Hepatitis C Updated Treatment Protocol (egytian guidelines)
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HCV treatment guidelines according to egyptian guidelines dec. 2016
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Hepatitis C Updated Treatment Protocol (egytian guidelines)
- 1. Hepatitis C Updated Treatment Protocol By:- Sayed Hanzal Ass. Lecturer of Hepatogastroenterology fayoum univ.
- 2. 5 Questions …..??? 1) Why should we treat HCV ? 2) Endpoint of therapy ?? 3) Drugs available and it’s mech. ??? 4) Egyptian guidelines for HCV ttt ????? Amazing patient’s questions
- 3. Why should we treat HCV ? 80 million people are chronically infected worldwide (3%) More then 350 000-500 000 people die every year from Hepatitis C related end-stage liver disease (cirrhoses, HCC, liver failure) 3-4 million people become infected with HCV annually
- 4. HCV in Egypt • Prevalence : 7% • Total number of cases: 6 million • Number of patients aware of infection: 1million • Number of yearly new diagnosed cases : 120,000 • Newly yearly infected cases: 120,000 – 150,000 • Number of yearly liver cancer cases caused by HCV : 16,000
- 5. Endpoint of therapy • undetectable HCV RNA 12 weeks (SVR12) and 24 weeks (SVR24) after the end of treatment
- 6. Drugs available and there mech. ????
- 8. HCV Life Cycle and DAA Targets Adapted from Manns MP, et al. 2007 Transport and release (+) RNA Translation and polyprotein processing RNA replication Virion assembly NS3/4A protease inhibitors NS5B polymerase inhibitors NS5A inhibitors “Previr’s” Boceprevir, Telaprevir, Simeprevir, Faldaprevir “Buvir’s” Sofosbuvir, Deleobuvir “Asvir’s” Daclatasvir, Ledipasvir DAA Uncoating Receptor binding
- 9. Egyptian guidelines for HCV ttt ?????
- 10. • All PCR +ve , ≥ 18 years except 1. Child C 2. Plt < 50 3. HCC, except 6 months after cure with no evidence of activity by dynamic (CT or MRI). 4. Extra-hepatic malignancy except after two years of disease-free interval except lymphomas 5. Pregnancy 6. (HbA1c>9 %)
- 11. Prvious ttt with DAAs naive easy difficult experienced Sof +dac Sof +sim
- 12. DAAs naïve (12Ws) Easy to treat group: • Treatment naïve • Total s. bil ≤ 1.2 mg/dl. • S. albumin ≥ 3.5 g/dl. • INR≤ 1.2. • Platelet ≥150.000/mm3. Difficult to treat group: • Peg-IFN ttt experienced • Total s. bil >1.2 mg/dl. • S. albumin <3.5 g/dl. • INR>1.2. • Platelet <150.000/mm3. SOF/DAC or Qurevo/RBV SOF/DAC/RBV
- 13. DAAs experience (12Ws) RBV ineligible: extend (24 Ws) • SOF/Qurevo/RBV OR SOF/SIM/DAC/RBV • Child’s B (specialized centers) SOF/DAC/RBV for 24Ws. • SOF/DAC/RBV SOF/DAC Failure SOF/SIM Failure Ribavirin dose : 1000 mg <75 kg. 1200 mg >75 kg
- 14. CKD according to eGFR • eGFR >30 ml/min by the usualttt regimens • eGFR ≤ 30 ml/min Qurevo/RBV In the conition that Child A or no cirrhosis Hb at least 10 g/dL no uncont. co-morbidity A nephrologist consult
- 15. post organ transplantation SOF/DAC/RBV for 24Ws
- 16. Combined HCV and HBV • treated with the same regimens If HBV replicates at significant levels before, during or after HCV clearance, concurrent HBV therapy is indicated.
- 17. Amazing patient’s questions • Did hcv reach my liver • Does hcv affect liver only • Does ttt curative or suppresive to the virus • What about relapse • Are there follow up after end of ttt (if there ,whome and how) • possibilty of Re-infection • What about hcv antibodies (presence , risk ,clearance )
Editor's Notes
- DAA, direct-acting antiviral; ER, endoplasmic reticulum; HCV, hepatitis C virus; LD, luminal domain; NS5A/B, nonstructural protein 5A/B. Now, one of the advantages of direct-antivirals for hepatitis C virus is that, unlike some of other virus, like HBV, for example, hepatitis C has a number of potential targets for drug development, and this has led to multiple classes of direct-acting antivirals being developed. So, if we look at this schematic of the HCV life cycle, you can see that after the virus enters the cell, the viral RNA is translated to lead to the viral proteins and then these are chopped up by the virally encoded protease. And of course, the first direct-acting antivirals were inhibitors of the NS3/4A protease. Subsequently, the viral RNA is replicated, and again, the HCV NS5B polymerase has been a target for inhibition, with both nucleotide polymerase inhibitors and nonnucleotide or nonnucleoside polymerase inhibitors, which act by a different mechanism of action but target the same enzyme. In addition, after viral replication occurs, the virus must be assembled and part of the replication complex involved in assembly is the nonstructural 5A protein—or NS5A—and a number of direct-acting antivirals target the NS5A protein. So, at least to date, the DAAs that have gone through clinical development include protease inhibitors, nucleotide and nonnucleotide polymerase inhibitors, and NS5A inhibitors.