current Hepatitis B infection(Hepatitis B Sero-Survey-2014, Epidemiology Unit-MRI joint Study) . A study done with 250 drug users in the Colombo district in 2005 revealed • 12.6% (CI 5.1-24.5) prevalence of ever injecting drug use • 7.6% Prevalence of HBV, but none were infective (HBsAg negative) • 0.4% Prevalence of anti-HCV • None tested positive for HIV (Tissera H. A, 2005). people interned in prisons A study among cohort of prison inmates(n=393) in Sri Lanka revealed low prevalence of • HBV (HBsAg-0.25%) • HCV (HCV RNA- 0.5%) • Injecting drug use (4.3%) None of the injecting drug users were positive for HBV-DNA or HCV-RNA (Niriella M. A et al)
- Samples: serum or plasma
- Genotype C –poor prognosis in terms of cirrhosis & HCC
- An accurate assessment of fibrosis is vital in assessing the urgency for treatment. The degree of hepatic fibrosis is one of the most robust prognostic factors used to predict disease progression and clinical outcomes. The most efficient approach to fibrosis assessment is to combine direct biomarkers and vibration-controlled transient liver elastography. A biopsy should be considered for any patient who has discordant results between the 2 modalities that would affect clinical decision making. For example, 1 shows cirrhosis and the other does not. The need for liver biopsy with this approach is markedly reduced.
- The first is to achieve sustained eradication of HCV (ie, SVR), SUSTAINED VIROLOGIC RESPONSE which is defined as the persistent absence of HCV RNA in serum 6 months or more after completing antiviral treatment.
- HBV genotype C , HCV Genotype 3
- Human plasma with high titer of Hep B antibody Not for treatment of hepatitis B not intra-venously
- in patients with symptomatic acute hepatitis B
- The endpoint of treatment for HBeAg-positive patients is HBeAg seroconversion.158-160 Liver chemistries should be monitored every 3 months and HBV DNA levels every 3-6 months while on therapy, and HBeAg and anti-HBe tested at the end of 1 year of treatment and every 3-6 months thereafter. Treatment may be discontinued in patients who have confirmed HBeAg seroconversion (HBeAg loss and anti-HBe detection on 2 occasions 1-3 months apart) and have completed at least 6 months of consolidation therapy after the appearance of anti-HBe. The durability of response after cessation of treatment is expected to be 70% to 90%
- only 11% of those who remain viremic at 6 months will spontaneously clear infection at some later time.
- The endpoint of treatment for HBeAg-positive patients is HBeAg seroconversion.158-160 Liver chemistries should be monitored every 3 months and HBV DNA levels every 3-6 months while on therapy, and HBeAg and anti-HBe tested at the end of 1 year of treatment and every 3-6 months thereafter. Treatment may be discontinued in patients who have confirmed HBeAg seroconversion (HBeAg loss and anti-HBe detection on 2 occasions 1-3 months apart) and have completed at least 6 months of consolidation therapy after the appearance of anti-HBe. The durability of response after cessation of treatment is expected to be 70% to 90%
- The treatment of hepatitis C has evolved over the years. Initial studies used IFN monotherapy. Subsequently, combination of ribavirin and IFN or of IFN to which polyethylene glycol (PEG) molecules have been added (ie, PEG-IFN) were used.
- The first protease inhibitor indicated for use in HCV infection, boceprevir. HCV NS5B polymerase inhibitor treatment duration 12 weeks for patients without cirrhosis 24 weeks for those with cirrhosis