1. Identifying and Managing Patients at Risk for HBV Reactivation
HBV, hepatitis B virus.
Supported by an independent educational grant from Gilead Sciences

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3. Program Chair
Robert P. Perrillo, MD, FAASLD Senior Investigator Hepatology Division Baylor University Medical Center Adjunct Professor of Medicine University of Texas Southwestern Medical Center Dallas, Texas
This slide lists the faculty who were involved in the production of these slides.

4. Faculty
Leonard H. Calabrese, DO Professor of Medicine Department of Rheumatology Cleveland Clinic Cleveland, Ohio Andrew D. Zelenetz, MD, PhD Medical Director, Quality Informatics Attending Physician, Lymphoma Service Department of Medicine Memorial Sloan Kettering Cancer Center Professor of Medicine Weill-Cornell Medical College New York, New York
This slide lists the faculty who were involved in the production of these slides.

5. Disclosures
Leonard H. Calabrese, DO, has disclosed that he has received fees for non-CME/CE services from AbbVie, Bristol-Myers Squibb, Genentech, GlaxoSmithKline, Janssen, Pfizer, and UCB. Robert P. Perrillo, MD, FAASLD, has disclosed that he has received consulting fees from Dynavax. Andrew D. Zelenetz, MD, PhD, has disclosed that he has received funds for research support from Bristol-Myers Squibb, Gilead, GlaxoSmithKline, Janssen, and Roche, consulting fees from Adaptive Biotechnology, Amgen, Celgene, Genentech/Roche, Gilead, GlaxoSmithKline, Hospira, Janssen, Nanostring Tech, Novartis, Portola Pharmaceuticals, and Takeda, and holds membership with a data monitoring committee with Boehringer Ingelheim.
This slide lists the disclosure information of the faculty and staff involved in the development of these slides.

6. Program Overview Defining HBV Reactivation
HBV Reactivation Risk, Screening, and Prophylaxis
Concerns for Specific Populations
Patients With Rheumatologic and Dermatologic Disorders
Patients With Oncologic Disorders
Current Areas of Need
HBV, hepatitis B virus.
Slide credit: clinicaloptions.com

7. Case: 55-Yr-Old Chinese Woman With Stage II Breast Cancer
Treated with doxorubicin, paclitaxel, dexamethasone, and cyclophosphamide
4000
Pt dies 20
3000 15
ALT Total bilirubin
Entecavir initiated
2000
Total Bilirubin (mg/dL)
Serum ALT (IU/L) 10
ALT, alanine aminotransferase.
Chemotherapy discontinued
1000 5
First abnormal ALT 20 40 60 80
Days Following Initiation of Chemotherapy
Slide credit: clinicaloptions.com

8. Defining HBV Reactivation
HBV, hepatitis B virus.

9. HBV Reactivation: Overview
Clinical syndrome characterized by an increase in HBV DNA and ALT/AST with or without symptoms or jaundice
Occurs in pts with active (HBsAg+) and resolved (HBsAg-, anti-HBc+) HBV infection
Wide clinical spectrum
Ranges from silent to liver failure
Can occur during treatment with many immunosuppressive agents
May also occur up to 12 mos after treatment
Preventable by antiviral prophylaxis
ALT, alanine aminotransferase; AST, aspartate aminotransferase; HBc, hepatitis B core antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.
Di Bisceglie AM, et al. Hepatology. 2015;61:
Perrillo RP, et al. Gastroenterology. 2015;148:
Slide credit: clinicaloptions.com

10. How Do You Define HBV Reactivation?
2 components
Virologic: increase in viral replication
Biochemical: increase in ALT and/or AST
Component
Criteria
Virologic
At least 10-fold (> 1 log10 IU/mL) increase in HBV DNA
De novo detection of HBV DNA or HBeAg
HBV DNA value above arbitrary cutoff in presence of biochemical worsening
Reverse HBsAg seroconversion
Biochemical
3-fold increase of ALT above baseline
Some studies use additional > 100 U/L
ALT, alanine aminotransferase; AST, aspartate aminotransferase; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.
Hoofnagle JH. Hepatology. 2009;49:S156-S165. Terrault NA, et al. Hepatology. 2016;63: Visram A, et al. Clin Liver Dis. 2015;5: Hwang JP, et al. Support Care Cancer. 2012;20:
Slide credit: clinicaloptions.com

11. HBV Reactivation Risk
HBV, hepatitis B virus.

12. HBV Reactivation Risk Assessment
Drug Immunosuppression Potency
Low
High X
Immune Control
Risk of Reactivation
Anti-HBs
Anti-HBc
Positive
Negative
HBc, hepatitis B core antibody; HBs, hepatitis B surface antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.
HBsAg
Negative
Positive
HBV DNA
Negative
Low Level
High Level
Resolved Infection
Occult Infection
Inactive HBsAg Carrier
Immune Active Chronic Hepatitis B
Perrillo RP, et al. Gastroenterology. 2015;148:
Bessone F, et al. World J Hepatol. 2016;8:
Slide credit: clinicaloptions.com

13. HBV Reactivation Risk Assessment
Drug Immunosuppression Potency
Low
High
Immune Control X
Risk of Reactivation
Anti-HBs
Anti-HBc
Positive
Negative
HBc, hepatitis B core antibody; HBs, hepatitis B surface antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.
HBsAg
Negative
Positive
HBV DNA
Negative
Low Level
High Level
Resolved Infection
Occult Infection
Inactive HBsAg Carrier
Immune Active Chronic Hepatitis B
Perrillo RP, et al. Gastroenterology. 2015;148:
Bessone F, et al. World J Hepatol. 2016;8:
Slide credit: clinicaloptions.com

14. HBV Reactivation Risk Assessment
Drug Immunosuppression Potency
Low
High
Immune Control X
Risk of Reactivation
Anti-HBs
Anti-HBc
Positive
Negative
HBc, hepatitis B core antibody; HBs, hepatitis B surface antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.
HBsAg
Negative
Positive
HBV DNA
Negative
Low Level
High Level
Resolved Infection
Occult Infection
Inactive HBsAg Carrier
Immune Active Chronic Hepatitis B
Perrillo RP, et al. Gastroenterology. 2015;148:
Bessone F, et al. World J Hepatol. 2016;8:
Slide credit: clinicaloptions.com

15. HBV Reactivation Risk Assessment
Drug Immunosuppression Potency
Low
High
Immune Control X X
Risk of Reactivation
Anti-HBs
Anti-HBc
Positive
Negative
HBc, hepatitis B core antibody; HBs, hepatitis B surface antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.
HBsAg
Negative
Positive
HBV DNA
Negative
Low Level
High Level
Resolved Infection
Occult Infection
Inactive HBsAg Carrier
Immune Active Chronic Hepatitis B
Perrillo RP, et al. Gastroenterology. 2015;148:
Bessone F, et al. World J Hepatol. 2016;8:
Slide credit: clinicaloptions.com

16. HBV Reactivation Risk Assessment
Drug Immunosuppression Potency
Low
High
Immune Control X
Risk of Reactivation
Anti-HBs
Anti-HBc
Positive
Negative
HBc, hepatitis B core antibody; HBs, hepatitis B surface antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.
HBsAg
Negative
Positive
HBV DNA
Negative
Low Level
High Level
Resolved Infection
Occult Infection
Inactive HBsAg Carrier
Immune Active Chronic Hepatitis B
Perrillo RP, et al. Gastroenterology. 2015;148:
Bessone F, et al. World J Hepatol. 2016;8:
Slide credit: clinicaloptions.com

17. Serological Risk Status Immunosuppressive Agent Risk Status
HBV Reactivation Risk Based on Serologic Status and Immunosuppressive Potency
Risk Level
Serological Risk Status
Immunosuppressive Agent Risk Status
High
HBsAg+,
high HBV DNA, or HBeAg+
B-cell–depleting agents
Systemic chemotherapy
Moderate/high-dose corticosteroids*
Intermediate
HBsAg-, anti-HBc+, anti-HBs-
TNF inhibitors
Tyrosine kinase inhibitors
Other cytokine and integrin inhibitors
Transarterial chemoembolization
Low/moderate/high-dose corticosteroids†
Low
HBsAg-, anti-HBc+, anti-HBs+
Methotrexate
Azathioprine
6-mercaptopurine
Low-dose corticosteroids‡
HBc, hepatitis B core antibody; HBeAg, hepatitis B e antigen; HBs, hepatitis B surface antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; TNF, tumor necrosis factor.
*≥ 10 mg for ≥ 4 wks for HBsAg+/anti-HBc+. †< 10 mg for ≥ 4 wks for HBsAg+/anti-HBc+; ≥ 10 mg for ≥ 4 wks for HBsAg-/anti-HBc+. ‡< 1 wk for HBsAg±/anti-HBc+; < 10 mg for ≥ 4 wks for HBsAg-/anti-HBc+.
Perrillo RP, et al. Gastroenterology. 2015;148: Reddy KR, et al. Gastroenterology. 2015;148:
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18. Who Should Receive HBV Screening Prior to Immunosuppressive Therapy?
HBV, hepatitis B virus.

19. HBV Screening Prior to Immunosuppressive Therapy
All pts should be screened
Supported by CDC,[1] EASL,[2] and APASL[3] guidelines
Some disagreement in guidelines: AASLD,[4] AGA,[5] and ASCO[6] recommend screening for pts based on HBV reactivation risk
Screening should include assessment of[1-6]:
HBsAg
Anti-HBc
Additional: HBV DNA levels[2,3,5,6]
AASLD, American Association for the Study of Liver Diseases; AGA, American Gastroenterological Association; APASL, Asian Pacific Association for the Study of the Liver; ASCO, American Society of Clinical Oncology; CDC, Centers for Disease Control and Prevention; EASL, European Association for the Study of the Liver; HBc, hepatitis B core antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.
1. Weinbaum CM, et al. MMWR Recomm Rep. 2008:57: EASL. J Hepatol. 2012;57:167‐ Sarin SK, et al. Hepatol Int. 2016;10: Lok AS, et al. Hepatology. 2009;50: Reddy KR, et al. Gastroenterology. 2015;148: Hwang JP, et al. J Clin Oncol. 2015;33:
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20. Risk Factors Do Not Accurately Identify Pts With HBV Infection
Antenatal screening studies
35% to 65% of pts with HBV would have been missed[1,2]
Pts do not know they are infected[3]
Healthcare access issues among minorities[4]
65% unaware of infection[3-5]
HBV, hepatitis B virus.
1. CDC. MMWR Morb Mortal Wkly Rep. 1988;37: , Brook MG, et al. Q J Med. 1989;71: Institute of Medicine Ward JW, et al. Hepatology. 2012;56: Hu DJ, et al. Hepatology. 2013;58: Lin SY, et al. Hepatology. 2007;46:
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21. Suboptimal Screening and Treatment: AASLD Survey
Survey of AASLD members regarding HBV reactivation experiences during cancer chemotherapy (N = 188 pts described)
HBV screening before chemotherapy occurred in 53% (100/188) of cases
More common with hematologic malignancies vs solid tumors (63% vs 29%; P ≤ .001)
More common in pts treated with vs without rituximab (73% vs 56%; P = .06)
Characteristic, %
Cases
(N = 188)
Type of screening
HBsAg and anti-HBc
39.9
HBsAg only
12.8
Anti-HBc only
0.5
None
31.9
Unknown
14.9
Antiviral therapy
After chemotherapy
72.9
Before chemotherapy
9.6
3.2
AASLD, American Association for the Study of Liver Diseases; HBc, hepatitis B core antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.
Slide credit: clinicaloptions.com
Hwang JP, et al. J Viral Hepat. 2015;22:

22. Who Should Receive HBV Prophylaxis?
HBV, hepatitis B virus.

23. HBV Prophylaxis for Pts Receiving Immunosuppressive Therapy
Candidates
HBsAg+[1-6]
HBsAg-/anti-HBc+ if
Receiving therapy associated with high HBV reactivation risk (AGA,[5] ASCO[6]*)
Detectable HBV DNA (EASL,[2] APASL[3], AASLD[4])
Timing of initiation[1-6]
At or before onset of immunosuppressive therapy
AASLD, American Association for the Study of Liver Diseases; AGA, American Gastroenterological Association; APASL, Asian Pacific Association for the Study of the Liver; ASCO, American Society of Clinical Oncology; EASL, European Association for the Study of the Liver; HBc, hepatitis B core antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.
*ASCO states that these pts may alternatively be monitored and treated with on-demand therapy as needed.
1. Weinbaum CM, et al. MMWR Recomm Rep. 2008:57: EASL. J Hepatol. 2012;57:167‐ Sarin SK, et al. Hepatol Int. 2016;10: Lok AS, et al. Hepatology. 2009;50: Reddy KR, et al. Gastroenterology. 2015;148: Hwang JP, et al. J Clin Oncol. 2015;33:
Slide credit: clinicaloptions.com

24. HBV Prophylaxis for Pts Receiving Immunosuppressive Therapy
Duration
Varies among guidelines
6 mos post immunosuppressive therapy if HBV DNA < 2000 IU OR until treatment goals reached if > 2000 IU (AASLD)[1]
6 mos post immunosuppressive therapy OR 12+ mos if B-cell–depleting agent (AGA, ASCO)[2,3]
12 mos post immunosuppressive therapy (EASL, APASL)[4,5]
AASLD, American Association for the Study of Liver Diseases; AGA, American Gastroenterological Association; APASL, Asian Pacific Association for the Study of the Liver; ASCO, American Society of Clinical Oncology; EASL, European Association for the Study of the Liver; HBc, hepatitis B core antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.
1. Lok AS, et al. Hepatology. 2009;50: Reddy KR, et al. Gastroenterology. 2015;148: Hwang JP, et al. J Clin Oncol. 2015;33: EASL. J Hepatol. 2012;57:167‐ Sarin SK, et al. Hepatol Int. 2016;10:1-98.
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25. Randomized, Controlled Trials of HBV Prophylaxis
Control Lamivudine
Control Entecavir
Control Tenofovir
Lamivudine Entecavir 70
P = .002 60 56 53
P = .001 50
P < .001 41 40
P = .001
P = .02 30
HBV Reactivation (%) 29 30
P = .03
P = NS 20 18 17 12
HBc, hepatitis B core antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; NS, not significant; TACE, transarterial chemoembolization.
References:
1. Lau GK, et al. Gastroenterology. 2003;125:
2. Jang JW, et al. Hepatology. 2006;43:
3. Hsu C, et al. Hepatology. 2008;47:
4. Long M, et al. Breast Cancer Res Treat. 2011;127:
5. Huang YH, et al. J Clin Oncol. 2013;31:
6. Buti M, et al. J Hepatology. 2014;60:S421-S422.
7. Huang H, et al. JAMA. 2014;312: 10 7 3 2
Lymphoma, HBsAg+ (N = 30)[1]
HCC, HBV DNA+ (N = 76)[2]
Lymphoma, HBsAg+ (N = 52)[3]
Breast Cancer, HBsAg+ (N = 42)[4]
Lymphoma, HBsAg- Anti-HBc+ (N = 80)[5]
Lymphoma, HBsAg- Anti-HBc+ (N = 30)[6]
Lymphoma, HBsAg+ (N = 121)[7]
Slide credit: clinicaloptions.com
References in slidenotes.

26. Choosing an Antiviral for HBV Prophylaxis
Drugs with high genetic barrier to resistance (tenofovir, entecavir) preferred[1]
Lamivudine associated with resistance[1]
Entecavir prophylaxis associated with a significantly lower incidence of HBV reactivation vs lamivudine in randomized controlled trial[2]
Adefovir less potent than tenofovir for treating HBV[3]
Lamivudine plus adefovir may be an option[4]
HBV, hepatitis B virus.
1. Reddy KR, et al. Gastroenterology. 2015;148: Huang H, et al. JAMA. 2014;312: Marcellin P, et al. N Engl J Med. 2008;359: Vassiliadis TG, et al. J Gastroenterol Hepatol. 2010;25:54-60.
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27. HBV Reactivation in Pts Receiving HCV Therapy

28. HBV Reactivation Risk in HBV/HCV Coinfected Pts Receiving HCV DAAs
Case reports of HBV reactivation in pts treated with SMV + SOF ± RBV,[1,2] DCV + ASV,[3,4] and LDV/SOF[5]
Observational study of Chinese pts treated with DAAs (N = 327 screened)[6]
3/10 HBsAg+ pts experienced hepatitis due to HBV reactivation
Of 124 HBsAg-/HBcAb+ pts, none experienced hepatitis due to HBV reactivation
Analysis of open-label phase IIIb trial[7]
No evidence of HBV reactivation in HBsAg-/HBcAb+ pts receiving LDV/SOF (n = 103)
FDA to require boxed warning for certain DAAs regarding the risk of HBV reactivation and need for HBV screening/monitoring for pts being treated with DAAs[8]
ASV, asunaprevir; DAA, direct-acting antiviral; DCV, daclatasvir; FDA, US Food and Drug Administration; LDV, ledipasvir; RBV, ribavirin; SMV, simeprevir; SOF, sofosbuvir.
References
1. Collins JM, et al. Clin Infect Dis. 2015;61:
2. Ende AR, et al. J Med Case Rep. 2015;9:164.
3. Hayashi K, et al. Clin J Gastroenterol. 2016;9:
4. Takayama H, et al. Hepatol Res. 2016;46:
5. De Monte A, et al. J Clin Virol. 2016;78:27-30.
6. Wang C, et al. Clin Gastroenterol Hepatol. 2016;[Epub ahead of print].
7. Sulkowski MS, et al. Clin Infect Dis. 2016;[Epub ahead of print].
8. FDA. Direct-Acting Antivirals for Hepatitis C: Drug Safety Communication - Risk of Hepatitis B Reactivating Available at: Accessed October 8, 2016.
Slide credit: clinicaloptions.com
References in slidenotes.

29. AASLD Guidance on HBV Reactivation in Pts Receiving HCV DAA Therapy
HBV vaccination recommended for all susceptible individuals (eg, no previous immunization, no evidence of immunization response)
All pts starting HCV DAA therapy should be assessed for HBV infection (HBsAg, anti-HBs, and anti-HBc testing)
If HBsAg+, assess HBV DNA prior to, during, and immediately after HCV DAA therapy
For active HBV infection, initiate HBV therapy before or simultaneously with HCV DAA therapy
For low or undetectable HBV DNA, monitor for HBV reactivation during HCV DAA therapy
Insufficient data to provide recommendations for pts who are HBsAg- and anti-HBc+ or anti-HBs+/anti-HBc+
Slide credit: clinicaloptions.com
AASLD/IDSA HCV Guidelines. September 2016.

30. Concerns in Patients With Rheumatologic and Dermatologic Disorders

31. HBV Reactivation and TNF Inhibitors
Analysis of cases of pts with autoimmune disease who were HBsAg+ or anti-HBc+ and had received TNF inhibitor therapy (N = 257)
Status
Findings
HBsAg+
(n = 89)
HBV reactivation: 35/89 (39%)
More frequent in pts with vs without prior immunosuppressive treatment (96% vs 70%; P = .033)
Less frequent in pts with vs without antiviral prophylaxis (23% vs 62%; P = .003)
Anti-HBc+
(n = 168)
HBV reactivation: 9/168 (5%)
Mean time to reactivation: 11 mos
No reactivating pt received antiviral prophylaxis
3 pts with HBV DNA > 100,000 IU/mL; 2 pts with symptoms of liver disease; 1 death
HBc, hepatitis core antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; TNF, tumor necrosis factor.
Slide credit: clinicaloptions.com
Perez-Alvarez R, et al. Medicine. 2011;90:

32. HBV Reactivation and Rituximab
Rituximab: B-cell–depleting agent often added to CHOP for treating NHL[1]
Increased reactivation risk in rituximab-treated pts
Can cause treatment delays, inferior outcomes, increased morbidity
May be preventable with antiviral prophylactic therapy
FDA Boxed Warning for HBV reactivation[2]
HBV reactivation reported in HBsAg+ and HBsAg-/anti-HBc+ pts and can result in fulminant hepatitis, hepatic failure, and death
All pts should be screened before and monitored during/after use
CHOP, cyclophosphamide, doxorubicin, vincristine, prednisone; HBc, hepatitis core antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; FDA, US Food and Drug Administration; NHL, non-Hodgkin’s lymphoma.
1. Villadolid J, et al. Oncologist. 2010;15:
2. Rituximab [package insert]. April 2016.
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33. HBV Reactivation and Abatacept
Abatacept: inhibitor of T-cell activation
Anecdotal data suggest it should be treated as a TNF inhibitor regarding HBV reactivation[1]
Clinical studies have excluded pts who tested positive for hepatitis during screening[2]
Package insert[2]
Pretreatment screening should be performed per guideline recommendations
HBV, hepatitis B virus; TNF, tumor necrosis factor.
1. Kim PS, et al. Arthritis Care Res. 2012;64:
2. Abatacept [package insert]. June 2016.
Slide credit: clinicaloptions.com

34. 2015 ACR RA Treatment Guidelines: HBV Recommendations
Screening
No specific recommendations[1]
2008 guidance[2]: screen pts receiving methotrexate or leflunomide if high risk for HBV infection exists
Prophylaxis/treatment[1]
Active HBV infection: immunosuppressive therapy can be administered with concomitant HBV treatment
HBsAg+: refer for HBV prophylaxis prior to immunosuppressive therapy
HBsAg-/anti-HBc+: monitor HBV DNA
ACR, American College of Rheumatology; HBc, hepatitis core antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; RA, rheumatoid arthritis.
1. Singh JA, et al. Arthritis Rheumatol. 2016;68:1-26.
2. Saag KG, et al. Arthritis Rheum. 2008;59:
Slide credit: clinicaloptions.com

35. Concerns in Patients With Oncologic Disorders

36. Single-Center HBV Reactivation Experience
Assessment after death from acute liver failure secondary to HBV reactivation was reported to hospital QA
Retrospective study assessed pts with HBV DNA > 1000 copies/mL receiving chemotherapy between and 2009 (N = 241)
Documented acute increase in serum ALT: n = 23
HBV reactivation: n = 22
ALT, alanine aminotransferase; HBV, hepatitis B virus; MSKCC, Memorial Sloan Kettering Cancer Center; QA, quality assurance.
Slide credit: clinicaloptions.com
Mendelsohn RB, et al. ASCO Abstract 9088.

37. Single-Center Experience: Characteristics of HBV Reactivation Cases (N = 22)
Country of Birth
Underlying Malignancy
China US
Other
Lymphoma
Leukemia
Solid tumors
32%
32%
50%
58%
18%
10%
HBV, hepatitis B virus; MSKCC, Memorial Sloan Kettering Cancer Center.
Slide credit: clinicaloptions.com
Mendelsohn RB, et al. ASCO Abstract 9088.

38. Single-Center Experience: HBV Reactivation Outcomes
4 of 22 pts experiencing HBV reactivation died
Additional HBV reactivation outcomes:
Hepatitis flare resolved, n/N = 15/22 (68%)
Altered outcomes, n/N = 4/22
Preclusion of BMT (n = 1)
Chemotherapy delay (n = 1)
Surgical resection delay leading to unresectable disease (n = 1)
Liver transplant required (n = 1)
HBV reactivation occurred in pts with known HBV history and unknown HBV exposure
BMT, bone marrow transplant; HBV, hepatitis B virus; MSKCC, Memorial Sloan Kettering Cancer Center.
Slide credit: clinicaloptions.com
Mendelsohn RB, et al. ASCO Abstract 9088.

39. AASLD Survey: HBV Reactivation by Cancer Type
Survey of AASLD members regarding HBV reactivation experiences during cancer chemotherapy (N = 188 pts described)
HBV Reactivation
HCC
Solid Hematologic
Unknown
Breast, n = 17 Lung, n = 4
Colon, n = 2
AASLD, American Association for the Study of Liver Diseases; HBV, hepatitis B virus; HCC, hepatocellular carcinoma.
Lymphoma, n = 88 Leukemia, n = 30
Other, n = 8
Hwang JP, et al. J Viral Hep. 2015;22:

40. Go Online for More CCO Coverage of HBV Reactivation!
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