Hepatitis A by dfhdhdhdhjr


									           Hepatitis A
Presented by James Hawk MD
          UNC Morning report
   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
   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
   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
   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
   Splenomegaly and cervical
    adenopathy present 10%
   Fulminant hepatitis is rare,
    but may occur in older
    persons and people with
    chronic liver disease

   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
   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
   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
   Healthy persons aged 12 months-40 years:
    HAV vaccine
   Persons > 40 years, <12 months, with
    chronic liver disease, or
    immunocompromised: IG +/- HAV vaccine

To top