Transcript Hepatitis B

Hepatitis B and
Acute Liver Failure
Jack Kuritzky, PGY-2
UNC Internal Medicine
Morning Report 3/12/10
HEP B - NATURAL HISTORY
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Mode of Infection
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Perinatal most common worldwide
In US, most commonly transmitted by sexual contact or IVDU
Incubation period 1-4 months
Symptoms
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Anorexia
Constitutional symptoms
Jaundice
Nausea
RUQ disomfort
HEP B – ACUTE PHASE
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Subclinical or anicteric hepatitis (70%)
Icteric hepatitis (30%)
Fulminant Hepatitis (0.1% - 0.5%)
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Acute Liver Failure: Rapid development of severe
acute liver failure with impaired synthetic function and
encephalopathy in a patient who previously had a
normal liver or well compensated liver disease
Development of encephalopathy within 8 weeks of
symptoms in a pt w/o liver disease
 Development of encephalopathy within 2 weeks of jaundice
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ACUTE LIVER FAILURE
Goldberg, E and Chopra, S. Acute liver failure: Definition; etiology; and prognostic indicators.
UpToDate, Sept. 2009.
CAUSES OF ACUTE LIVER
FAILURE
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Data from 17 US sites, 308 consecutive patients
with acute liver failure (Ostapowicz G, et al. Results of a prospective study of acute
liver failure at 17 tertiary care centers in the United States. Ann Intern Med 2002 Dec 17;137(12):947-54.)
Acetaminophen overdose (39 percent)
 Indeterminate (17 percent)
 Drug reactions (13 percent)
 Viral hepatitis A or B (12 percent)
 survival at 3 weeks was 67%.
 29% had liver transplantation and 43% survived
without transplantation
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HEP B – RESOLUTION OF
INFECTION
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Previous infection without further virologic,
biochemical, or histologic evidence of disease
Symptoms typically improve in 1-3 months
 >95% of cases resolve in adults
 >90% progress in neonatal hepatitis and 20-50%
progress in patients 1-5 yrs old
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HEP B – CHRONIC PHASE
Less than 5% of infected adults
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Asymptomatic carrier state
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HBsAg+ but no chronic, active inflammatory damage
Chronic hepatitis
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Chronic "necroinflammatory infection", subdivided with
HBeAg positive and HBeAg negative
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12-20% progress cirrhosis
Cirrhosis
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HBeAg is a marker of viral replication and infectivity
6-15% of compensated cirrhosis progress to HCC
Hepatocellular carcinoma
HEP B - TREATMENT
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SUPPORTIVE
Antiviral options: lamivudine, adefovir, entecavir,
telivudine, and tenofivir
Who to treat--Acute HepB:
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Trial of 71 patients with lamivudine for acute HepB (Kumar, et al. A
randomized controlled trial of lamivudine to treat acute hepatitis B. Hepatology. 2007 Jan;45(1):97-101.)
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No difference in clinical or biochemical outcomes
No difference in patients with severe disease, though numbers limited
Fulminant HepB, immunocompromised, prolonged course (>4
weeks), pre-existing liver disease, coinfection with HepC/D
Who to treat--Chronic HepB
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Compensated cirrhosis w/HBV DNA >2,000 IU/mL
Decompensated cirrhosis w/detectable viral load
HEP B - VACCINE
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Series of 3 injections at time 0, 1 month, and 6 months
Indicated for health-care workers, dialysis patients,
patients w/chronic liver disease, patients with high-risk
sexual practices, and IV drug users
Good response is determined by an anti-HepB surface Ag
titer of >10 mIU/mL
Available US vaccines are 95% effective in healthy adults
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Post vaccination testing only recommended for health-care
workers, dialysis patients, and other selected patient populations
Non-responders should complete a second 3-dose regimen
(successful in 50-70% of patients)
SOURCES
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Goldberg, E and Chopra, S. Acute liver failure: Definition;
etiology; and prognostic indicators. UpToDate, Sept 2009.
Kumar, et al. A randomized controlled trial of lamivudine
to treat acute hepatitis B. Hepatology. 2007 Jan;45(1):97101
Lok, A. Clinical manifestations and natural history of
hepatitis B virus infection. UpToDate, Sept 2009.
Ostapowicz G, et al. Results of a prospective study of
acute liver failure at 17 tertiary care centers in the United
States. Ann Intern Med 2002 Dec 17;137(12):947-54.
QUESTIONS?