Transcript African Americans and Hepatitis C

African Americans and
Hepatitis C
Marlene Taylor PA-C
HIV/HCV Primary Care Provider
Montefiore Medical Center
• African Americans are twice as likely to be
infected with the hepatitis C virus (HCV)
compared to the general U.S. population,
according to the CDC. While African Americans
represent only 12 percent of the U.S.
population, they make up roughly 22 percent
of the estimated 3.2 million persons with
chronic HCV infection. Moreover, chronic liver
disease, often hepatitis C-related, is a leading
cause of death among African Americans
ages 45-64.
Hepatitis C Facts
• Hepatitis C is a liver disease caused by a virus.
• Hepatitis C is usually spread when blood from a person
infected with the hepatitis C virus enters the body of
someone who is not infected. This can happen from
sharing equipment for injecting drugs, receiving blood
transfusions or organ transplants before 1992, getting a
needlestick injury in health care settings, and even being
born to a mother who has Hepatitis C. And some people
don’t know how they got infected. Hepatitis C can
spread through sexual intercourse, but it’s rare.
• Anyone can get hepatitis C, but African
Americans – as well as people born between
1945-1965, (“babyboomers” )– bear a
disproportionate burden of disease.
Hepatitis C Facts
• Most people living with hepatitis C do not know they are
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infected.
The hepatitis C virus (HCV) can cause chronic hepatitis,
in which the infection is prolonged, sometimes lifelong.
Chronic hepatitis can lead to cirrhosis, liver failure, and
liver cancer. In fact, viral hepatitis is the leading cause
of liver cancer and the most common reason for liver
transplantation.
Most people living with HCV infection often have no
symptoms until significant damage has been done.
There is no vaccine to prevent hepatitis C infection.
Getting tested is the only way to know if you have been
exposed to hepatitis C.
There are new and improved treatments exists for
hepatitis C.
Features of Hepatitis C Virus
Infection
Incubation period
Range 2-26 weeks
Acute illness (jaundice)
Chronic infection
Cirrhosis
Mortality from CLD
Liver Cancer
Average 6-7 weeks
Mild (<20%)
75%-85%
10%-20%
1%-5%
1%
Serologic Pattern of Acute HCV
Infection with Progression to
Chronic Infection antiHCV
Symptoms +/-
Titer
HCV RNA
ALT
Normal
0
1
2
3 4
Months
5
6
1
Time after Exposure
3
2
Years
4
Transmission of HCV
– Injecting drug use
– Blood Transfusion, transplant from infected
donor,(before screening available in 1992 )
– Therapeutic (contaminated equipment,
unsafe injection practices)
– Occupational (needlestick)
– Perinatal (mother to child)
– Sexual
– Sharing Contaminated items with infected
blood( ie toothbrush, razor, )
Signs and Symptoms
• Persons with newly acquired HCV infection usually are
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asymptomatic or have mild symptoms that are unlikely
to prompt a visit to a health care professional. When
symptoms occur, they can include
Fever
Fatigue
Dark urine
Clay-colored stool
Abdominal pain
Loss of appetite
Nausea
Vomiting
Joint pain
Jaundice
Signs and Symptoms
Most persons with chronic HCV infection are
asymptomatic. However, many have chronic liver
disease, which can range from mild to severe, including
cirrhosis and liver cancer. Chronic liver disease in HCVinfected persons is usually insidious, progressing slowly
without any signs or symptoms for several decades. In
fact, HCV infection is often not recognized until
asymptomatic persons are identified as HCV-positive
when screened for blood donation or when elevated
alanine aminotransferase (ALT, a liver enzyme) levels
are detected during routine examinations.
Medical Work up
• History and Physical
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HCV antibody result
Hepatitis C Viral RNA if HCVab +
Check HIV status
HepA ab /HepBsab status – vaccinate if neg
Liver enzymes(ALT/AST SGOT/SGPT)
Metabolic panel (check glucose, kidney fct)
Genotype
Abdominal ultrasound
Liver Biopsy +/-
Progression of Fibrosis on
Biopsy
No Fibrosis
Stage 1: Fibrous
expansion of
some portal areas
Stage 3: Fibrous
expansion of
most portal areas
with occasional
portal to portal
bridging
Courtesy of Gregory Everson, MD.
Stage 4: Fibrous
expansion of portal
areas with marked
bridging (portal to
portal and portal to
central)
Stage 5,6: Cirrhosis,
probable or defined
Cirrhotic liver:
Gross anatomy of
cadaver
Challenges
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Genotype
Fewer Blacks in Clinical trials
Stigma
Co morbid conditions
Neutropenia
Disease progression (Fibrosis)
Treatment Response
IL28B
Access to care/ Insurance/
Treatment
• Important to understand that currently available treatment must be
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individualized –(treatment experienced or naïve, genotype, liver bx etc)
Early 2000-Combination therapy Pegylated interferon, and ribavirin,
2011 in addition to the above two protease drugs (Bocepravir or Telapravir
FDA approved and one combined with peg and riba for treatment,
Studies show that currently available treatment improved because of
shorter duration
Better clincal outcomes (SVR’s)
Improved tolerability, less side effects
Treatment is defined as undetectable HCV RNA in the patient's blood 24
weeks after the end of treatment
At least six distinct HCV genotypes (genotypes 1–6) and more than 50
subtypes have been identified. Genotype 1 is the most common HCV
genotype in the United States and the most common in African Americans.
Patients with genotypes 2 and 3 are almost three times more likely than
patients with genotype 1 to respond to therapy
DAA Combinations Phase III (without interferon
Drug Name/
Category Drug Name/
Category CompanyVerifiedABT-450/r
(Protease Inhibitor)ABT-267
(NS5A Inhibitor) and/or
ABT-333
(Polymerase Inhibitor)Abbott / EnantaJuly 3, 2013 Daclatasvir
(BMS-790052)
(NS5A Inhibitor)Asunaprevir
(BMS-650032)
(Protease Inhibitor)Bristol-Myers SquibbJuly 3, 2013 Faldaprevir
(BI 201335)
Protease InhibitorDeleobuvir
BI 207127 Polymerase Inhibitor Boehringer IngelheimJuly 3, 2013
Sofosbuvir
(GS-7977)
(Polymerase Inhibitor)Ledipasvir
(GS-5885)
(NS5A Inhibitor)GileadJuly 3, 2013
Phase III (with PegINF plus RBV
• Phase III (with PegINF plus RBV)
Drug Name Drug Category
CompanyVerifiedDaclatasvir
(BMS-790052)NS5A Inhibitor Bristol-Myers SquibbJuly
3, 2013 Faldaprevir
(BI 201335)Protease Inhibitor Boehringer IngelheimJuly
3, 2013 Simeprevir
(TMC435)Protease Inhibitor JanssenJuly 3, 2013
Sofosbuvir
(GS-7977)Polymerase Inhibitor GileadJuly 3, 2013
Case
• RT is a 26 yo AA female who presented to the local medical clinic for
a routine physical . Her previous clinic “closed down “ and she
needs an exam to return to school and work.
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PMH- Denies DM, HTN, CVS Ds, Pneumnia, Asthma or TB, last
PPD 2011 negative,
Gyn Hx- G0 P0 – last pap neg, Neg HPV 2012 ,sexually active ,
heterosexual with 2 partners, uses condoms ‘”most of the time” No
h/o GC, Chlamydia or HSV, tested HIV negative 2010
ROS- tired most of the time for past 3- 4 yrs , generalized itching
on and off, occ nausea , no fevers diarrhea or wgt loss, has good
appetite despite intermittent nausea is able to go to school and work.
Allergies- NKA
Meds- Multivitamin daily
Social Hx- single, P/T college student x 2 yrs, F/T work as unit clerk
in local hospital x 5 years, no h/o smoking , +Social drinker once a
moth with the girls” few glasses wine” , no h/o IVDA or illicit drug
use. Hobbies include being a Big Sister to a 9 yo girl twice a month
who sleeps over “sometimes she forgets to bring toiletries but I keep
a supply of mine for her”
Family Hx- Mother and Father both deceased AIDS related
complications 1992, 5 siblings 1 she recalls with “yellow jaundice” as
a child
Case
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PE : Thin AA female in NAD vital signs stable
HEENT- anicteric, throat clear no lymph node enlargement
Lungs- clear
CVS- S1 S2
Abdomen- soft + BS, slight RUQ tenderness, no hepatomegaly
no spleenomegaly, no fluid wave
Extremity- no clubbing cyanosis or edema, no palmar erythema
Neuro- no deficits
Skin- no rashes or petichiae no spider angiomas
Mental status- pleasant, alert, oriented , appropriate
Genitalia- wnl no lesions or rashes
Pelvic –no d/c , no cmt, no lesions or adnexal tenderness
Ut antverted nl size
Labs
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CBC and PLT’s - wnl
Metabolic Panel-wnl
LFT- elevated ALT (83), AST (37)
alk phos112
HepAsab-Negative
HepBsag- Negative/ HepBsab- Positive
HCV Ab- positive
RPR- Non reactive
Urine GC and Chlamydia - negative
Urinalysis – wnl
Quantiferon – negative
Pap- negative malignant cells , negative HPV
Questions
• What is the diagnosis in this patient?
• What was the most likely mode of transmission?
• What are the next diagnostic steps in her medical work
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up?
Is she cleared to go to return to school? to work?
What would you advise this patient to do immediately?
Would you refer this patient to a specialist for treatment
? Why or why not?
What important information is missing in the history
essential for the management of this patient?
Despite the seriousness of this health problem in
the African American community, too few
African Americans know about the disease or
get tested for it. Early detection of chronic viral
hepatitis infection can save lives,” observes Dr.
Ronald Valdiserri, MD, MPH, Deputy Assistant
Secretary for Health, Infectious Diseases and
Director, Office of HIV/AIDS and Infectious
Disease Policy at the U.S. Department of Health
and Human Services
Thank You!
Marlene Taylor PA-C
[email protected]
718 920-8542