treatment of hepatitis b in children (-) - naspghan homepage
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Treatment of Hepatitis B in Children
• Kathleen B. Schwarz, M.D.
Johns Hopkins Children’s Center
President‐Elect of NASPGHAN
• In the past 12 months, I have had the following relevant financial relationships with the following manufacturer(s) of any commercial product(s) and/or provider(s) of commercialservices discussed in this CME activity:
Research grants from Gilead, Roche, BMS, NIDDK
• Consulting – Novartis, Hepatitis B Foundation
I do not intend to discuss an unapproved or investigative use of a commercial product or device in my presentation.
Moderators
Regino Gonzalez‐Peralta, M.D. –University of Florida
Barbara Haber, M.D. – CHOPhild ’Maureen Jonas, M.D. – Boston Children’s
Karen Murray, M.D. – University of Washington
Michael Narkewicz, M.D. – University of Colorado
Moderator disclosures
• Gonzalez‐Peralta
• Haber
• Jonas
• Murray – research support – Roche, Gilead
• Narkewicz
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Outline
• Epidemiology and natural history
• Usual treatment candidates
• Antiviral agents
–4 FDA approved for <18 years
–3 more approved for 18 years and older
• Special populations
• Three cases
• In much of the world, the lifetime risk of contracting HBV is >60%• 2 billion infected, ~350 million chronic carriers
• In the US, universal infant vaccination was instituted in 1991– The incidence of acute hepatitis B has declined significantly– Chronic hepatitis B remains a substantial problem due toC o c epat t s e a s a substa t a p ob e due to
Vertical transmissionImmigration from areas of endemicityInfection by HBsAg+ household contacts
• Chronic HBV infection develops in – 90% of infants infected as neonates– 25-50% of children aged 1-5 years who are acutely infected
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Phase Labs and Histology Note
Immune Tolerant
DNA>20,000 IU/ml ALT normalHBsAg and HBeAg detectable Minimal liver inflammation and fibrosis
Antiviral therapies are generally ineffective Risk of drug resistance if treated
Immune Active
DNA levels declineALT elevated
Most children still show no signs or symptoms of disease
Phases of Chronic Hepatitis B Infection
HBsAg and HBeAg remain detectable Liver inflammation and fibrosis can develop
Inactive HBsAgCarrier
DNA<2,000 IU/ml or undetectable ALT normalizes HBeAg undetectable, anti-HBe presentNo liver inflammation, fibrosis may regress
Age at serocoversion appears to be influenced by HBV genotypeRisk of developing cirrhosis and HCC declines
Reactivation DNA levels increase ALT normal or elevated HBeAg remains undetectable
Occurs in 20-30 % of patients e-antigen-negative diseaseUsually due to a mutant virus
Haber, BA, et al. Pediatrics. published online Oct 5, 2009. (doi: 10.1542/peds.2009-0567)
920 Liver biopsies on HBV‐infected children from 11 medical centers.
Inter‐observer variability in histopathological assessmentof liver biopsies taken in a pediatric open label therapeuticprogram for chronic HBV infection treatment
World J Gastroenterol 2006 March 21; 12(11): 1713‐1717
Biopsies were independently reviewed by6 pathologists from academic centers who assessedBatts‐Ludwig score for grading and staging.
Satisfactory inter‐observer agreement forgrading was obtained in 51.6% and for staging in 75.7%of biopsies. Satisfactory dispersion for grading scoreswas observed in 44.5% and for staging in 72.7% of cases
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24 Year Follow of 67 HBV‐infected Children
Peters M. HEPATOLOGY 2009;49:S146‐S155
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HBV Genotypes and response to treatment
• Pegylated interferon – HBsAg loss– A 14%, B 9%, C 3%, D 2%
• Interferon and pegylated interferonC (40 20% i l i )– B >C (40 vs. 20% virologic response)
– A>D (49 vs. 26% virologic response)
• Lamivudine – resistance A>D
• Adefovir dipivoxil and entecavir – no genotype effect
Sites of action of various anti‐viral agents
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Goals of treatment
• Eliminate HBV (unlikely)
• Decrease risk of chronic liver disease/HCC
• Decrease social stigma/isolation
• Decrease transmission
• Decrease HBV DNA to <2000 IU/ml or less
Goals of HBV Therapy
• In HBeAg‐positive patients – HBeAg loss and seroconversion represent a secondary form of treatment success
• Associated with improved long‐term outcomes
I HB A iti d HB A ti ti t• In HBeAg‐positive and HBeAg‐negative patients – HBsAg loss and seroconversion ultimate form of HBV treatment success
• Best predictor of durable viral suppression • Strongest indicator of best long term outcome, lowest risk of cirrhosis and liver cancer
• Not achieved by the majority of patients
• Children born in countries endemic for HBV — even if they received hepatitis B vaccine in their country of origin
– All of Asia– All of Africa– South- and mid-Pacific Islands– Europe (Eastern and Mediterranean countries), Greenland, and Russia– Middle East– South America: Amazon Basin
Caribbean
Children Who Should Be Screened for Chronic HBV Infection
– Caribbean– Indigenous populations from the Arctic, Australia, and New Zealand
• Children born in the US to immigrant parents from endemic areas
• Infants born to HBsAg+ mothers
• Children living with an HBsAg+ individual – Including children who received hepatitis B vaccine after birth who were not screened
before vaccination
Haber, BA, et al. Pediatrics. published online Oct 5, 2009. (doi: 10.1542/peds.2009-0567)Adapted from Weinbaum CM, et al, MMWR Recomm Rep. 2008;57(RR-8):1–20
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Recommended approach to monitoring children with
chronic hepatitis B infection
Hepatitis B Foundation
www.hepb.org
Lamivudine
Peginterferon alfa‐2a
TenofovirEntecavir
Evolution of Approved HBV Therapy Over Time
Interferon alfa‐2b Adefovir Telbivudine
1990 1998 2002 2005 2006 2008
Serving Size 2 Chewable Animal‐Shaped Tablets
Supplement FactsStandard vitamins
Proprietary Kids Immune Booster Blend
i (f d l h l f ) hi (d ff i d)
First therapy to show up when you Google Treatment for HBV in Children!
Grape Juice Concentrate (fermented, alcohol free), Chinese Green Tea (decaffeinated), Turmeric, Garlic (odor‐modified), Olive Leaf, Shiitake Mushroom (Lentinus edodes mycelia) 30 mg
Lactobacillus acidophilus (4 million viable cells at time of manufacture) 1 mg
Percent Daily Values are based on a 2,000 calorie diet. Daily Value (DV) not established.
Other Ingredients: Fructose, natural flavors, microcrystalline cellulose, stearic acid, magnesium stearate, citric acid, natural color Standardized Extract
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
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Drug Labeled for NoteAdefovir ≥ 12 years old Less potent
Risk of drug resistance
• 7 antiviral drugs are currently approved for use in adults• 4 of these are labeled for use in children (<18 years old)• Only 2 are available for younger children
Antiviral Therapy for < 18 years of age
g
Entecavir ≥ 16 years old Older teens only
Interferon alfa-2b ≥ 12 months old Potential adverse effects
Lamivudine ≥ 3 years old Less potentRisk of drug resistance
Haber, BA, et al. Pediatrics. published online Oct 5, 2009. (doi: 10.1542/peds.2009-0567)
Antiviral agents for 18 years and older
•Pegylated interferon alfa• Telbivudine• Tenofovir
Treatment outcomes inHBV infected children
IFN‐a (Sokal) Lamivudine (Jonas) Adefovir dipivoxil(Jonas)
HBeAg clearance 23* 26* 16
HBeAg 54 (7 years) 23* 16HBeAgseroconversion
54 (7 years) 23 16
Suppression of HBV DNA
29* 61* 23*
Side effects yes no no
Resistance to antiviral agent
no 19% no
HBsAg clearance 8.9% (7 years) 2% 0.5%
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Recommended pediatric doses
• Interferon alfa 2b –3 M IU/m2 subcutaneously tiw x 1 week then 6 M IU/m2 (max 10 MIU) x 16 – 24 weeks
• Lamivudine 3mg/kg/day in one daily oral dose (max 100 mg daily) (5mg/ml or 100 mg tab) – safety and efficacy not established > 1 yearefficacy not established > 1 year
• Adefovir dipivoxil 10 mg in one daily oral dose – safety and efficacy not established > 1 year (10 mg tablet)
• Entecavir – 0.5 mg in one daily oral dose (0.5 and 1 mg tablet, 0.05mg/ml oral solution) ‐ “Optimal duration of treatment not established”
Undetectable* HBV DNA in HBV Adults After 1 Year of Treatment
Not head‐to‐head trials; different patient populations and trial designs
HBeAg Positive HBeAg Negative
DNA (%
) 100
8067
76
90 88 91100
80
*By PCR‐based assay (LLD ~ 50 IU/mL) except for some LAM studies.
Lok A, et al. Hepatology. 2007;45:507‐539. EASL HBV Guidelines. Journal of Hepatology. 2009;50:227‐242.
Und
etectable*
HBV
D
60
40
20
0LAM ADV ETV LdT TDF
40‐44
13‐21
6760 60‐73
51‐6360
40
20
0LAM ADV ETV LdT TDF
HBeAg Loss/Seroconversion in HBeAg‐Positive Adults After 1 Year of Treatment
ersion
(%)
Not head‐to‐head trials; different patient populations and trial designs
HBeAg Loss HBeAg Seroconversion100
80
100
80
HBe
Ag Loss/Serocon
ve
Lau GK, et al. N Engl J Med. 2005;352:2682‐2695. Marcellin P, et al. N Engl J Med. 2003;348:808‐816 Chang TT, et al. N Engl J Med. 2006;354:1001‐1010. Lai CL, et al. N Engl J Med. 2007;357:2576‐2588. Marcellin P, et al. N Engl J Med. 2008;359:2442‐2455.
60
40
20
0LAM ADV ETV LdT TDF
3224 22 26
2212‐18
21 23 21
60
40
20
0LAM ADV ETV LdT TDF
NR
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10
nts (%
)
HBeAg Seroconversion in HBeAg‐Positive
Patients on Extended Treatment*
Not head‐to‐head trials; different patient populations and trial designs100
80
60
4047 50 48
LAM ADV ETV LdT TDF
Years of Therapy
Patie
*With sustained undetectable HBV DNA.
Chang TT, et al. N Engl J Med. 2006;354:1001‐1010. Lai CL, et al. N Engl J Med. 2007;357:2576‐2588. Marcellin P, et al.N Engl J Med. 2003;348:808‐816. Marcellin P, et al. N Engl J Med. 2008;359:2442‐2455. Lok AS, et al. Gastroenterology. 2003;125:1714‐1722. Leung NW, et al. Hepatology. 2001;33:1527‐1532. Dienstag JL, et al. Hepatology. 2003;37:748‐755. Marcellin P, et al. Hepatology. 2008;48:750‐758. Liaw YF, et al. Gastroenterology. 2009;136:486‐495. Gane E, et al. AASLD 2008. Abstract 729. Heathcote E, et al. AASLD 2008. Abstract 158.
40
20
01 2 3 4 5
22
1221 23 21
29 31 29 27
40 37
Cumulative Rates of Resistance With Oral Agents in Nucleos(t)ide‐Naive Patients
Not head‐to‐head trials; different patient populations and trial designs
100
LAM ADV ETV LdT TDF
EASL HBV Guidelines. J Hepatol. 2009;50:227‐242. Tenny DJ, et al. EASL 2009. Abstract 20.
Year
0
24
49
67 70
38
1 2 3 4 5
Patie
nts (%
)
80
40
60
20
03
1118
29
0.2 1.2 1.24
00
17
1.2
6
1.20.5
What Determines Rate of Resistance? Potency vs Genetic Barrier
• Potency is only 1 part of the equation• Pharmacologic barrier to resistance
– Dose/safety profile– Blood levels– Tissue concentration
• Genetic barrier to resistance – The number of substitutions needed for primary antiviral drug resistance
– Probably at least as important as potency
Allen MI, et al. Hepatology. 1998;27:1670‐1677. Yatsuji H, et al. Antimicrob Agents Chemother. 2006;50: 3867‐3874. Qi X, et al. Antivir Ther. 2007;12:355‐362. Villeneuve JP, et al. J Hepatol. 2003;39:1085‐1089. Baldick CJ, et al. Hepatology. 2008;47:1473‐1482. Seifer M, et al. Antiviral Res. 2009;81:147‐155. Heathcote E, et al. AASLD 2008. Abstract 158. Marcellin P, et al. AASLD 2008. Abstract 146.
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What Determines Rate of Resistance? Potency vsGenetic Barrier (cont)
• LAM: rtM204V/I and rtA181T (also possibly V) – Compensatory mutations: rtL180M, rtV173L, and rtL80V/I
• LdT: rtM204I (not rtM204V)• ADV: rtA181T and rtN236T
C bi ti f l ti b i d t l t 2• Combination of low genetic barrier drugs: at least 2 mutations required
• ETV: at least 3 mutations required– rtL180M + rtM204V + 1 of the following: rtT184G or rtS202I or
rtM250V change• TDF: no signature resistance mutations identified at 2 years
Allen MI, et al. Hepatology. 1998;27:1670‐1677. Yatsuji H, et al. Antimicrob Agents Chemother. 2006;50: 3867‐3874. Qi X, et al. Antivir Ther. 2007;12:355‐362. Villeneuve JP, et al. J Hepatol. 2003;39:1085‐1089. Baldick CJ, et al. Hepatology. 2008;47:1473‐1482. Seifer M, et al. Antiviral Res. 2009;81:147‐155. Heathcote E, et al. AASLD 2008. Abstract 158. Marcellin P, et al. AASLD 2008. Abstract 146.
HBsAg Level as Predictor of Long‐term Durability of PegIFN Response in HBeAg(‐)
• 4‐yr and 6‐mo response rates higher with Wk 12 HBsAg level ≤ 1500 IU/mL vs > 1500 IU/mL in long‐term cohort
6 mos posttreatment
HBsAg ≤ 1500 IU/mL
nse
6 mos posttreatment
HBsAg > 1500 IU/mL
nse
100
80
100
80
Marcellin P, et al. AASLD 2008. Abstract 919.
6 mos posttreatment4 yrs posttreatment
HBV DNA ≤10,000
copies/mL
HBV DNA ≤400
copies/mL
HBsAg Clearance
Patie
nts With
Respo
(%)
59
39 3931
7
23
60
40
20
0
6 mos posttreatment4 yrs posttreatment
HBV DNA ≤ 10,000
copies/mL
HBV DNA ≤400
copies/mL
HBsAg Clearance
Patie
nts With
Respo
(%)
34
12 9 82 4
60
40
20
0
80 80
Predictors of response to therapy
higher response rates
• < 5 years
• ALT >> normal
• Low HBV DNA
Lower response rates• > 5 years• Normal ALT• High HBV DNA• Liver failure
• Compensated liver disease
• HBV genotype A and B
• Low drug resistant mutant rates
• HBeAg + hepatitis
• Low HBsAg levels
• Liver failure• HBV genotype C and D• High drug resistance mutant
rates• HBeAg negative hepatitis• HDV• High HBsAg levels
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Recommendations for Treatment Initiation in
HBeAg‐Positive Adults
AASLD 2007[1] US Algorithm 2008[2] EASL 2009[3]
HBV DNA, IU/mL > 20,000 > 20,000 ≥ 2,000
ALT, x ULN* > 2 > 1 > 1
Disease stage/grade Moderate/severe necroinflammation/ f fDisease stage/grade and/or significant fibrosis
First-line therapy ADV,† ETV, pegIFN
ETV, TDF,pegIFN
ETV, TDF,pegIFN
1. Lok A, et al. Hepatology. 2007;45:507‐539. 2. Keeffe EB, et al. Clin Gastroenterol Hepatol. 2008;6:1315‐1341. 3. EASL HBV Guidelines. J Hepatology. 2009;50:227‐242.
*Persistent (> 3‐6 mos). †TDF not FDA approved at time of publication.
Criteria for HBV DNA, ALT and disease stage/grade must all be met
– If not, guidelines recommend monitoring and consideration of treatment based on individual’s age, health status, and stage of infection/disease
Recommendations for Treatment Initiation in HBeAg‐Negative Adults
AASLD 2007[1] US Algorithm 2008[2] EASL 2009[3]
HBV DNA, IU/mL > 20,000‡ > 2000 ≥ 2000
ALT, x ULN* 1 to > 2 > 1 > 1
Disease stage/grade Moderate/severe necroinflammationand/or significant fibrosis
First-line therapy ADV,† ETV, pegIFN
ETV, TDF,pegIFN
ETV, TDF,pegIFN
*Persistent (> 3‐6 mos). †TDF not FDA approved at time of publication. ‡ Consider liver biopsy if > 2000 IU/mL and treat if moderate/severe inflammation and/or fibrosis found.
Criteria for HBV DNA, ALT and disease stage/grade must all be met
– If not, guidelines recommend monitoring and consideration of treatment based on individual’s age, health status, and stage of infection/disease
1. Lok A, et al. Hepatology. 2007;45:507‐539. 2. Keeffe EB, et al. Clin Gastroenterol Hepatol. 2008;6:1315‐1341. 3. EASL HBV Guidelines. Journal of Hepatology. 2009;50:227‐242.
Special Populations That Should Also Be Considered for HBV Treatment
• Regardless of HBV DNA and ALT levels– Patients with rapid deterioration of liver function
– Patients with compensated cirrhosis • If DNA > 2 000 IU/mL regardless of ALT• If DNA > 2,000 IU/mL, regardless of ALT
– Patients with decompensated cirrhosis (IFN contraindicated)
– Recurrent HBV infection post liver transplantation
– HBV carriers undergoing immunosuppressive or cytotoxic chemotherapy
Lok A, et al. Hepatology. 2007;45:507‐539. Keeffe EB, et al. Clin Gastroenterol Hepatol. 2008;6:1315‐1341. EASL HBV Guidelines. Journal of Hepatology. 2009;50:227–242. Sorrell MF, et al. Ann Intern Med. 2009;150:104‐110.
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Special Populations That Should Also Be Considered for HBV Treatment
• Regardless of HBV DNA and ALT levels– Patients with rapid deterioration of liver function
– Patients with compensated cirrhosis • If DNA > 2 000 IU/mL regardless of ALT• If DNA > 2,000 IU/mL, regardless of ALT
– Patients with decompensated cirrhosis (IFN contraindicated)
– Recurrent HBV infection post liver transplantation
– HBV carriers undergoing immunosuppressive or cytotoxic chemotherapy
Lok A, et al. Hepatology. 2007;45:507‐539. Keeffe EB, et al. Clin Gastroenterol Hepatol. 2008;6:1315‐1341. EASL HBV Guidelines. Journal of Hepatology. 2009;50:227–242. Sorrell MF, et al. Ann Intern Med. 2009;150:104‐110.
• Despite immunoprophylaxis, perinatal transmission still occurs
• Highest in those who are eAg+• Rates 7-28%
SPECIAL CONSIDERATIONS OF PREGNANT FEMALES – PERINATAL TRANSMISSION
Rates 7-28%• High level of viremia thought to be the most important
factor• Wiseman 2009 reported 9% in 4/47 women with HBV
viral load >108 copies/ml• Limitations of studies to date
– small numbers, retrospective data– Little data in US patients
Recommendations for HBsAg+ HBV DNA + pregnant women at 28 weeks
Previous child HBV NEG
• If HBV DNA >108 cpmconsider treatment with lamivudine, tenofovir or t lbi di t 32 k d
Previous child HBV POS
• If HBV DNA >106cpm consider treatment
telbivudine at 32 weeks and HBIG and vaccine at birth
• If HBV DNA <108 cpmmonitor and give infant HBIG and vaccine at birth
• If HBV DNA <106 cpmmonitor and give infant HBIG and vaccine at birth
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Summary of FDA Approved Oral HBV Treatments for Adults
Oral Drug
Antiviral Potency*
Pharmacologic Barrier
Genetic Barrier†
Adverse Events‡
LAM + + 1 --ADV ++ + 1 Nephrotoxicity (≤1% per year)ETV ++++ ++++ 3
*Approximate and relative. †Number of mutations needed for primary antiviral drug resistance.‡Only includes reported adverse events that may differ in historical incidence associated with LAM and, therefore, potentially affecting selection vs other agents. Pancreatitis has been reported as a class effect and all agents have to be dose adjusted for renal insufficiency.§ From HIV databases
ETV ++++ ++++ 3 --LdT ++ ++ 1 Myalgia, myositis, neuropathy,
cardiac arrhythmia (rare)TDF ++++ ++++ ? Nephrotoxicity§
Case #1
• 3 year old treatment naive adopted Nigerian male with Giardia lamblia, presumed perinatalacquisition of HBV
• Physical exam: normal• Physical exam: normal
• LABS: ALT 39, 78, 65, 77 IU/L q 6 months x 4
• HBsAg +, HBeAg+
• Genotype E
• HBV DNA 10,000 IU/ml
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Case #1 continued
• Consider treatment?
• Consider liver biopsy?
• If treatment, what agent?
Case #2
• 12 year old adopted Romanian female with presumed perinatal acquisition of HBV, lamivudine resistant
• Physical exam normal• Physical exam normal
• LABS: ALT 150 IU/l
• HBsAg+, HBeAg+
• HBV DNA 5M IU/L
• Genotype C
Case #2 cont
• Consider treatment?
• Consider liver biopsy?
• If treatment, what agent?
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Case #3
• 16 year old treatment naïve African American female with IVDU – mode of acquisition either IVDU or perinatal
• Physical exam: hepatomegaly• LABS: ALT 234 IU/L• HBsAg+ HBeAg neg• HBV DNA 1 M IU/L• Genotype A•
Case #3 cont
• Consider treatment?
• Consider liver biopsy?
• If treatment, what agent?