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
Mode of Infection
Perinatal most common worldwide
In US, most commonly transmitted by sexual contact or IVDU
Incubation period 1-4 months
Symptoms
Anorexia
Constitutional symptoms
Jaundice
Nausea
RUQ disomfort
HEP B – ACUTE PHASE
Subclinical or anicteric hepatitis (70%)
Icteric hepatitis (30%)
Fulminant Hepatitis (0.1% - 0.5%)
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
ACUTE LIVER FAILURE
Goldberg, E and Chopra, S. Acute liver failure: Definition; etiology; and prognostic indicators.
UpToDate, Sept. 2009.
CAUSES OF ACUTE LIVER
FAILURE
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
HEP B – RESOLUTION OF
INFECTION
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
HEP B – CHRONIC PHASE
Less than 5% of infected adults
Asymptomatic carrier state
HBsAg+ but no chronic, active inflammatory damage
Chronic hepatitis
Chronic "necroinflammatory infection", subdivided with
HBeAg positive and HBeAg negative
12-20% progress cirrhosis
Cirrhosis
HBeAg is a marker of viral replication and infectivity
6-15% of compensated cirrhosis progress to HCC
Hepatocellular carcinoma
HEP B - TREATMENT
SUPPORTIVE
Antiviral options: lamivudine, adefovir, entecavir,
telivudine, and tenofivir
Who to treat--Acute HepB:
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.)
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
Compensated cirrhosis w/HBV DNA >2,000 IU/mL
Decompensated cirrhosis w/detectable viral load
HEP B - VACCINE
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
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
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.
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