Hepatitis A
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Hepatitis A
Presented by James Hawk MD
UNC Morning report
3/31/08
HAV
Noneveloped RNA virus
Hepatovirus genus
Picornavirus Family
Incubation Period: 15-45
days (mean 30 days)
Virus not known to be
cytopathic to hepatocytes-
disease process is due to
immunologic response
Transmission of HAV
Almost exclusively fecal-oral
Viral replication limited to liver, but virus is
present in liver, bile, stools, and blood during
late incubation phase and acute pre-icteric
phase
When jaundice becomes apparent, viral
shedding in feces, viremia, and infectivity
diminish rapidly
Transmission of HAV
Transmission enhanced by poor personal
hygiene and overcrowding
Populations at risk: citizens of and travelers
to developing countries, children in daycare
centers, men who have sex with men, drug
users
Since availability of HAV vaccine in 1995,
infection rate has decreased 89% in US
(incidence now 1.2 cases/100,000)
Clinical Presentation: 3 phases
Prodrome
Icteric Phase : >70% of cases
Recovery
Most patients recover completely
Fatality rate 1.8% in patient > 60 years old
Prodrome
Precedes onset of jaundice
by 1-2 weeks
Rise in AST/ ALT
Symptoms are quite
variable. May include:
Nausea/ vomiting
Low-grade fever (38-39 C)
HA/ photophobia
Arthralgia/ Myalgia
Pharyngitis / Cough
Icteric Phase
Elevated bilirubin level
follows transaminitis, and
may persist longer
At onset of jaundice,
constitution symptoms
usually start to resolve
Liver may become enlarged
and tender, causing RUQ
pain
Splenomegaly and cervical
adenopathy present 10%
Fulminant hepatitis is rare,
but may occur in older
persons and people with
chronic liver disease
Recovery
Usually within1-2 months
Constitution symptoms resolve
Liver enlargement may persist, along with LFT
abnormalities during this phase, but elevated LFTs
rarely persist up to 1 year
HAV does NOT progress to chronic liver disease
Relapsing Hepatitis: may occur weeks to months
after apparent resolution
Diagnosis
Anti-HAV IgM class antibodies present during
acute illness (while AST/ALT elevated and
viral shedding still occurring), and may be
present for several months
IgG class anti-HAV demonstrates previous
infection or vaccination and immunity
Differential Diagnosis
Viral diseases causing elevated AST/ALT (less
frequently hyperbilirubinemia): infectious
mononucleosis, CMV, HSV, Coxsackieviruses
Other rare infectious causes of liver injury:
toxoplasmosis, leptospirosis, Candida, brucella,
mycobacteria, Pnuomocystis
Drugs!
Acute cholecystitis, common bile duct stone,
ascending cholangitis
Vaccination
Two commercially available vaccines, Havrix
and Vaqta. Both are inactivated, single
antigen. Both require two doses, the second
one six months after first.
Twinrix is a combined HAV and HBV
inactivated vaccine
Who Should Be Vaccinated?
All children at age 1 year
Persons traveling to countries with high rates
of HAV
Men who have sex with men
Users of injection and non-injection drugs
Chronic liver disease patients
Pts with clotting factor disorders
Pts with occupational exposure (Note: NOT
health care workers)
Postexposure Prophylaxis
AICP recommendations as of June 2007.
Based upon a noninferiority trial of IG vs HAV
vaccine after exposure to HAV (NEJM 2007)
Prophylaxis should be provided to household
members and sexual contacts of persons
with serologically confirmed HAV, or others
with “close personal contact”
Efficacy of prophylaxis greater than two
weeks after contact is unknown
Postexposure Prophylaxis
IG and HAV vaccine provide good protection
(~96%)
Healthy persons aged 12 months-40 years:
HAV vaccine
Persons > 40 years, <12 months, with
chronic liver disease, or
immunocompromised: IG +/- HAV vaccine
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