Brilliant Answers Brilliant Answers Jennifer Price, MD, PhD - - PDF document

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10 Important Liver Care Questions and 10 Brilliant Answers

Jennifer Price, MD, PhD UCSF Hepatology December 8, 2017

10 Important Liver Care Questions and 10 Brilliant Answers

Jennifer Price, MD, PhD UCSF Hepatology December 8, 2017

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Disclosures

• Grant support: Gilead, Merck
• Advisory board: Intercept
• Ownership interest: Bristol-Myers Squibb,

Johnson and Johnson, Merck, Abbvie

Outline

• Complications of cirrhosis

– Surveillance for hepatocellular carcinoma (HCC) – Risk of HCC with DAA’s – Surveillance for esophageal varices

• Timing of HCV treatment in transplant candidates
• Hepatitis B virus

– Isolated HBcAb+ – New treatments

• Nonalcoholic fatty liver disease (NAFLD)

– Diagnosis and management

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Acute hepatitis C Chronic infection Chronic hepatitis Cirrhosis Time (yr) 55 - 85% 70% 20%

10 20 30 Decompensation Hepatocellular Carcinoma

1-4%/yr 4-5%/yr

Natural History of Chronic Liver Disease (HCV example) HCC Surveillance: U/S +/- AFP every 6 months

• Rising incidence over past 20 years

– Estimated 39,230 cases and 27,170 deaths in 2016 – Aging HCV+ population, increasing NAFLD – Incidence expected to rise until 2030

• High risk groups:

– Cirrhosis – Chronic HBV – F3 fibrosis

• Observational studies in cirrhosis: screening associated

with improved survival, detection of early-stage HCC

Heimbach J, AASLD Practice Guidelines, 2017.

HCC Surveillance: Chronic HBV

• 1. How should we approach HCC screening in patients

with HIV/HBV?

HCC Surveillance: Chronic HBV

Bruix J, AASLD Practice Guidelines, 2011.

Surveillance recommended HBV Population Group Threshold incidence for efficacy of surveillance Incidence of HCC Cirrhosis 0.2-1.5%/yr 3-8%/yr Family h/o HCC 0.2%/yr Incidence higher than without family history Asian male >40 years 0.2%/yr 0.4-0.6%/yr Asian female >50 years 0.2%/yr 0.3-0.6%/yr African/North American Blacks 0.2%/yr Occurs at earlier age Benefit uncertain Males <40, Females <50 0.2%/yr <0.2%/yr

• 1. How should we approach HCC screening in patients

with HIV/HBV?

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HCC Surveillance: Chronic HBV

Bruix J, AASLD Practice Guidelines, 2011.

Surveillance recommended HBV Population Group Cirrhosis Family h/o HCC Asian male >40 years Asian female >50 years African/North American Blacks Benefit uncertain Males <40, Females <50

• 1. How should we approach HCC screening in patients

with HIV/HBV?

What about Caucasian pts?

HCC Surveillance: Chronic HBV

Bruix J, AASLD Practice Guidelines, 2011.

Surveillance recommended HBV Population Group Cirrhosis Family h/o HCC Asian male >40 years Asian female >50 years African/North American Blacks Benefit uncertain Males <40, Females <50

• 1. How should we approach HCC screening in patients

with HIV/HBV?

What about Caucasian pts?

─ If no cirrhosis and chronic inactive HBV (long-term normal ALT, low HBV DNA) “the incidence of HCC is probably too low to make surveillance worthwhile” ─ However… “additional risk factors have to be taken into account including older age, persistence of viral replication, co- infection with HCV or HIV, or presence

• f other liver disease”

─ …“Caucasian pts with active HBV are likely at risk for HCC and should be screened”

HCC Surveillance: Chronic HBV

Bruix J, AASLD Practice Guidelines, 2011.

Surveillance recommended HBV Population Group Cirrhosis Family h/o HCC Asian male >40 years Asian female >50 years African/North American Blacks Benefit uncertain Males <40, Females <50

• 1. How should we approach HCC screening in patients

with HIV/HBV?

What about Caucasian pts?

─ If no cirrhosis and chronic inactive HBV (long-term normal ALT, low HBV DNA) “the incidence of HCC is probably too low to make surveillance worthwhile” ─ However… “additional risk factors have to be taken into account including older age, persistence of viral replication, co- infection with HCV or HIV, or presence

• f other liver disease”

─ …“Caucasian pts with active HBV are likely at risk for HCC and should be screened”

HCC Surveillance: Chronic HBV

• 2. How should we approach HCC screening in non-

cirrhotic pts with isolated HBcAb+:

• Isolated HBcAb+:
• Isolated HBcAb+ associated with increased HCC risk in Japanese

pts with non-HBV, non-HCV cirrhosis1

• High prevalence of HBcAb+ in Korean pts with non-HBV, non-

HCV HCC2

• HBcAb+ not associated with HCC in U.S. HCV cohort3
• Systematic review suggested increased risk of HCC4

─ Mostly case/control, few adjustments for confounders, only 1 in US

• Insufficient evidence to support surveillance in this group

1Ikeda K, J Viral Hepat, 2009. 2Lee SB, Liver Int, 2016. 3Lok AS, Hepatology, 2011. 4Lee SB, Liver Int, 2016.

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HCC Surveillance: Chronic HBV

• 2. How should we approach HCC screening in non-

cirrhotic pts with HBsAg loss (spontaneous or due to tx)?

1Sung JJY, Aliment Pharmacol Therp, 2008. 2Hung CH, J Viral Hepat, 2017. 3KimGA, J Hepatol, 2015. 4EASL-EORTC

Guidelines, 2012.

• HBsAg loss
• HBV tx reduces (but does not

eliminate) risk of HCC1

• HCC still occurs in pts who lose

HBsAg spontaneously or with tx2,3

• Factors predicting HCC: age ≥50 at

seroclearance, cirrhosis, low albumin, male sex3

• Continue surveillance in pts at risk due to baseline factors4

HCC Surveillance: HCV

• 3. Should we screen in HCV+ pts with F3 fibrosis?

HCC Surveillance: HCV

Lok AS, Gastroenterology, 2009.

• 3. Should we screen in HCV+ pts with F3 fibrosis?
• HCV+ pts with F3 fibrosis have elevated HCC risk

HCC Surveillance: HCV

Lok AS, Gastroenterology, 2009.

• 3. Should we screen in HCV+ pts with F3 fibrosis?
• HCV+ pts with F3 fibrosis have elevated HCC risk
• HCC guidelines are conflicting

– Recommended for F3 fibrosis in HCV by EASL (2012) – Benefit uncertain in AASLD guidelines (2010)

• Post-SVR Treatment guidelines are consistent and

recommend surveillance in pts with F3 fibrosis

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HCC Surveillance: HCV

AASLD/IDSA HCV Guidelines, 2017.

• 3. Should we screen in HCV+ pts with F3 fibrosis?

HCC Surveillance: HCV

EASL HCV Guidelines, 2017.

• 3. Should we screen in HCV+ pts with F3 fibrosis?

HCC Surveillance: HCV

• 3. Should we screen in HCV+ pts with F3 fibrosis?

Yes!

• Essential to adequately stage fibrosis prior to HCV tx

– Nearly 50% of pts with F3 fibrosis on pre-treatment Fibroscan (≥9.5 kPa) will have post-SVR Fibroscan <9.5 kPa – Fibroscan and other non-invasive fibrosis surrogates have not been validated in post-SVR pts – Limited evidence comparing post-SVR biopsy with Fibroscan shows you will underestimate fibrosis stage if you rely on post-SVR results

• 5 UCSF pts with ≥F3 fibrosis on post-SVR biopsy: 3 (60%) had post-

SVR Fibroscan <9.5; 1 of these developed HCC post-SVR

HCC Risk with HCV DAA’s

• 4. Do DAA’s increase the risk of HCC?

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HCC Risk with HCV DAA’s

• 4. Do DAA’s increase the risk of HCC? Incident HCC risk

HCC Risk with HCV DAA’s

• 4. Do DAA’s increase the risk of HCC? Incident HCC risk
• High de novo HCC occurrence rates within 12 months
• f DAA cessation reported in 3 early studies

HCC Risk with HCV DAA’s

• 4. Do DAA’s increase the risk of HCC? Incident HCC risk
• High de novo HCC occurrence rates within 12 months
• f DAA cessation reported in 3 early studies
• Subsequent larger studies showed no increased risk

HCC Risk with HCV DAA’s

• 4. Do DAA’s increase the risk of HCC? Incident HCC risk
• High de novo HCC occurrence rates within 12 months
• f DAA cessation reported in 3 early studies
• Subsequent larger studies showed no increased risk

HR 0.28 (95% CI 0.22-0.36)

• Large VA study of 22,500

pts (39% with cirrhosis): SVR after DAAs reduced risk of HCC

Kanwal F, Gastroenterology, 2017.

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HCC Risk with HCV DAA’s

• 4. Do DAA’s increase the risk of HCC? Incident HCC risk

Llovet JM, Nat Rev Gastro Hepatol, 2016. SVR (DAA-based tx) 1.5-4% per year

• We are now treating older pts with more advanced liver

disease (higher risk for HCC) DAAs are not associated with increased INCIDENT HCC

HCC Risk with HCV DAA’s

• 4. Do DAA’s increase the risk of HCC? Recurrence risk

HCC Risk with HCV DAA’s

• 4. Do DAA’s increase the risk of HCC? Recurrence risk
• Some data suggests possibility of early recurrence of

HCC with DAA therapy

HCC Risk with HCV DAA’s

• 4. Do DAA’s increase the risk of HCC? Recurrence risk
• Some data suggests possibility of early recurrence of

HCC with DAA therapy

• Several studies show no

increased risk

ANRS Study Group, J Hepatology, 2016.

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HCC Risk with HCV DAA’s

• 4. Do DAA’s increase the risk of HCC? Recurrence risk
• Some data suggests possibility of early recurrence of

HCC with DAA therapy

ANRS Study Group, J Hepatology, 2016.

• Several studies show no

increased risk

• For pts with HCC and

complete response with resection or locoregional tx, there is insufficient evidence to justify withholding DAA’s

Esophageal Varices Screening

• 5. Who should be screened for varices with EGD and

how often should this be repeated after initial EGD?

Esophageal Varices Screening

• Seen in 45-50% of patients with cirrhosis

– 40% in CPT A, 60% in CPT B, 80% in CPT C

• Active bleed is associated with 20-30% mortality
• Primary prophylaxis: non-selective beta blockers or

band ligation

Small varices Large varices No varices

8%/year 8%/year

D’Amico G. Portal Hypertension in the 21St Century, 2004

Esophageal Varices Screening

• Seen in 45-50% of patients with cirrhosis

– 40% in CPT A, 60% in CPT B, 80% in CPT C

• Active bleed is associated with 20-30% mortality
• Primary prophylaxis: non-selective beta blockers or

band ligation

Small varices Large varices No varices

8%/year 8%/year

D’Amico G. Portal Hypertension in the 21St Century, 2004

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Diagnosis of Cirrhosis Endoscopy

No Varices

Follow-up EGD in 2-3 years*

Small Varices

Follow-up EGD in 1-2 years*

Medium/Large Varices

• Step-wise increase until maximally tolerated dose
• Continue beta-blocker (life-long)

No Contraindications Contraindications

• r

Beta-blocker intolerance

Beta-blocker therapy Endoscopic Variceal Band Ligation *EGD every year in decompensated cirrhosis

Esophageal Varices Screening Esophageal Varices Screening

• 5. Who should be screened for varices with EGD and

how often should this be repeated after initial EGD?

• All patients with cirrhosis (traditional criteria)
• Pts with clinically significant portal hypertension

(HVPG ≥10 mmHg) are at risk of bleeding

• Patients with compensated cirrhosis, Fibroscan LS

<20 kPa and platelets >150,000 mm3 have very low probability (<5%) of having high-risk varices and EGD can be safely avoided (aka Baveno VI criteria)

Garcia-Tsao G, AASLD Guidelines, 2016. Maurice JB, J Hepatol, 2016.

Timing of HCC Treatment in Transplant Candidates

• 6. How do you approach HCV treatment in liver or kidney

transplant candidates?

Timing of HCC Treatment in Transplant Candidates

• 6. How do you approach HCV treatment in liver or kidney

transplant candidates?

• In vast majority of pts: wait until after transplant

─ Ability to receive a HCV+ kidney significantly reduces waitlist time ─ HCV can be safely treated post-transplant

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Timing of HCC Treatment in Transplant Candidates

• 6. How do you approach HCV treatment in liver or kidney

transplant candidates?

• In vast majority of pts: wait until after transplant

─ Ability to receive a HCV+ kidney significantly reduces waitlist time ─ HCV can be safely treated post-transplant

• In some pts with cirrhosis, treatment is considered to

decrease need for combined liver/kidney

Timing of HCC Treatment in Transplant Candidates

• 6. How do you approach HCV treatment in liver or kidney

transplant candidates?

• In vast majority of pts: wait until after transplant

─ Ability to receive a HCV+ kidney significantly reduces waitlist time ─ HCV can be safely treated post-transplant

• In some pts with cirrhosis, treatment is considered to

decrease need for combined liver/kidney

• Do not treat HCV are candidates for kidney transplant

until after they are evaluated by transplant nephrology and hepatology

Timing of HCC Treatment in Transplant Candidates

• 6. How do you approach HCV treatment in liver or kidney

transplant candidates?

Timing of HCC Treatment in Transplant Candidates

• 6. How do you approach HCV treatment in liver or kidney

transplant candidates?

• Trickier and transplant region-specific

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Timing of HCC Treatment in Transplant Candidates

• 6. How do you approach HCV treatment in liver or kidney

transplant candidates?

• Trickier and transplant region-specific
• Pts with HCC: often wait until after transplant

– Lower SVR rates in pts with HCC – 25% waitlist drop-off for HCC pts in our region; allows for expanded donor pool – Will consider tx to prevent decompensation, allowing for locoregional therapy while waiting

Timing of HCC Treatment in Transplant Candidates

• 6. How do you approach HCV treatment in liver or kidney

transplant candidates?

• Trickier and transplant region-specific
• Pts with HCC: often wait until after transplant

– Lower SVR rates in pts with HCC – 25% waitlist drop-off for HCC pts in our region; allows for expanded donor pool – Will consider tx to prevent decompensation, allowing for locoregional therapy while waiting

• Pts with decompensated cirrhosis

§Compensated cirrhosis §Child-Pugh A §MELD <10 §Decompensated cirrhosis §Child-Pugh C §MELD cut-off??? §Significant renal dysfunction § Treat all unless HCC (concern of inability to get to LT with exception status) § Don’t treat unless LT is not an option and expected to survival at least 6 months §Decompensated cirrhosis §Child-Pugh B §Less severe portal HTN § Treat most patients § Consider age, severity

• f PHT complications,

severity of necroinflammation

Timing of HCC Treatment in Transplant Candidates

Transplant Candidates

HBV

• 7. How do you approach isolated HBcAb+ patients?

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HBV

• 7. How do you approach isolated HBcAb+ patients?
• Potential scenarios:

a) “Window phase” of acute HBV recovery

─ Check HBsAb 1-3 months

HBV

• 7. How do you approach isolated HBcAb+ patients?
• Potential scenarios:

a) “Window phase” of acute HBV recovery

─ Check HBsAb 1-3 months

b) Occult HBV

─ Rates vary depending on study ─ Check HBV DNA (I reserve for HIV+, ESRD on HD, cirrhosis, immunocompromised)

HBV

• 7. How do you approach isolated HBcAb+ patients?
• Potential scenarios:

a) “Window phase” of acute HBV recovery

─ Check HBsAb 1-3 months

b) Occult HBV

─ Rates vary depending on study ─ Check HBV DNA (I reserve for HIV+, ESRD on HD, cirrhosis, immunocompromised)

c) Prior exposure with loss of HBsAb

─ Most common scenario; if risk factors for prior exposure, no vaccination needed unless HIV+ or immunocompromised

HBV

• 7. How do you approach isolated HBcAb+ patients?
• Potential scenarios:

a) “Window phase” of acute HBV recovery

─ Check HBsAb 1-3 months

b) Occult HBV

─ Rates vary depending on study ─ Check HBV DNA (I reserve for HIV+, ESRD on HD, cirrhosis, immunocompromised)

c) Prior exposure with loss of HBsAb

─ Most common scenario; if risk factors for prior exposure, no vaccination needed unless HIV+ or immunocompromised

d) False positive

─ Higher suspicion if no risk factors for exposure- give full series vaccine if indicated and unsure of exposure history

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362 pts with isolated HBcAb+ (Paris) 11 false positive (3%) 1 “Window phase” (0.3%) 10 HBV DNA+ (3%) 341 HBV DNA- (94%)

Repeat HBcAb HBc IgM HBV DNA

HBV

• 7. How do you approach isolated HBcAb+ patients?

Launay O, J Viral Hep, 2011.

362 pts with isolated HBcAb+ (Paris) 11 false positive (3%) 1 “Window phase” (0.3%) 10 HBV DNA+ (3%) 341 HBV DNA- (94%)

Repeat HBcAb HBc IgM HBV DNA

HBV

• 7. How do you approach isolated HBcAb+ patients?

Launay O, J Viral Hep, 2011. Risk of reactivation with immunosuppression, HCV DAA treatment

HBV

• 8. Is tenofovir alafenamide (TAF) effective in HBV?

HBV

• 8. Is tenofovir alafenamide (TAF) effective in HBV?
• Tenofovir prodrug with greater plasma

stability than TDF

• Enhances delivery of active drug to

hepatocytes

• TAF non-inferior to TDF at wks 48 and 96
• Small and similar % of pts with HBV

DNA ≥69 IU/mL

• Virologic breakthrough infrequent
• No resistance to TAF detected

through 96 wks

Agarwal K, EASL 2017, FRI-153. Brunetto MR, EASL 2017, PS-042. Chen HLY, AASLD 2017, Abstract 26.

12/8/17 14

HBV: What is on the horizon?

Mechanism Drug

Entry inhibitors Myrcludex Polymerase inhibitors TAF, CMX-157, AGX-1009, Besifovir, Lagociclovir Capsid blockers GLS-4, NVR 3-778 Release inhibitors Rep-2139, Rep-2165 cccDNA cleavage (gene editing) CRISPR/Cas9, TALENS, ZFNs Transcription inhibitors (RNA interference) ARC-520, ARC-521 Innate immunity GS-9620, Birinapant Adaptive immunity Therapeutic vaccines (GS- 4774), Engineered T cells Soriano V, Expert Opin Investig Drugs, 2017. Virus life cycle (antivirals) Host immune response (immunomodulators)

NAFLD/NASH

~30% ~3-10% ~0.3-2%

NAFLD/NASH

HIV+ similar to HIV- Likely higher in HIV+ (42% NASH, 22% ≥F2) Is it higher in HIV?

~30% ~3-10% ~0.3-2%

NAFLD/NASH

• 9. How do you make the diagnosis of NAFLD, and when

should we biopsy patients with suspected NAFLD/NASH?

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NAFLD/NASH

• 9. How do you make the diagnosis of NAFLD, and when

should we biopsy patients with suspected NAFLD/NASH?

• Suspect NAFLD if:

– Metabolic syndrome, history of d-drug use – Abnormal liver enzymes (not necessary for NAFLD) in absence

• f other chronic liver disease or heavy EtOH use

– Ultrasound suggests NAFLD

NAFLD/NASH

• 9. How do you make the diagnosis of NAFLD, and when

should we biopsy patients with suspected NAFLD/NASH?

• Suspect NAFLD if:

– Metabolic syndrome, history of d-drug use – Abnormal liver enzymes (not necessary for NAFLD) in absence

• f other chronic liver disease or heavy EtOH use

– Ultrasound suggests NAFLD

• It remains undiagnosed in the majority of pts

– Fibroscan with controlled attenuation parameter (CAP) can be used to screen

• Not recommended yet in primary care clinics

– MR imaging (MRS, MRI-PDFF) is non-invasive gold standard

NAFLD Simple Steatosis NASH Nonprogressive Progressive Borderline NASH Simple Steatosis (n = 8) NASH (n = 109)

Survival

1.00 0.75 0.50 0.25 10 20 30

Years

Söderberg C, Hepatology, 2010.

Slide credit: clinicaloptions.com

NAFLD/NASH: Why Biopsy?

Biopsy is needed to differentiate simple steatosis vs NASH

NAFLD/NASH: Approach to Biopsy

Elevated liver enzymes or evidence of hepatic steatosis on imaging Trial of 3-6 mos of diet and exercise for weight loss Reassess every 6-12 mos Liver biopsy Consider biopsy if undergoing cholecystectomy or bariatric surgery Presence of:

• Diabetes
• Metabolic syndrome
• Older age

Baseline workup:

• CBC, platelets, ALT, AST, ALP, GGT, INR, total bili, albumin
• Rule out other causes of chronic liver disease (eg, viral

hepatitis, autoimmune)

• Fasting glucose and lipid levels, A1C

Unsuccessful No Yes

• High AST:ALT
• High AST:platelet
• Decreased albumin or plts

Noureddin M,Clin Liver Dis, 2012.. Slide credit: clinicaloptions.com

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NAFLD/NASH: Approach to Biopsy

Elevated liver enzymes or evidence of hepatic steatosis on imaging Trial of 3-6 mos of diet and exercise for weight loss Reassess every 6-12 mos Liver biopsy Consider biopsy if undergoing cholecystectomy or bariatric surgery Presence of:

• Diabetes
• Metabolic syndrome
• Older age

Baseline workup:

• CBC, platelets, ALT, AST, ALP, GGT, INR, total bili, albumin
• Rule out other causes of chronic liver disease (eg, viral

hepatitis, autoimmune)

• Fasting glucose and lipid levels, A1C

Unsuccessful No Yes

• High AST:ALT
• High AST:platelet
• Decreased albumin or plts

Noureddin M,Clin Liver Dis, 2012.. Slide credit: clinicaloptions.com

HIV

HIV and NASH Prevalence

NASH Fibrosis

Median (IQR) or % HIV- monoinfected (n=18) Uninfected (n=17) Age 53 (46, 57) 54 (44, 59) Male 28% 24% Hispanic 22% 6% Race: African American 39% 59% White 33% 24% Other 28% 18% BMI (kg/m2) 29.7 (25.5, 33.6) 34.4 (30.1, 38.3) Waist circumference (cm) 101 (95, 114) 116 (105, 122) Fasting glucose ≥126 22% 29% ALT 26.5 (16, 42) 18 (13, 23) AST 25.5 (17, 32) 20 (17, 25) Liver stiffness kPa 4.3 (3.9, 6.7) 4.4 (3.5, 5.6) CAP dB/m 306 (261, 324) 286 (248, 347)

p=0.03 p=0.03 Price JC, unpublished data.

NAFLD/NASH

• 10. How do you treat NAFLD/NASH?

NAFLD/NASH

• 10. How do you treat NAFLD/NASH?

Treat

• NASH
• NASH with fibrosis
• Advanced fibrosis
• NASH-related cirrhosis

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NAFLD/NASH

• 10. How do you treat NAFLD/NASH?

Treat

• NASH
• NASH with fibrosis
• Advanced fibrosis
• NASH-related cirrhosis

Do Not Treat

• Pts without biopsy-

confirmed NASH

• Simple steatosis

─ Focus on CVD risk factor modification

NAFLD/NASH

• 10. How do you treat NAFLD/NASH?
• Weight loss: goal ≥10% weight loss

─ Improves NASH and fibrosis

NAFLD/NASH

• 10. How do you treat NAFLD/NASH?
• Weight loss: goal ≥10% weight loss

─ Improves NASH and fibrosis

• Treat diabetes, hypertension, dyslipidemia

NAFLD/NASH

• 10. How do you treat NAFLD/NASH?
• Weight loss: goal ≥10% weight loss

─ Improves NASH and fibrosis

• Treat diabetes, hypertension, dyslipidemia
• Vitamin E for confirmed NASH; 800 IU/day

─ Improved NASH in PIVENS trial ─ Increased risk of bleeding, prostate cancer in older men, and possibly hemorrhagic stroke

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NAFLD/NASH

• 10. How do you treat NAFLD/NASH?
• Weight loss: goal ≥10% weight loss

─ Improves NASH and fibrosis

• Treat diabetes, hypertension, dyslipidemia
• Vitamin E for confirmed NASH; 800 IU/day

─ Improved NASH in PIVENS trial ─ Increased risk of bleeding, prostate cancer in older men, and possibly hemorrhagic stroke

• Pioglitazone

─ Improved NASH and fibrosis in PIVENS trial ─ Associated with weight gain, bone fractures, ?long-term safety

NAFLD/NASH: Emerging Treatments, Phase III

Slide credit: clinicaloptions.com

1ClinicalTrials.gov. NCT02704403. 2ClinicalTrials.gov. NCT02548351. 3ClinicalTrials.gov. NCT03053050. 4ClinicalTrials.gov. NCT03053063. 5ClinicalTrials.gov. NCT03028740.

NAFLD/NASH: Emerging Treatments, Phase III

Slide credit: clinicaloptions.com

1ClinicalTrials.gov. NCT02704403. 2ClinicalTrials.gov. NCT02548351. 3ClinicalTrials.gov. NCT03053050. 4ClinicalTrials.gov. NCT03053063. 5ClinicalTrials.gov. NCT03028740.

Studies in HIV: Aramchol, Tesamorelin

Questions?