Case Studies: HBeAg Negative Chronic Hepatitis B
•Transferir como PPT, PDF•
8 gostaram•6,936 visualizações
Real case studies. Discussion on management for each case based on available evidence at the time.
![Case Study ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
Recomendados
Recomendados
Mais conteúdo relacionado
Mais procurados
Mais procurados (20)
Semelhante a Case Studies: HBeAg Negative Chronic Hepatitis B
Semelhante a Case Studies: HBeAg Negative Chronic Hepatitis B (20)
Último
Último (20)
Case Studies: HBeAg Negative Chronic Hepatitis B
- 1. Clinical Case Scenario : Chronic Hepatitis B HBeAg Negative Dr Yeong Yeh Lee MD, MRCP (UK), MMed May 2007
- 6. REVEAL: High HBV Viral Load is associated with increased incidence of HCC Chen CJ, et al. JAMA 2006; 295:65–73 HBeAg negative, normal ALT, no liver cirrhosis at entry (n=2,925) .14 .12 .1 .08 .06 .04 .02 0 0 1 2 3 4 5 6 7 8 9 10 11 12 13 Cumulative incidence of HCC Year of follow-up Baseline HBV DNA Level ≥ 10 6 10 5 –<10 6 10 4 –<10 5 300–10 4 <300
- 7. Haimen City Cohort: HBV V iral L oad at B aseline is A ssociated with HCC M ortality 1.00 0.96 0.92 0.88 0.84 0.80 0 1 2 3 4 5 6 7 8 9 10 11 12 Survival distribution function Survival time (Years) HBV DNA >10 5 RR=9.9 (3.2–31.0) HBV DNA >10 3 – <10 5 RR=1.8 (0.5–5.8) HBV DNA <10 3 Chen et al. Am J Gastroenterol 2006; 101:1797-1803
- 10. Liver biopsy : bridging necrosis and fibrosis Ishak Staging for fibrosis Score 3
- 13. FDA Approved Therapies for Chronic Hepatitis B Oct 28, 2006 Idenix/Novartis TYZEKA ™ Telbivudine March 29, 2005 Bristol-Myers Squibb BARACLUDE ™ Entecavir May 13, 2005 Hoffmann La-Roche Inc. PEGASYS ® Peginterferon alfa-2a 2002 Gilead Sciences HEPSERA ™ Adefovir dipivoxil 1998 GlaxoSmithKline EPIVIR-HBV ® Lamivudine 1992 Schering Corporation INTRON ® A Interferon alfa-2b, recombinant Date Approved in US Manufacturer Trade Name Generic Name
- 14. HBV DNA suppression: Comparison of treatments at 1 year in naïve patients* Lai CL, et al. Hepatology 2005; 42(Suppl 1):748A (abstract LB01); Lau G, et al. NEJM 2005; 352:2882–2695; Chang T-T, et al. NEJM 2006; 354:1000–1010; Lai CL, et al. NEJM 2006; 354:1011–1020; Marcellin P, et al. NEJM 2003; 348:808 – 816; Marcellin P, et al. NEJM 2004; 348:1206 – 1217; Hadziyannis SJ, et al. NEJM 2003;348:800–807 *Collation of currently available data – not from head-to-head studies Peg IFN # Lamivudine* Adefovir # Telbivudine* HBV DNA undetectable (% patients) 36 67 60 0 20 40 60 80 HBeAg(+) HBeAg(-) 0 20 40 60 80 100 72 90 88 *Undetectable <300 copies/mL # Undetectable <400 copies/mL Entecavir* 21 25 63 51
- 19. Lamivudine-resistant mutations result in reduced treatment efficacy and poorer patient outcomes Adapted from Liaw. Semin Liver Dis 2005; 25:40–47; Liaw et al. N Eng J Med 2004; 351:1521–1531 Wild-type (n = 221) Time after randomisation (months) 0 5 10 15 20 25 0 6 12 18 24 30 36 Percentage of patients with disease progression Placebo (n = 215) 5% 21% M204I/V mutations (n = 209, 49%) 13%
Notas do Editor
- ALT N Men 30 Female 19
- A1 : Yes. A viral load is indicated here especially his ALT=2xULN A2: Both a+b true. Log 4 treat if liver biopsy shows inflam and fibrosis Based on REVEAL study; risk of progression to cirrhosis and HCC high with log 4 independent of ALT
- Data from the REVEAL study shows that patients with DNA ≥104 <105 and normal ALT have an increased risk of disease progression… Therefore such patients may warrant therapy. This new data may prompt an update of the guidelines BACKGROUND INFO ON DATA : Viral Load as a Risk Factor for HCC 1,678 men and women had a serum HBV DNA level of ≥10 4 copies/mL at cohort entry. The serum samples collected at the last follow-up health examination or at the follow-up examination preceding the HCC diagnosis (for cases) were tested for serum HBV DNA level. 1,376 of 1,678 (82%) had serum samples collected at follow-up health examination available for HBV DNA testing. Samples from subjects with entry HBV DNA level < 10 4 copies/mL were not re-tested as this was the control group. HCC incidence rate per 100,000 person-years was 145.2, 112.5, 314.9, 952.1, and 1,149.5 respectively, for patients with HBV DNA <300, 300-9.9x10 3 , 1.0-9.9x10 4 , 1.0-9.9X10 5 , and ≥10 6 copies/mL Reference Chen C-J, et al. DDW 2005. Poster #M917.
- 1 iu/ml=5.1 copies/ml (AASLD 2003) A3: Yes. His HBV DNA = 11,000 iu/ml (betw 2000 – 20,000). Based on AASLD 2007, with borderline ALT 2xULN and DNA>2,000 then liver biopsy indicated if plan for treatment
- A4: Endpoint should be undetectable HBV DNA and ALT normalisation. LMV should continue till endpoints met. If HBV DNA at week 24 < log 3 then chances of response high at week 48. Otherwise the real duration unknown
- Speaker Notes Communication objectives HBV DNA suppression: Cross-study comparison of treatment outcomes at 1 year in nucleoside-naïve patients Approximately ~20-70% of HBeAg(+) patients, and ~ 50-90% HBeAg(-) patients achieve undetectable viral load at one year. Antivirals provide higher response rates (proportion of patients with undetectable HBV DNA) than IFN. ETV results compare favourably to other antivirals. References Lai CL, et al. Hepatology 2005; 42(Suppl):748A (AASLD abstract LB01) Lau G, et al. N Engl J Med 2005; 352:2882–2695 Chang T-T, et al. N Engl J Med 2006; 354:1000–1010 Lai CL, et al. N Engl J Med 2006; 354:1011–1020 Marcellin P, et al. N Engl J Med 2003; 348:808 – 816 Marcellin P, et al. N Engl J Med 2004; 348:1206 – 1217
- Speaker Notes Communication objectives Resistance emerges when HBV replication occurs in the presence of antivirals, leading to selection pressure and increased probability of HBV mutation. In patients treated with lamivudine, initial improvements in disease are rarely sustained due to development of drug resistance. The prevalence of lamivudine resistance increases with the duration of therapy; after five years, resistance will develop in about 70% of patients. References Liaw Y-F. Semin Liver Dis 2005; 25:40–47 Liaw Y-F, et al. N Eng J Med 2004 ; 351:1521–1531