transmission of hcv in the united states (cdc estimate)
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Transmission of HCV in the United States (CDC estimate)
Infected 20+ years
Overall prevalence
Past and Future US Incidenceand Prevalence of HCV Infection
Armstrong GL, et al. Hepatology. 2000;31:777-782. Graphic courtesy of the CDC.
Decline among IDUs
Overall incidence
Often a Silent Disease until its too late
Over the last 20 to 30 years, liver disease in many undiagnosed or untreated hepatitis C patients has silently progressed:
-In the 1990s, the most common finding on liver biopsy was stage 0 (no liver damage). -Now 20 years later the most common finding will soon be Stage 4 (cirrhosis).
1990s 2015
Good news- Less new cases of Hepatitis C over the last 20 years
Bad news- many of the millions of people infected in the 1970’s and 1980’s are silently progressing to cirrhosis and liver failure
Vertex Pharmaceuticals Incorporated, March 2010
Does curing Hepatitis C alter the patient’s prognosis?YES!!!
Curing HCV has many benefits:
I. Actual regression (improvement) of the liver scars
II. Decreased incidence of liver failure
III. Decreased incidence of liver cancer
IV. Reduced all-cause mortality
V. Improved life expectancy
VI. Prevent viral transmission to others
How to work up your patient with Hepatitis C
You screened your patient, and now the HCV antibody test ispositive. What do you do next?
1.To confirm active disease obtain:
Virus (HCV), Quantitative, PCR (QuantaSURE®)
If HCV RNA is detectable- they have active disease
If HCV RNA is not-detectable- the disease has resolved- either spontaneously or due to prior successful treatment .
A positive HCV antibody test only means they have been exposed to HCV. About 20 % of patients will spontaneously clear the infection, but their antibody test will remain positive. They do not need treatment!
Blood work
1. HCV Genotype – over time, HCV has evolved into different strains, referred to as genotypes 1 thru 6. Some HCV drugs may only block viral replication in a specific genotype, while other drugs may work against all genotypes. Genotype 1, the most common genotype in the United States is broken down further into genotype 1a and 1b.
It is critical to determine the genotype before prescribing therapy.
In the United States:
Genotype 1a – 55% genotype 3- 14%
genotype 1b- 15% genotype 4- 1%
genotype 2 15 %
Other blood tests:
Chemistry panel and ProTime – evaluates liver function – albumin, t.bili and ProTime; and inflammation- AST and ALT
CBC- thrombocytopenia is a good predictor of cirrhosis
Iron panel and ferritin- increased levels could mean hemochromatosis or cirrhosis
AFP- elevated levels seen in cirrhosis and liver cancer
Hepatitis A antibody, total and Hepatitis B Surface ag and Surface ab- if not immune, good to vaccinate these patients against HAV and/or HBV
HIV screen
Other tests:
Liver /spleen Ultrasound- don’t order an abdominal ultrasound, L/S ultrasound is cheaper and it is all you need: write “evaluate Hepatitis C” – this way the radiologist knows to look for signs of cirrhosis, portal hypertension and hepatoma
Hepatitis C FibroSURE© – (A LabCorp test) A blood test that takes a number of lab values and correlates them with stage of liver disease.
Stage of Disease-how much damage has occurred to the liverDoes your patient have cirrhosis?
1. Need to know if the patient has cirrhosis, since this is when the risk of liver cancer or decompensation increases, and the course of therapy may need to be extended
2. Degree of liver damage is described by Stage, and reflects the amount of scarring to the liver
3. At this time- most insurances only cover therapy if patient has moderate to advanced liver disease
Stage of liver disease – based on Metavir Scale from 0 to 4- how much scarring (fibrosis) is present in the liver
Stage 0- no damage
Stage 1 – mild scarring
Stage 2- moderate scarring
Stage 3- advanced disease
Stage 4- severe scarring with distortion of the liverstructure-this stage is called cirrhosis
Options for Liver Fibrosis Assessment
Liver BiopsySerum
Biomarkers
Liver biopsy: gold standard
Axial CT/MRI, US can demonstrate cirrhotic morphology, portal hypertension
Serum markers of fibrosis
Elastography: approved in United States
HCV life cycle and how the new drugs work -Right now there are three important enzymes ( a protease, a polymerase and an enzyme involved in viral replication) which are the targets of the new anti-viral drugs. If you can block these enzymes effectively enough- then the virus has no where to hide and the infection resolves . Two or three potent anti-virals working together at different sites in the life cycle are enough to cure most patients
Treatment :For Genotype 1a or 1b:Two choices : Either a combination of two antiviral drugs Sofosbuvir and Ledipasvir (in one tablet called Harvoni®) Or three antivirals in a BID regimen called Viekira Pak® +/- ribavirinFor Genotype 2 or 3:Sofosbuvir (Sovaldi®) and ribavirin together 90 to 100% of all patients can be cured with these regimens!
Three Hepatitis C treatment terms to know:
1. SVR12- (Sustained Virologic Response, week 12)- this is
the accepted definition of cure. It means at 12 weeks after completion of therapy, the HCV remains non-detectable. Very rare to relapse after that time period.
2. Treatment naïve- patient has never been treated before
3. Treatment experienced- the patient has been treated with but
not cured previously with dual therapy (interferon and ribavirin) or triple therapy (interferon, ribavirin and a protease inhibitor). These patients may not respond as quickly to the new therapies as a treatment naïve patient, and may therefore require a longer course of medication to achieve SVR12.
Case #1- 65 year old vet with mild disease
Used drugs in the late 1960s in the service, hospitalized with hepatitis. None since
No alcohol for 27 years
Diagnosed at VA when established care in 2008
Liver biopsy showed Stage 1 fibrosis in 2008
Had some depression, decided against therapy with interferon and ribavirin then
Recently saw a TV ad about new HCV meds, decided to come to see if he was a candidate
HCV antibody test is positive
Case 1, cont
PMH- none
PE- sharp, palpable liver edge
NO palmer erythema or spider angiomata
Case 1-Lab results
Platelets- 280,000
AST/ALT- 45/73
Albumin – 4.2, T. bilirubin 0.9mg/dl
INR- nl
Fe/TIBC- 34%
AFP- 4.2
Genotype – 1a
HCV viral load- 695, 657 copies/ml
HIV- neg, HAV IgG +, HBV Sag-/Sab-
APRI score- (45/33)/280 x 100 = 1.1 (mild fibrosis)
Ultrasound- mildly enlarged liver, no masses or portal hypertension
Questions ?
In 2008, how did we confirm he has active Hepatitis C?
It is an active infection, so what is the utility now of each of the following tests in evaluating your patient?
1. CBC
2. Chemistry panel, PT/INR
3. Fe/TIBC
4. Genotype
5. Ultrasound and AFP
6. HIV, HAV IgG , HBV Sag and Sab
Started on Harvoni daily for 8 weeks, so far non-detectable week 4. Cure rate > 95%
Case #2- 65 year old alcoholic with cirrhosis
Used nasal cocaine in the 1970s and 1980s, none for 30 years. No combat, no tattoos, no transfusions
Retired, plays golf and has 3 to 4 hard drinks a few times a week with his buddies
Diagnosed in 2014 at the VA with HCV
No other major medical problems
Case #2, cont.
PE:
tremulous, has rosacea
enlarged liver, possible spleen tip
palmer erythema
distended veins on abdomen
Case 2-Lab results
Platelets- 94,000
AST/ALT- 48/51
Albumin – 3.5 mg, T. bilirubin 0.6mg/dl
INR- nl
Fe/TIBC- 34%
AFP- 9.6
Genotype – 1b
HCV viral load- 388,800 copies/ml
HIV- neg, HAV IgG -, HBV Sag-/Sab-
APRI score- (48/33)/94 x 100 = 1.6 (advanced fibrosis)
Ultrasound- mildly enlarged, nodular liver, no masses or portal hypertension, c/w cirrhosis (Stage 4)
Case #2, cont.
Patient told unless he completely stops drinking , will not be offered HCV therapy and likely to die in relatively near future of liver failure
Over next 6 months switches to Coors non-alcohol beer after golfing, loses 30 pounds. Appears motivated
To start Viekira Pak with ribavirin for 12 weeks this week – cure rate > 95%
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