1

This enduring activity is supported by educational grants from AbbVie & Gilead Sciences, Inc.

This webcast is not sanctioned by the AASLD conference organizers,

nor is it an official part of the conference proceedings.

2

Poor Adherence to Hepatocellular Carcinoma

(HCC) Surveillance in a U.S. Cohort of 2376

Patients with Chronic Hepatitis C (CHC)

and Cirrhosis

Abstract #57

Sally A. Tran1,4, Joseph K. Hoang1, An K. Le1, Changqing Zhao1,2,

Lee Ann Yasukawa3, Susan C. Weber3, Mindie H. Nguyen1;

1. Division of Gastroenterology and Hepatology, Stanford University Medical Center, Palo Alto, CA;

2. Department of Cirrhosis, Shuguang Hospital, Shanghai, China;

3. Center for Clinical Informatics, Stanford University School of Medicine, Palo Alto, CA;

4. Stanford University, Palo Alto, CA

3

0

5

10

15

20

25

30

35

40

45

50

Optimal (Imaging every 6mo)

Fair (Imaging every 6-12mo)

Poor (Imaging every 12-24mo)

Very Poor (Imaging < every24 months/no screening)

Pati

en

ts (

%)

18.8% 16.9%

18.5%

45.8% • 2376 patients monitored for at least 1 year

• Median follow-up = 45.4 months (range: 12-231)

• Mean age = 54+10 yo; 63% male

4

• No significant difference in surveillance between men and women.

• Patients >55 yo had higher rates of optimal surveillance (21.4% vs. 16.2%,

p<0.0001), as well as decompensated patients compared to compensated

patients (22.7% vs. 10.9%, p<0.0001) and Asian patients compared to non-

Asians (30.6% vs. 17.4%, p<0.0001).

• 435 patients developed HCC during follow-up

– 30.2% (90/298) Asians

– 13.2% (345/2619) non-Asians

• The 5-year cumulative incidences of HCC were greater in Asians (15.2% vs.

28.6%, p<0.00001).

• HCC patients who had optimal/fair adherence to surveillance (imaging at least

every 12 months) had less portal vein thrombosis (6.7% vs. 21.3%, P<0.0001).

• HCC patients who have had optimal/fair surveillance were also more likely to

meet the Milan criteria for liver transplants (66.0% vs. 50.0%, p<0.037) and

UCSF criteria for liver transplants (81.9% vs. 67.9%, p<0.031).

5

The impact of sustained virological response to

HCV infection on long term risk of hepatocellular

carcinoma: The BC Hepatitis Testers Cohort

Abstract #175

Naveed Z. Janjua1,2, Mei Y. Chong1, Margot E. Kuo1,

Amanda Yu1, Hasina Samji1, Zahid Butt1,2, Maria Alvarez1, Darrel Cook1,

Jason Wong1,2, Ryan Woods3, Mark Tyndall1,2, Morris Sherman4,

Eric M. Yoshida2, Mel Krajden1,2;

1. BC Centre for Disease Control,Vancouver, BC, Canada;

2. University of British Columbia, Vancouver, BC, Canada;

3. BC Cancer Agency, Vancouver, BC, Canada;

4. Medicine, University of Toronto, Toronto, ON, Canada

6

• The risk of hepatocellular carcinoma(HCC) post HCV cure

is not well-established for the North American population.

• We assessed the effect of sustained virologic

response(SVR) on the risk of HCC among a large

population based cohort in Canada.

7

• The BC Hepatitis Testers Cohort includes ~1.5 million individuals

tested for HCV between 1990–2013, linked with data on medical

visits, hospitalizations, cancers, prescription drugs and mortality.

• Patients who received IFN based treatments were followed from

the end of last treatment to HCC occurrence, death or December

31, 2012.

• Examined HCC risk among those who did

and did not achieve SVR using cumulative

incidence function and multivariable Cox proportional hazard

models.

• 8147 patients initiated treatment and 57% achieved SVR.

• Median follow up: 5.6 yr (range: 0.5-12.9)

8

Cumulative HCC Incidence by SVR

Person years at risk

Cu

mu

lati

ve

In

cid

en

ce

0.0

0.0 2.5 5.0

No SVR SVRTreatment outcome

Gray’s Test p<.0001

7.5 10.0 12.5

0.1

0.2

0.3

• HCC incidence rate (IR)

was 1.1/1000 person-yr

(PY) in the SVR and

7.2/1000 PY in the

no-SVR groups.

• The IR was higher among

those with cirrhosis at

treatment (SVR: 6.4, no-

SVR: 21.0/1000 PY).

• In those with SVR, cirrhosis

(HR=3.16), older age (50-

59 yr: HR=4.73; 60+yr:

HR=5.44 vs. ≤49 yr),

and being male (HR=3.3)

were associated with higher

HCC risk.

9

Liver-related morbidity and mortality in patients with

Chronic Hepatitis C and cirrhosis with and without

sustained virologic response

Abstract #176

Sofie Hallager1, Steen Ladelund2, Peer B. Christensen3,4,

Mette Clausen5, Alex L. Laursen6, Axel M.ller7, Poul Schlicthting8,

Lone Galmstrup Madsen9, Jan Gerstoft10, Suzanne Lunding11,

Karin Elmegaard Gronb.aek12, Henrik Krarup13, Nina Weis1,14;

1. Infectious Diseases, Copenhagen University Hospital,

Hvidovre, K.benhavn., Denmark;

2. Clinical research Center, Hvidovre Hospital,

Hvidovre, Denmark;

3. Infectious Diseases, Odense University Hospital,

Odense, Denmark;

4. Clinical Institute, University of Southern Denmark,

Odense, Denmark;

5. Hepatology, Rigshospitalet, Copenhagen, Denmark;

6. Infectious Diseases, Skejby Sygehus, Aarhus, Denmark;

7. Internal Medicine, Kolding Sygehus, Kolding, Denmark;

8. Hepatology, Herlev Hospital, Copenhagen, Denmark;

9. Gastroenterology, K.ge Sygehus, K.ge, Denmark;

10. Infectious Diseases, Rigshospitalet, Copenhagen, Denmark;

11. Lung and infectious diseases, Nordsj.llands Hospital,

Hiller.d, Denmark;

12. gastroenterology, Hvidovre Hospital, Hvidovre, Denmark;

13. Section of Molecular Diagnostics, Clinical Biochemistry and

Department of Gastroenterology, Aalborg Sygehus,

Aalborg, Denmark;

14. Faculty of Health and Medical Sciences, Department of Clinical

Medicine, University of Copenhagen, Copenhagen, Denmark

10

• Patients registered in DANHEP (Danish Database for

Hepatitis B and C), with CHC and cirrhosis diagnosed

before 31 December 2012 were eligible.

• Cirrhosis was based on liver biopsy, transient elastography

≥ 17 kPa, and clinical cirrhosis.

• 988 patients included: 68% male, median age 52, 43% GT1

and 37% GT3.

• Median follow-up 3.5 years [range 0 – 10.5]

• 44% achieved SVR

11

Time [Years]

Cu

mu

lati

ve I

ncid

en

ce Morbidity

Decompensation

HCC

Ascites

EVH

Hepatic Encephalopathy

SBP

0.0

0.0

0.1

0.2

2.5 5.0 7.5 10.0

12

• Crude all-cause and liver-related mortality

rates were 7.3/100 person years (PY) [6.5; 8.2] and

4.6/100 PY [4.0; 5.2], respectively, for the entire cohort.

• Liver-related and liver-unrelated mortality rate ratios for

patients with SVR vs non- SVR were 0.6 [0.4; 0.9] and

0.7 [0.5; 1.1], respectively, when adjusting for

confounders.

13

Optimal Timing of Hepatitis C Treatment for

Patients on the Liver Transplant Waiting List

Abstract #254

Jagpreet Chhatwal6,1, Sumeyye Samur6,1, Brian Kues2,

Turgay Ayer2, Mark S. Roberts3, Fasiha Kanwal4,5, Chin Hur6,1,

Drew M. Donnell3, Raymond T. Chung1,6;

1. Harvard Medical School, Boston, MA;

2. Georgia Institute of Technology, Atlanta, GA;

3. University of Pittsburgh, Pittsburgh, PA;

4. Baylor College of Medicine, Houston, TX;

5. Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX;

6. Massachusetts General Hospital, Boston, MA

14

• There is a tradeoff between pre- versus post-LT

treatment of HCV—treatment can improve liver

functions but decrease the likelihood of LT.

• Objective: Identify LT-eligible patients with decomp

cirrhosis who will benefit/not benefit) from pre-LT

treatment based on their MELD scores.

15

• We simulated a virtual trial comparing long-term outcomes

of pre- versus post-LT HCV treatment with oral DAAs for

genotype 1 and 4 patients having MELD scores between10-

40.

• Markov-based microsimulation model, SIM-LT (simulation of

liver transplant candidates), which simulated the life course

of patients on the transplant waiting list.

• SIM-LT integrated data from recent trials of oral DAAs

(SOLAR 1 and 2), United Network for Organ Sharing

(UNOS), and other published studies.

16

• SIM-LT followed patients on the transplant waiting list,

tracked their MELD scores over time, and projected the

natural history of their disease

after LT.

• The outcomes of the model included expected life years,

quality-adjusted life years (QALYs), 1-year and 5-year

patient survival, and death from background and liver-

related causes.

• Model-predicted patient-survival was validated

with UNOS data.

17

10

MELD

Ch

an

ge i

n L

ife

Yea

rs

-1

0

1

2

3

4

5

6

7

8

9

12 14 16 18 20 22 24 26 28 30 32 34 36 38 40

• On average, treating HCV before LT would

increase life expectancy (and QALYs) if

MELD ≤ 26, and could decrease at higher

MELD.

• Threshold to treat HCV pre-LT varied

between 22 and 26, depending on the

UNOS region; lower for UNOS regions 3, 10

& 11, and higher for regions 1, 2, 4, 5, 8 & 9.

18

Reduction in Liver Transplant Wait-Listing in

the Era of Direct Acting Anti-Viral Therapy

LB-23

Jennifer A. Flemming1, W. Ray Kim2, Carol L. Brosgart3, Norah Terrault3;

1. Medicine and Public Health Services, Queens University, Kingston, ON, Canada;

2. Medicine, Stanford University, Palo Alto, CA;

3. University of California San Francisco, San Francisco, CA

19

• Cohort study using the Scientific Registry of Transplant

Recipients database from 2003-2015.

• 47,591 adults wait-listed for LT due to HCV, HBV and NASH

were identified.

• LT indication was defined as decompensated cirrhosis if the

model for MELD at wait listing was

≥ 15 or HCC.

• Era of listing was divided into “interferon” ([IFN] 2003-2010),

“protease inhibitor” ([PI] 2011-2013), and “direct-acting

antiviral” ([DAA] 2014-2015).

20

Figure: Annual standardized incidence rates (ASIR) of LT wait-listing per

100,000 US population by etiology of liver disease and indication for wait-

listing. X-axis is the year of LT wait-listing registration. PI: protease

inhibitor; DAA: direct acting antiviral

200

3

0LT

WL

ra

te p

er

10

0,0

00

US

po

pu

lati

on

1

2

3

4

5

6

7

8

9

106

5

5

4

3

2

1

0

4

3

2

1

0

Interferon

HBV HCV NASH

A) Overall B) Decompensated cirrhosis C) HCC

PI DAA Interferon

Year of wait-list registration

PI DAA Interferon PI DAA

20

04

20

05

20

06

20

07

20

08

20

09

20

10

20

11

20

12

20

13

20

14

20

15

20

03

20

04

20

05

20

06

20

07

200

8

200

9

201

0

2011

201

2

201

3

201

4

201

5

20

03

20

04

20

05

20

06

20

07

200

8

200

9

201

0

2011

201

2

201

3

201

4

201

5

21

Eight weeks treatment duration with

Ledipasvir/Sofosbuvir (LDV/SOF) is effective for

appropriately selected patients with genotype 1

Hepatitis C virus (HCV) infection: an analysis of

multiple real world cohorts totaling >6,500 patients

LB-16

Vinay Sundaram1, Christie Jeon1, Kamran Qureshi3, Nyan L. Latt4,

Amandeep K. Sahota4, Michael P. Curry5, Naoky C. Tsai6,

Nathorn Chaiyakunapruk7, Yoori Lee8, Stephen Lott10,

Joerg Petersen9, Peter Buggisch9, Kris V. Kowdley2;

1. Cedars-Sinai Medical Center, Los Angeles, CA;

2. Swedish Medical Center, Seattle, WA;

3. Temple University, Philadelphia, PA;

4. Kaiser Permanente, Los Angeles, CA;

5. Beth Israel Deaconness, Boston, MA;

6. Queens Medical Center, Honolulu, HI;

7. Monash University, Subang Jaya, Malaysia;

8. Trio Health, La Jolla, CA;

9. Institut fur Interdisziplinäre Medizin, Hamburg, Germany;

10. Burmans-Diplomat Specialty Pharmacy, Flint, MI

22

• A post-hoc analysis of the ION-3 trial indicated that 8 weeks of

treatment with LDV/SOF is effective in selected patients with

genotype 1 chronic HCV.

• Several real-world cohort studies also suggest that SVR rates

with an 8 week regimen is comparable to a 12 week course.

• However, these studies are limited by lack of uniform data

regarding fibrosis stage or risk factors for relapse.

• Therefore, current guidelines do not routinely recommend an

8-week regimen.

• Using individual patient data from multiple real world cohorts, we

determined the effectiveness of 8 weeks of treatment, examined

variables associated with relapse and compared the efficacy of 8

weeks with 12 weeks of therapy.

23

8 weeks treatment (n=868)

95% Confidence Interval

Overal SVR12 ITT: 845/868 (97.3%)

PP: 845/857 (98.6%)

96.2-98.4

97.8-99.3

Age > 65 years ITT: 157/161 (97.5%)

PP: 157/160 (98.1%)

95.1-100

96.0-100

HIV co-infection ITT: 19/19 (100%)

PP: 19/19 (100%)

n/a

n/a

Caucasian African-American

ITT: 508/517 (98.2%)

PP: 508/512 (99.2%)

ITT: 197/207 (95.2%)

PP: 197/204 (96.6%)

97.1-99.4

98.4-99.9

92.2-98.0

94.0-99.0

Fibrosis Stage 0 Fibrosis Stage 1 Fibrosis Stage 2 Fibrosis Stage 3

ITT: 167/170 (98.2%)

PP: 167/167 (100%)

ITT: 244/251 (97.2%)

PP: 244/248 (98.4%)

ITT: 263/268 (98.1%)

PP: 263/264 (99.6%)

ITT: 142/150 (94.6%)

PP: 142/149 (95.3%)

96.2-100

n/a

95.1-99.2

96.8-99.9

96.5-99.7

98.8-100

91.1-98.2

91.9-98.7

Genotype 1a Genotype 1b

ITT: 551/566 (97.3%)

PP: 551/560 (98.4%)

ITT: 261/267(97.8%)

PP: 261/263 (99.2%)

96.0-98.7

97.4-99.4

95.9-99.5

98.1-100

24

• Random effects meta-analysis of 6 additional real world

cohorts (n=5,641) demonstrated similar efficacy with 8

weeks (2168/2278, 95.2%) as 12 weeks (3266/3363,

97.1%) duration of treatment (RR=0.99, 95% CI 0.97-1.02).

• Real-world data from a large individual patient data cohort

and a meta-analysis of additional cohort studies

demonstrates that 8 weeks of LDV/SOF achieves high SVR

rates >95% in appropriately selected patients, regardless of

fibrosis stage, race or HIV co-infection and has comparable

outcomes to 12 weeks duration.

25

Virological failures to direct acting antivirals (DAA)

regimens in a real life setting show frequent resistance

associated variants and may require

re-treatment with unconventional strategies

Abstract #1944

Velia Chiara Di Maio1, Valeria Cento1, Ilaria Lenci2, Marianna Aragri1, Silvia Barbaliscia1, Simona Francioso2, Stefania Paolucci3, Michela

Melis4, Gabriella Verucchi5, Nicola Coppola6, Carlo F. Magni7, Francesco Santopaolo2, Simona Landonio7, Valeria Ghisetti8, Mario Starace6,

Cecilia D’Ambrosio9, Vincenza Calvaruso10, Nicola Caporaso11, Caterina Pasquazzi12, Ivana Maida4, Antonino Picciotto13, Antonio Di Biagio14,

Laura Sticchi15, Raffaele Cozzolongo16, Dante Romagnoli17, Marco Biolato18, Jacopo Vecchiet19, Gabriella D’Ettorre20, Manuela Merli21,

Giovanni B. Gaeta22, Alessia Ciancio23, Letizia Marinaro8, Pietro Andreone24, Giorgio -. Barbarini25, Roberto Gulminetti26, Valeria Pace Palitti27,

Perluigi Tarquini28, Massimo Puoti29, Vincenzo Sangiovanni30, Maurizio Paoloni31, Sergio Babudieri4, Giuliano Rizzardini7,

Savino Bruno32, Massimo Andreoni33, Adriano M. Pellicelli9, Giustino Parruti34, Antonio Crax.10, Mario Angelico2,

Carlo F. Perno1, Francesca Ceccherini-Silberstein1;

1. Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy;

2. Hepatology Unit, University Hospital of Rome Tor Vergata,

Rome, Italy;

3. Virologia Molecolare, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy;

4. Infectious Diseases Unit, University of Sassari, Sassari, Italy;

5. Policlinico S. Orsola-Malpighi, Bologna, Italy;

6. Infectious Diseases, Second University of Naples, Naples, Italy;

7. Division of Infectious Disease, Hospital Sacco of Milan, Milan, Italy;

8. Infectious Diseases, “Amedeo di Savoia” Hospital, Turin, Italy;

9. Hepatology Unit, San Camillo Forlanini Hospital, Rome, Italy;

10. Gastroenterology, “P. Giaccone” University Hospital, Palermo, Italy;

11. Department of Clinical Medicine and Surgery, University “Federico II” of Naples, Naples, Italy;

12. Infectious Diseases, Sant’Andrea Hospital – “La Sapienza” University, Rome, Italy;

13. Division of Hepatology, IRCCS San Martino, IST Genova,

Genova, Italy;

14. Infectious Disease, IRCCS AOU San Martino - IST, Genova, Italy;

15. Hygiene Unit, IRCCS AOU San Martino-IST, Genova, Italy;

16. Department of Gastroenterology, Scientific Institute for Digestive Disease “Saverio de Bellis”

Hospital, Castellana Grotte, Bari, Italy;

17. Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio

Emilia, Modena, Italy;

18. Liver Transplant Unit, Catholic University of Rome, Rome, Italy;

19. Infectious Disease Clinic, Hospital of Chieti, Chieti, Italy;

20. Policlinico Umberto I Roma, Rome, Italy;

21. Gastroenterology, “La Sapienza” University of Rome, Rome, Italy;

22. Viral Hepatitis Unit, Second University, Naples, Italy;

23. Unit of Gastroenterology, University of Turin, Department of Medical Sciences, Citt. della salute e

della scienza di Torino Molinette Hospital, Turin, Italy;

24. Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy;

25. Division of Infectious and Tropical Diseases,, Fondazione IRCCS Policlinico San Matteo, Pavia,

Italy;

26. Institute of Infectious Diseases, University of Pavia, Pavia, Italy;

27. Hepatology Unit, Ospedale San Massimo, Penne, Italy;

28. Infectious Disease, Hospital “G. Mazzini”, Teramo, Italy;

29. Hospital Niguarda Ca’Granda, Milan, Italy;

30. Hospital Cotugno, Naples, Italy;

31. Infectious Disease Unit, Avezzano General Hospital, Avezzano, Italy;

32. Internal Medicine,, Humanitas University, Rozzano, Milan, Italy;

33. Infectious Diseases, University Hospital of Rome Tor Vergata,

Rome, Italy;

34. Infectious Disease Unit, Pescara General Hospital, Pescara, Italy

26

• Analysis of 182 patients who failed a DAA regimen

– GT1a: 21%, GT1b: 33%, GT2c: 5%, GT3a:

23% and GT4a/d/n/r: 18%

– 65% treatment-experienced (9% with prior NS3

protease inhibitor)

– 81% cirrhotic

– 81% relapsed, 12% had on-treatment breakthrough

and 7% were nonresponders

• 49% failed a regimen now known to be

suboptimal/not recommended

27

• Overall, 53% of pts showed >1 RAV related to the DAA-

failure; RAVs prevalence was higher in breakthrough/non

responders than in relapsers (94% vs 43%,p<0.001).

• RAVs related to the DAA-class at failure varied in

prevalence according to the inhibitors used:

– 92% NS5A-RAVs in NS5A-failing pts (N=51)

– 77% NS3-RAVs in NS3-failures (N=82)

– 20% NS5B-RAVs in SOF-failures (N=152)

– 23% NS5B-RAVs in dasabuvir-failures (N=17)

28

• 46% of pts treated with >2 DAA classes showed RAVs on

>2 DAA-targets, including 13/13 NS3-NS5A-failures, and

10/17 (59%) in 3D-failures.

• Overall, 13% of pts showed resistance to a class different

than the DAAs class used, probably due to natural

resistance.

• 50% (5/10) SOF breakthrough/non-responders showed the

SOF S282T RAV (3 GT4: SMV/LDV+SOF+RBV;

1 GT1b: SOF+SIM; 1 GT3: SOF alone).

• SOF RAV L159F detected in 14% (20/142) of SOF

relapsers (35% GT1b, 9% GT3).

29

• Due to natural RAVs, HCV resistance test

at failure should be recommended for all 3 genes

(NS3/NS5A/NS5B).

• In a real life setting, RAVs prevalence at failure was

remarkably high in all genes tested (with a partial exception

for NS5B, whose limited resistance is still higher than

previously reported).

• Must consider appropriate retreatment regimens,

sometimes based upon unconventional, more

aggressive/prolonged regimens able to overcome the

natural/acquired resistance and to warrant high success

rates.

30

ENDURANCE-4: Efficacy and Safety of ABT-

493/ABT-530 in Patients with Chronic HCV

Genotype 4, 5, or 6 Infection

Abstract #114

Tarik Asselah1, Christophe Hezode2, Neddie Zadeikis6,

Dr. Magdy Elkhashab7, Massimo Colombo8, Rui T. Marinho3, Kosh Agarwal4,

Frederik Nevens5, Ran Liu6, Teresa Ng6, Federico Mensa6;

1. Centre de Recherche sur l’Inflammation, Clichy, France;

2. H.pital Henri Mondor, AP-HP, Universit. Paris-Est,

Creteil, France;

3. Hospital S. Maria, Medical School of Lisbon, Lisbon, Portugal;

4. Institute of Liver Studies, Kings College Hospital, London,

United Kingdom;

5. University Hospitals KU, Leuven, Belgium;

6. AbbVie, Inc., North Chicago, IL;

7. Toronto Liver Centre, Toronto, ON, Canada;

8. Policlinic Hospital IRCCS & University, Milan, Italy

31

• The phase 2b study SURVEYOR-II (NCT02243293) demonstrated

100% SVR12 rates in 34 patients with GT4,5, or 6 infection without

cirrhosis following treatment with G/P for 12 weeks

• ENDURANCE-4 (NCT02636595) is a multicenter, open-label, single-

arm phase 3 study investigating the safety and efficacy of 12-week,

ribavirin-free treatment with G/P in treatment-naïve or treatment-

experienced patients with chronic HCV GT4, 5 or 6 infection without

cirrhosis

G/P

Wk 12Day 0

GT4, 5, 6N = 121

Open-label Treatment

G/P is co-formulated and dosed once daily as three 100 mg/40 mg pills for a total dose of 300 mg/120 mg

Wk 24

SVR12

Wk 48

32

Characteristic G/P

N = 121

HCV RNA* Median (range), log10 IU/mL ≥ 6 million IU/mL, n (%)

6.3 (3.6-7.3)

22 (18)

Fibrosis Stage, n (%)

F0-1 104 (86)

F2 8 (7)

F3 9 (7)

Treatment naïve, n (%) 82 (68)

Treatment experienced, n (%) 39 (32)

SOF-based, n/N (%) 0

IFN-based, n/N (%) 39 (100)

PPI use, n (%) 11 (9)

33

% P

ati

en

ts w

ith

SV

R12

100

99 99 100 100 100 100 100 100

Overall

GT4

GT5

GT6

80

60

40

20 120___

121

120___

121

75*___

76

75___

75

26___

26

26___

26

19___

19

19___

190

ITT mITT

*One GT4 patient

discontinued treatment

on day 12 and did not

achieve SVR12

34

High Efficacy in Real-World Treatment of

Cirrhotic Patients by Non-Specialist Providers

Abstract #22

Benjamin Emmanuel1, Chloe Gross1, Henry Masur2,

Shyam Kottilil1, Sarah Kattakuzhy1;

1. Division of Clinical Care and Research, Institute of Human Virology, University of Maryland School of Medicine, Baltimore, MD.

2. Critical Care, National Institutes of Health, Bethesda, MD.

35

• Although sustained virologic response utilizing direct acting

antivirals (DAA) has led to high efficacy across patient

subgroups, patients are

still managed by experienced specialist physicians.

• We compared patients with and without cirrhosis for efficacy

and adherence to DAA therapy

in a task-shifting model among community-

based providers.

36

SV

R1

2 (

%)

94% 96% 92% 93% 92% 91%

95%

0

20

40

60

80

100

Nurse Practitioners Primary Care Physicians Specialists (ID orhepatologist)

SVR12 (overall) SVR12 (cirrhotics) SVR12 (non-cirrhotics)

85%

97%

• 600 patients between

MAY-NOV 2015 in

Washington DC

• Demographics – 96% black

– 72% GT1a

– 82% treatment naïve

– 20% cirrhotic

– 24% HIV/HCV coinfected

• No statistical

difference

in overall SVR12 by

treater type

• Adherence to

treatment visits – No difference between

cirrhotics vs non-cirrhotics

– Lowest amongst specialists

(56%) vs primary care (63%)

vs nurse practitioners (73%)

(p<0.0001)

37

Hepatitis C Treatment with Direct Acting Antiviral

Therapy: Report of a Global Survey

Abstract #938

Maen Masadeh, Huafeng Shen, Yazan Hasan, Andrew Johannes, Antonio J. Sanchez;

1. Division of Gastroenterology and Hepatology, University of Iowa Hospitals and Clinics, Iowa City, IA

38

• An Institutional Review Board approved survey was emailed

to members of the American Association for the Study of

Liver Diseases (AASLD) and Infectious Diseases Society of

America (IDSA).

• All responses were anonymous.

• 19% (801/4224) responded; of those, 295 treat HCV

patients and are the focus of this survey

• More AASLD respondents treat HCV than IDSA

respondents (94% vs 66%, P< 0.001).

39

• Therapy of choice for treatment naive patients

– GT1: LDV/SOF (93%)

– GT2: SOF/RBV (75%)

– GT3: DCV/SOF (80%)

– GT4: LDV/SOF (78%)

• Liver specialists treat more HCV in decompensated

cirrhosis than ID specialists (86% vs 34%, p<0.001) and

HCV recurrence after liver transplant (74% vs.11.3%,

p<0.0001).

• Insurance coverage was a major limiting

factor preventing initiation of DAAs in 86%

of practitioners.

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• Years of experience treating HCV did not affect approach to HCV

treatment failure or hepatic fibrosis assessment methods before

HCV treatment.

Hepatology (n=132)

Infectious disease (n=153)

P-value £

Assesment of hepatic fibrosis 0.004

Liver biopsy 13 (9.9%) 10 (6.5%)

Fibrosure/Fibrospect 36 (27.3%) 74 (48.4%)

Fibroscan/Elastography 71 (53.8%) 60 (39.2%)

Other 12 (9.1%) 9 (5.9%)

Approach to DAA failure 0.537

Wait for new DAA’s to be approved 56 (53.3%) 30 (48.4%)

Treat with a different DAA 49 (46.7%) 32 (51.6%)

HCV Practice Patterns By Specialty

Values are numbers (%). £ Fisher’s exact test.

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This enduring activity is supported by educational grants from

AbbVie & Gilead Sciences, Inc.