Beruflich Dokumente
Kultur Dokumente
AM Report 5/19/09
Anne Peery MD
Hepatitis A
Pathophysiology
HAV is a small non-enveloped RNA hepatovirus
HAV is exclusively a virus of humans and primates
Transmitted by the fecal-oral route
Absorbed in the small intestine and replicates in the liver
HAV is secreted in the bile and shed in feces for 1-2 weeks
BEFORE clinical illness and approximately 1 week after
the onset
Incubation period is 15-50 days (on average 30 days)
There is NO chronic carrier state
Hepatitis A
Epidemiology
Transmitted by the fecal-oral route
The largest known modern epidemic of hepatitis A was from
consumption of contaminated seafood. In Shanghai, China,
292,301 cases of acute hepatitis were attributed to eating
raw clams
Spread of hepatitis A has been reported in the United States
and Europe following consumption of contaminated lettuce,
ice slush beverages, frozen strawberries, and salad food
items
The virus is hardy, surviving on human hands and inanimate
objects (fomites) . Transmission of hepatitis A from
hospitalized patients with unsuspected disease to staff is
well recognized
Hepatitis A
Epidemiology
Prevalent in the economically developing regions of
Africa, Asia and Latin America where seroprevalence rates
approach 100% and most infections occurs by age 5
Infection confers lifelong immunity
Seroprevalence rates are approximately 33% in the US
Rates of HAV have been decreasing over past 20yrs
secondary use of vaccine and improvements in hygiene,
sewage disposal and food safety
Hepatitis A
Clinical Presentation
Often asymtomatic in children
May begin with nonspecific prodrome of fever, malaise,
weakness, anorexia, nausea, vomitting, arthralgias,
mylagias and upper respiratory symptoms
This is followed by 1-2 wks dark urine, jaundice, mild
pruritus and slight liver enlargement and tenderness
Labs reflect hepatocellular injury and aminotransferase
levels may be elevated between 500 and 5000; serum
bilirubin usually peaks later then transaminase levels but
usually remains less then 10mg/dl
Most patients have normalization of LFTs within 6 months
Hepatitis A
Relapsing hepatitis A
Recurrent hepatitis secondary to primary infection
The severity of symptoms and biochemical abnormalities
during second phase tend to be the same as observed
during the initial illness except for a tendency to greater
cholestasis
The rate of hepatitis A relapse varies in different case
series from 1.5% to 11.9%
Hepatitis A
Diagnosis
Diagnosis requires presence of serum HAV IgM; IgM
antibody persists for 3-6 months after onset of symptoms
Hepatitis A
Differential diagnosis
(Mild transaminitis < 5x nl)
Hepatic: ALT predominant Hepatic: AST predominant
Chronic hepatitis C Alcohol-related liver injury
Chronic hepatitis B
Steatosis/steatohepatitis
Acute viral hepatitis (A-E, EBV,
CMV) Cirrhosis
Steatosis/steatohepatitis Nonhepatic
Hemachromatosis Hemolysis
Medications/toxins
Myopathy
Autoimmune hepatitis
Thyroid disease
Alpha1-antitrypsin deficiency
Wilson’s disease Strenuous exercise
Celiac disease
Hepatitis A
Differential diagnosis (Severe transaminitis > 15x nl)
Acute viral hepatitis (A-E, herpes)
Medications/toxins
Ischemic hepatitis
Autoimmune hepatitis
Wilson’s disease
Acute bile duct obstruction
Acute Budd-Chiari syndrome
Hepatic artery ligation
Hepatitis A
Treatment
There is no treatment
Prognosis
HAV is usually a benign course in young, healthy people
and is associated with a low mortality
Older adults, immunosuppresed patients and those with
chronic liver disease have greater morbidity and mortality
Mortality 0.1-2%
Hepatitis A
Prevention
Immune globulin (IG)
Available since 1940
Immunoglobins administered low dose provides
protection for 1-2 months
Inactivated HAV vaccine
Available since 1992
Hepatitis A
Post exposure prophylaxis
Close personal contacts
Household and sex contacts
Persons who have shared illicit drugs with someone with
hepatitis A
Child-care center staff, attendees, and attendees'
household members
Persons exposed to a common source, such as an infected
food handler. If a food handler receives a diagnosis of
hepatitis A, PEP should be administered to other food
handlers at the same establishment.
Hepatitis A
Post exposure prophylaxis
Until recently, immune globulin (IG) was the only recommended way to protect
people after they have been exposed to hepatitis A virus.
In June 2007, U.S. guidelines were revised to allow for hepatitis A vaccine to be
used after exposure to prevent infection in healthy persons aged 1–40 years.
Healthy persons aged 12 months – 40 years, who have recently been exposed to
HAV and who have not been vaccinated previously should be administered a single
dose of hepatitis A vaccine, within 2 weeks after exposure.
For persons aged >40 years, IG is preferred because of the absence of information
regarding vaccine performance in this age group and because of the more severe
manifestations of hepatitis A in older adults. Vaccine can be used if IG cannot be
obtained.
For children aged <12 months, immunocompromised persons, persons with chronic
liver disease, and persons who are allergic to the vaccine or a vaccine component,
IG should be used.
Hepatitis A
Prevention
Pre exposure prophylaxis
Indications for HAV vaccination:
People planning to travel to endemic areas
The risk for hepatitis A exists even for travelers to urban areas, those who
stay in luxury hotels, and those who report that they have good hygiene
and that they are careful about what they drink and eat
Men who have sex with men
Illicit drug users
People with chronic liver disease
Recipients of clotting factor concentrates
Hepatitis A
Prevention
Advisory Committee on Immunization Practices (ACIP)
recommends one dose of single-antigen hepatitis A
vaccine administered at any time before departure may
provide adequate protection for most healthy persons.
For optimal protection, older adults,
immunocompromised persons, and persons with chronic
liver disease or other chronic medical conditions who are
planning to depart in <2 weeks should receive the initial
dose of vaccine and also can simultaneously be
administered IG (0.02 mL/kg) at a separate anatomic
injection site.
Hepatitis E
Pathophysiology
HEV is a small non-enveloped single strain RNA virus
HEV can infect humans, primates, swine
Transmitted by the fecal-oral route; thought to spread
zoonotically (principally through swine)
Absorbed in the small intestine and replicates in the liver
HAV is secreted in the bile and shed in feces for 1-2 weeks
BEFORE clinical illness and approximately 1 week after
the onset
Incubation period is on average 40 days
There is NO chronic carrier state
Hepatitis E
Epidemiology
First recognized as a disease in 1980
Considered most important or second most important
cause of acute clinical hepatitis in adults throughout Asia,
Middle East and Africa
Rare in industrialized countries but antibody is found
worldwide
Diagnostic tests vary greatly in specificity, sensitivity, and
availabilty
Hepatitis E is probably underdiagnosed
Fewer then a dozen cases have been reported in the US
Hepatitis E
Clinical Presentation
Similar to HAV
Relapsing hepatitis is rare
Diagnosis
Diagnosis requires presence of serum HEV IgM
Mayo send out $123.90
Hepatitis E
Prognosis
Self limited disease
Mortality 1-4%
Mortality is approximately 20% in pregnant women
Transmission of HEV from pregnant mother to fetus can
result in fetal demise
Hepatitis E
Treatment
No treatment available
Prevention
GlaxoSmithKline has developed a HEV vaccine
Double blind study 2000 adults 95.5% efficacious and
minimal adverse events
The vaccine is not commercially available