This document discusses viral hepatitis, focusing on hepatitis A, B, C, D, and E. It provides details on the definition, causes, epidemiology, transmission, signs and symptoms, diagnosis, treatment and prevention of each type of viral hepatitis. Key points include that hepatitis A, B, C, D and E viruses are the main causes of viral hepatitis in humans. They differ in their transmission routes, clinical presentations, risk of chronic infection and availability of treatment. Vaccination is an effective way to prevent hepatitis A and B infection.

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Viral hepatitis
Definition: Hepatitis is a condition where the inflammation of the liver occurs
that can be caused by viruses, medications and immunological abnormalities.
Hepatitis is of different types based on types of viruses causing it. There are as
follows:
Hepatitiscaused by common viruses:
1. Hepatitis A, caused by hepatitis A virus (HAV)
2. Hepatitis B, caused by hepatitis B virus (HBV)
3. Delta hepatitis, caused by hepatitis D virus (HOV)
4. Hepatitis C, caused by hepatitis C virus (HCV)
5. Hepatitis E, caused by hepatitis E virus (HEV)
Hepatitiscaused by other viruses:
1. Cytomegalovirus
2. Epstein-Barr virus
3. Herpes simplex virus
4. Yellow fever virus
5. Hepatitis G virus
HEPATITIS A
Aetiology
 Caused by hepatitis A virus (HAV), aRNA virus belonging to the
picomavirus group.
 HAV survives on human hands and fomites, and requires temperatures
higher than 185°F (85°C) for inactivation.
 It is resistant to freezing, detergents and acids, but it is inactivated by
formalin and chlorine.
Epidemiology
1. Incubation period is 30 days (15-45 days).
2. HAV infection has a worldwide distribution, and infections can be
sporadic or occurin epidemic outbreaks.

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3. The incidence of acute cases and the seroprevalence vary according to the
hygiene, sanitation, housing, and socioeconomic standards of the region,
with seroprevalences as low as about 13% in Sweden but up to 100% in
many developing countries.
4. In developing countries, infection generally occurs at a young age, and
most of the population has been exposed and is protected after age 10
years.
5. In developed countries, however, infection can occurat any age, and the
prevalence of exposed, immune subjects slowly increases with age.
6. In the United States, the incidence of acute hepatitis A has declined from
12.0 cases per 100,000 individuals in 1995 to 1.0 case per 100,000
individuals in 2007.
Transimission
1. Oral-fecal route, (most often directly from person to person or through
the ingestion of fecally contaminated food or wate)
2. Blood transfusion
3. High-risk groups for acute hepatitis A include travelers to developing
countries, children in day care centers and their parents, men who have
sex with men, injection drug users, hemophiliacswho receive plasma
products, and persons in institutions.
Signsand symptoms
1. The preicteric phase brings nonspecific influenza-like symptoms
consisting of anorexia, nausea, fatigue, and malaise
2. Abrupt onset of anorexia, nausea, vomiting, malaise, fever, headache, and
right upper quadrant abdominal pain with acute illness
3. Icteric hepatitis is generally accompanied by dark urine, acholic (light
colored) stools, and worsening of systemic symptoms
4. Pruritus is often a major complaint of icteric patients
Physical examination
a. Icteric sclera, skin, and secretions
b. Mild weight loss of 2–5 kg
c. Hepatomegaly

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Laboratory tests
1. Positive serum immunoglobulin M anti–hepatitis A virus
2. Mild elevations of serum bilirubin, γ-globulin, and hepatic transaminase
(ALT [alanine transaminase] and aspartate transaminase [AST]) values to
about twice normal in acute anicteric disease
3. Elevations of alkaline phosphatase, γ-glutamyl transferase, and total
bilirubin in patients with cholestatic illness
Prevention
1. Prevention of hepatitis A infection can be achieved through
immunoprophylactic measures.
2. Immuno prophylaxis may be passive, active, or a combination of both. In
passive immunization, temporary protective antibody in the form of
immunoglobulin is administered.
3. In active immunization, a vaccine is administered to induce the formation
of protective antibody.
4. Prophylaxis can be administered before (pre-exposure prophylaxis) or
after exposure (postexposureprophylaxis).
Pre-Exposure Prophylaxis
Immunoglobulin
1. Before hepatitis A vaccine was available, the sole therapy for pre
exposure prophylaxis of hepatitis A infection was immunoglobulin.
2. Although passive immunization with immunoglobulin alone is highly
effective in preventing HAV infection,
3. The duration of protection is short.
4. When used for pre-exposure prophylaxis
5. A dose of 0.02 mL/kg of immunoglobulin administered intramuscularly
(IM) confers protection for less than 3 months, and an IM dose of 0.06
mL/kg confers protection for 5 months or longer for travellers.
Vaccine
1. Active immunization with hepatitis A vaccine has largely supplanted the
use of immunoglobulin for pre-exposure prophylaxis of infection caused
by HAV.

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2. Formulations of inactivated hepatitis A vaccine available in the United
States include Havrix and Vaqta.
3. Both vaccines are formalin-inactivated preparations of attenuated HAV
strains. The manufacturers use differing units to express antigen content
of their respective vaccines.
4. Havrix dosages are expressed in ELISA units, and Vaqta dosages are
expressed as units of hepatitis A antigen.
Dosing Regimen
1. Havrix is availablein two formulations that differ according to age:
(i) For persons 12 months to 18 years of age, 720 ELISA units
(0.5 mL) per dosein a two-doseschedule and
(ii) For persons older than 19 years of age, 1,440 ELISA units
(1.0 mL) per dosein a two-doseschedule.
a. This vaccine is usually injected IM into the deltoid muscle with a
boosterdoseadministered 6 to 12 months later.
b. The pediatric Havrix formulation (three-dose schedule) is no longer
available.
2. Vaqta is available in two formulations, and the formulations differ
according to the person’s age:
(i) For persons 12 months to 18 years of age, 25 units (0.5 mL)
in a two-dose schedule
(ii) For persons older than 19 years of age, 50 units (1.0 mL) per
dose in a two-dose schedule.
a. This vaccine is usually injected IM into the deltoid muscle with a
boosterdoseadministered 6 to 18 months later.
Combination Vaccine
 The US Food and Drug Administration (FDA) has also licensed a
combined HAV and HBV vaccine (Twinrix) for use in persons aged 18
years or older. Twinrix is composed ofthe same antigenic components
used in Havrix and Engerix-B.
 Each doseof Twinrix contains at least 720 ELISA unitsof inactivated
HAV and 20 mcg of recombinantHBsAg. Traceamounts of thimerosal
(<1 mcg) are also present from the manufacturing process.Primary
immunization consists of three doses, given on a 0-, 1-, and 6- month
schedule, the same that is used for single-antigen hepatitis B vaccine.

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 Any person18 years of age or older having an indication for both
hepatitis A and hepatitis B vaccine can be given Twinrix, including
patients with chronic liver disease, users of illicit injectable drugs, men
who have sex with men, and persons with clotting factor disorders who
receive therapeutic blood products.
 For international travel, hepatitis A vaccine is recommended; hepatitis B
vaccine is recommended for travelers to areas of high or intermediate
hepatitis B endemicity who plan to stay for longer than 6 months and
have frequent close contactwith the local population.
 At 1 month after completion of the three-dose series, seroconversion for
anti-HAV (titer>20 milli-international units/mL) was elicited in 99.9% of
vaccines, and protective antibodies against HBsAg (anti-HBs>10 milli-
international units/mL) were elicited in 98.5% of vaccinees.
 The persistence of anti-HAV and antibody to HBsAg (anti-HBs) after
administration is similar to that after single-antigen hepatitis A and B
vaccine administration at 4-year follow-up.
 Observed adverse effects were generally similar in type and frequency to
those reported after vaccination with monovalent hepatitis A and B
vaccines.
VIRUS HAV HBV HCV HDV HEV
Genome RNA DNA RNA RNA RNA
Family Picornavirus Hepadnavirus Flavivirus Satellite Hepeviridae
Size (nm) 27 42 30-60 40 32
Incubation (days)
[mean]
15–50 [30] 45–180[80] 15–160 21–140[35] 15–65 [42]
Transmission
Oral
Percutaneous
Sexual
Perinatal
Common
Rare
No
No
Rare
Common
Common
Common
Rare
Common
Common
Rare
No
Common
Common
Common
Yes, common
Unknown
No
Rare

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Onset Sudden Insidious Insidious Insidious Sudden
Clinical illness 70%-80% adults
5%children
10%–15% 5%–10% 10% 70%–80%adults
Icteric presentation
Children
Adults
<10%
30%
30%
5%–20%
25%
5%–10%
Unknown
25%
Unknown
Common
Peak alanine aminotransferase
(ALT) (units/L)
800–1,000 1,000–1,500 300–800 1,000–1,500 800–1,000
Incidence of acute liverfailure (%) <1 <1 <1 2–7.5 <1; higher in
pregnant women
Serum diagnosis
Acute infection
Chronic infection
Anti-HAVIgM HBsAg, anti-HBc
IgM
HBsAg
Anti-HBc IgG
HCV-RNA (anti-
HCV)
Anti-HCV(ELISA)
RIBA
Anti-HDVIgM
Anti-HDVIgG
Anti-HEVIgG
(seroconversion)
NA
Viral markers HAV RNA HBV DNA
DNA polymerase
HCV RNA HDV RNA Viruslike particles
Immunity Anti-HAV, IgG Anti-HBs NA NA Anti-HEVIgG
Case-fatality rate 0.1%–2.7%
0.15%–1.7%
1%–3% 1%–2% <1% coinfect 0.5%–4%
1.5%–21% pregnant
women
Completerecovery >97% 85%–97% 50% 90% 99%
Incidence of
chronic infection
0% 2%–7%
>90% neonates
50% 80% superinfect
≤5% coinfection
0%
Carrier state No Yes Yes Yes No
Risk of hepatocellular
Carcinoma
No Yes Yes Yes No
Drug treatment None Pegylated
interferon,
interferon,
tenofovir,
entecavir,
adefovir,
telbivudine,
lamivudine
Pegylatedinterferon
+
ribavirin, pegylated
interferon,
interferon,
telaprevir,
boceprevir
Pegylatedinterferon,
interferon
None
*ELISA, enzyme-linked immunosorbent assay; NA, not applicable; RIBA0, recombinant immunoblot assay.*
Hepatitis B

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Aetiology
a. Caused by hepatitis B virus (HBY), belonging to the group of
hepadna viruses.
b. HBY comprises a surface envelope [antigen expressed on it is
called hepatitis B surface antigen (HBsAg)] and a nucleocapsid
core containing DNA [antigen expressed on its surface is called
hepatitis B core antigen (HBcAg), while another soluble antigen in
the nucleocapsid is called hepatitis Be antigen (HBeAg)].
Nucleocapsid core also bas DNA polymerase enzyme.
c. The correspondingantibodies are:
 Anti-HBs
 Anti-HBc
 Anti-HBe.
d. HBsAg-positive serum containing HBeAg is more likely to be
highly infectious than HBeAg-negative or anti-HBe positive
serum.
Epidemiology
1. Incubation period is about 90 days (50--150 days). Hepatitis B is one of
the most common causes of chronic liver disease and hepatocellular
carcinoma worldwide.
2. Approximately one-third of the world’s population have serological
evidence of past or current infection with hepatitis B and approximately
350–400 million people are chronic HBsAg carriers.
3. It is estimated that 1.25 million people in the United States are
chronically infected with hepatitis B virus.
4. Approximately 78,000 people per year becomeacutely infected with the
hepatitis B virus in the United States.
5. Of those infected, 70% become symptomatic; 26% are hospitalized; 90%
of infants infected at birth, 30% of children infected at age 1 to 5 years,
and 6% of those infected over 5 years of age develop chronic infections;
and 1% from acute disease and 15% to 25% from chronic disease die
each year.
6. 14 Patients with cirrhosis are at a much greater risk for developing liver
cancer (12 to 300 times normal risk).
Transmission

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 Transmitted through parenteral but occasionally non-parenteral
 Transfusion of infected blood or blood products, injections with
contaminated needles, intravenous drug use with needle sharing, tattooing
and acupuncture.
 Non-parenteral means of transmission include spread through bodyfluids
like saliva, urine, semen and vaginal secretions. However, this requires
close personal contact, sexual intercourse and male homosexuality.
 Mother-to-child spread (perinatal transmission) is also common. It could
be either transplacental transmission or transmission at or soonafter birth.
Signsand symptoms
• Easy fatigability, anxiety, anorexia, and malaise
• Ascites, jaundice, variceal bleeding, and hepatic encephalopathy can
manifest with liver decompensation
• Hepatic encephalopathy is associated with hyperexcitability, impaired
mentation, confusion, obtundation, and eventually coma
• Vomiting and seizures
Physical examination
• Icteric sclera, skin, and secretions
• Decreased bowel sounds, increased abdominal girth, and detectable fluid
wave
• Asterixis
• Spider angiomata
Laboratory tests
• Presence of hepatitis B surface antigen for >6 months
• Intermittent elevations of hepatic transaminase (alanine transaminase [ALT]
and aspartate transaminase [AST]) and hepatitis B virus DNA >20,000 IU/mL
(105 copies/mL or 108 copies/L)
• Liver biopsies for pathologic classification aschronic persistent hepatitis,
chronic active hepatitis, or cirrhosis

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Prevention
Alterations in sexual behavior, screening of high-risk patients or settings (e.g.,
STD and HIV testing and treatment facilities, drug abuse treatment and
prevention settings, heath care settings targeting services to IV drug users, heath
care settings targeting services to men having sex with men, and correctional
facilities) and blood products, developing needle exchange programs, and
cultural outreach and education may have an impact on HBV transmission. The
goals of preventive therapy should be to identify all persons who require
immunoprophylaxis for the prevention of infection and provide long-term
protection through vaccination to decrease the risk of chronic HBV infection
and its subsequent complications, as well as minimizing adverse effects and cost
of therapy.
Pre-Exposure Prophylaxis
Manufactured using recombinant DNA technology, Recombivax HB (10 mg
HBsAg/mL) and Engerix-B (20 mg HBsAg/mL) are yeast-derived HBV
vaccines that induce an immunologic responsesimilar to the plasma-derived
vaccine (no longer used). Because P.G. will come in contact with potentially
infectious bodily secretions during her rotations, she should be immunized
against hepatitis B with either Recombivax HB or Engerix-B.
DOSING
REGIMEN
1. The
recommended doses
of available hepatitis
B vaccines are
shown below
2. HBV injection

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to the buttocks have a signifificantly higher responsewhen vaccinated in
the arm.
3. P.G. should be immunized with either Recombivax HB (10 mcg) or
Engerix-B (20 mcg) administered as a 1-mL IM injection in the deltoid
muscle.
Postexposure Prophylaxis
Percutaneous Exposure
After exposure to HBV, prophylactic treatment with hepatitis B vaccination and
possibly passive immunization with hepatitis B immunoglobulin (HBIG) should
be considered. The ACIP recommendations for postexposure immune
prophylaxis after hepatitis B exposure are shown in Table
Sexual Exposure
CASE77-9
1. Sexual transmission of HBV is an important cause of HBV infection,
accounting for approximately 30% to 60% of all new cases annually.
2. Passive immunization with a single 5-mL doseof HBIG was found
highly effective in preventing HBV infection after sexual exposure when
compared with a control globulin (with no anti-HBs activity).
3. The CDC recommends that susceptible persons exposed to HBV through
sexual contact with a personwho has acute or chronic HBV infection
should receive postexposureprophylaxis with 0.06 mL/kg of HBIG as a
single IM dosewithin 14 days of the last exposure.

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4. Patients also should receive the standard three-dose immunization series
with hepatitis B vaccine beginning at the time of HBIG administration.
Perinatal Exposure
1. In many Asian and developing countries, perinatal (vertical) transmission
accounts for most HBV infections.
2. Infants bornto HBV-infected mothers have a greater than 85% risk of
acquiring HBV during the perinatal period.
3. Of those who become infected, 80% to 90% becomechronic HBsAg
carriers. Although fulminant cases have been reported, most hepatitis
infections in neonates are asymptomatic.
4. Despite the usually innocuous initial disease, signifificant adverse
consequences are associated with chronic HBsAg carriage in neonates.
5. Chronic hepatitis B infection is associated with chronic liver disease and
has been clearly implicated as a major risk factor in the development of
primary HCC.
6. Screening pregnant women for the presence of HBeAg and
administration of HBIG and hepatitis B vaccine is 85% to 98% effective
in preventing HBV infection and the chronic carrier state.56,60,62 This
compares with a 71% effificacy rate for administration of HBIG alone.
7. Simultaneous administration of HBIG and hepatitis B vaccine does not
adversely affect the productionof anti-HBs in neonates.56,60,62 Infants
born to mothers who are HBsAg positive should receive simultaneous IM
injections of the appropriate doses ofhepatitis B vaccine and HBIG (0.5
mL) within 12 hours of birth.
8. The injections should be administered at separate sites. S.L. should
receive HBIG (0.5 mL) as soonas possible after birth, administered as an
IM injection and
9. 0.5 mL of either Recombivax HB (5 mcg) or Engerix-B (10 mcg) as an
IM injection at a separate site.
Hepatitis C

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Aetiology
• Previously called blood-bornenon-A, non-B hepatitis.
• It is a single-stranded RNA virus belonging to the family Flaviviridae.
• HCV has six genotypes. Chronic HCV 1 infection has poorresponseto
therapy. In India, HCV 3 is mostprevalent.
• HCV-RNA can be detected within a few days of infection, well before
the appearance of antibodies to HCV (anti-HCV).
Epidemiology
• Incubation period is 50 days (15-160 days).
Transmission
 Transmission is through parenteral route.
 More than 90% of cases of post-transfusion hepatitis are caused by HCV.
Also common in drug addicts.
 Common sources of infection are blood and blood products capableof
transmitting hepatitis B, particularly coagulation factor concentrates.
 Other modes include perinatal and sexual transmission.
 Transmission of hepatitis C through needle-stick injury is 1-3%.
 HCV is not transmitted by breastfeeding.
 Nearly 80% develop chronic hepatitis.
 Prevention by vaccine or immunoglobulin not possible.
Signsand symptoms
 HCV RNA becomes detectable in the serum 3 to 7 days after exposure.
HCV RNA levels rise rapidly during the first weeks, followed by serum
aminotransferase levels 2 to 8 weeks after exposure.
 Anti-HCV antibodies arise late in the course of acute hepatitis C and may
not be present at the onset of symptoms and serum aminotransferase
elevation.
 After an incubation period that ranges from 15 to 120 days, acute
hepatitis C usually remains asymptomatic and is undiagnosed.
 Nonspecific symptoms such as fatigue, low-grade fever, myalgias,
nausea, vomiting, or itching may be present.

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 Jaundice occurs in only 20 to 30% of patients, usually 2 to 12 weeks after
infection.
 Serum aminotransferase levels commonly exceed 10 times the upper limit
of normal in the acute stage, even in the absence of symptoms.
 Fulminant hepatitis C has been reported but appears to be exceptional in
the absence of another chronic underlying liver disease
Diagnosis
 Anti-HCV-appears after infection; disappears after recovery; persists in
chronic hepatitis C
 HCV-RNA-after exposure, HCV-RNA becomes detectable in serum after
7-14 days, followed by aminotransferase elevation and later (after 4-10
weeks) by presence of antibodies.
 Remains detectable in most, continuously or intermittently .
Prevention
Pre-Exposure Prophylaxis
1. No vaccines are effective against HCV, and current measures to prevent
hepatitis C infection have largely focused on identifying high-risk
uninfected persons and counseling them on risk reducing strategies to
prevent infection.
2. The CDC and the National Institutes of Health have published
recommendations that address these issues. Suggested primary preventive
measures are
 In monogamous long-term relationships, transmission is rare.
 Although HCV-positive individuals and their partners should be
informed of the potential for transmission.
 It is recommended that sexual partners of infected patients should
be tested for antibody to HCV.
 In households with an HCV-positive member, sharing razors and
toothbrushes should be avoided.
 Covering open wounds is recommended.
 Injection needles should be carefully disposed ofusing universal
precaution techniques.

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 It is not necessary to avoid close contact with family members or to
avoid sharing meals or utensils.
 Additionally, pregnancy is not contraindicated in HCV infected
individuals. Perinatal transmission from mother to baby occurs in
less than 6% of instances.
 No evidence indicates that breast-feeding transmits HCV from
mother to baby
 Babies born to HCV-positive mothers should be tested for anti-
HCV at 1 year.
 It is important that clear and evidence-based information be
provided to both patients and physicians regarding the natural
history, means of prevention, management, and therapy of hepatitis
C.
Postexposure Prophylaxis
 Immunoglobulin is no longer recommended for postexposureprophylaxis
of hepatitis C infection because it is not effective.
Delta Hepatitis
Aetiology
1. Caused by hepatitis D virus (HDV), which is a defective RNA
virus. The RNA genome is covered by an outer coat of HBsAg.
2. It has no independent existence. It requires HBV for replication
and expression.
3. HDV can infect a personsimultaneously with HBV (coinfection).
4. HDV can superinfect a person who is already a chronic carrier of
HBV (superinfection).
Epidemiology
 Two epidemiologic patterns exist:
o Delta infection being endemic among those with hepatitis B,
predominantly transmitted by non-parenteral route, especially close
personal contact.

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o In non-endemic areas, delta infection is confined to persons
exposed frequently to blood and blood products, mainly
intravenous drug addicts and haemophiliacs.
 Five percent of chronic HBV carriers, or 15 million to 20 million
individuals worldwide, are also infected with HDV.
 The prevalence of HDV infection in HBV-infected patients varies
according to the geographic area because it is transmitted primarily
through parenteral exposure.
 As a result, its prevalence is relatively higher in HBsAg-positive
intravenous drug users in Western countries, where approximately 8 to
12% of HBsAg-positive patients are infected with HDV.
 By comparison, the prevalence of HDV has decreased substantially in
southern Europe, probably owing to universal HBV vaccination
programs, improvement in hygiene and living conditions, and
implementation of standard precautions to prevent HIV infection.
 The incidence of HDV is increasing in Russia, eastern Europe, Japan, and
India.
Transmission
 Transmitted by parenteral route.
 Coinfection gives rise to severe acute hepatitis that is limited by recovery
from HBV infection.
 Superinfection causes rapidly progressive chronic hepatitis, with episodes
of acute hepatitis.
 It can cause fulminant liver failure and rapid progression to cirrhosis as
well as an increased risk of liver cancer.
Signsand symptoms
 HDV can be acquired at the same time as HBV (coinfection) or by a
chronic HBsAg carrier (superinfection).
 Coinfection is characterized by one or two episodes of acute hepatitis,
depending on the respective amounts of HBV and HDV present in the
inoculum; acute hepatitis can range from mild to fulminant.
 In contrast, when chronic HBV carriers are superinfected by HDV, acute
hepatitis D is generally severe, often fulminant, and chronic.
Diagnosis

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o Delta antigen-occasionally detectable
o Anti-delta-initially of lgM type and later lgG type
o HOV-RNA-most reliable.
Prevention
 Hepatitis D virus replication is dependent on HBV replication; therefore,
successfulimmunization with HBV vaccine also prevents HDV infection.
 No immunoprophylactic therapies are available for patients with chronic
HBV infection who are also at risk for superinfection with HDV.
 Prevention of HDV superinfection is based on behavioral modifification,
such as the use of condoms to prevent sexual transmission and needle
exchange programs to minimize transmission by IV drug use.
Treatment
The goal of treatment is to eradicate HDV along with HBV.
Hepatitis E
Aetiology
• Previously called epidemic or enterically transmitted non-A, non-B hepatitis.
• It is a single-stranded RNA virus.
Epidemiology
• Incubation period is 40 days (15-60 days).
• Primarily enteric mode of transmission.
• Accounts for epidemic, water-borne hepatitis; common in India.
• Commonly occurs after contamination of water supplies as after monsoon
flooding.
Diagnosis
• Anti-HEV-both lgM and lgG are present at onset
Prevention and treatment

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 No immunoprophylactic measures exist for HEV disease, and effective
prevention strategies are dependent on improved sanitation in endemic
areas.
 Travelers going to endemic areas should be educated regarding the risks
of drinking water, eating ice, or eating uncooked shellfish or uncooked
and peeled fruits and vegetables.
 Drinking water should be boiled to inactivate HEV.
 No vaccines or postexposureprophylaxis treatments are currently
available to prevent HEV infection.
 However, results from a phase II randomized trial using 20 mcg of a
recombinant 56-kDa truncated open reading frame-2 vaccine in young
healthy men suggest that these agents could be effective in the prevention
of HEV infection.
 Others have reported limited success with oral ribavirin (12 mg/kg daily
for 12 weeks) in a kidney and pancreas transplant recipient with chronic
HEV infection.
 Clearly, an appropriately designed clinical trial is required to defifine the
role of ribavirin for chronic HEV infection.
Complications of Acute Viral Hepatitis
1. Fulminant hepatic failure
2. Relapsing hepatitis
3. Cholestatic hepatitis
4. Post-hepatitis syndrome
5. Aplastic anaemia
6. Polyarteritis nodosa
7. Transverse myelitis
8. Renal failure
9. Henoch-Schonlein purpura
10.Chronic hepatitis
11.Cirrhosis
12.Hepatocellular carcinoma
13.Myocarditis
14.Peripheral neuropathy

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Poor Prognostic Features
1. Marked increase in AST and ALT
2. Bilirubin >20 mg/dl
3. Liver not enlarged
4. Prolongation of prothrombin time by 5 seconds
5. Recurring attacks of hypoglycaemia
6. Renal failure
7. Associated conditions
8. HBV, HCV or HDV infection
Treatment
 Rest
 During the acute symptomatic period, complete rest and thereafter
gradual ambulation.
 In high-risk patients (patients more than 50 years, pregnant and those
with other major diseases) rest is continued till symptoms and signs
have disappeared, and liver function tests have returned to near
normal.
 Diet
 Nutritious general diet of 2000-3000 kcal/day. In the initial stage, when
good diet is not tolerated, give a light diet, fruit drinks and glucose. There
is no need to avoid fatty diets, but most patients cannot tolerate these
diets.
 Encourage good protein intake.
 If vomiting is severe, intravenous fluids are given.
 Drugs
 Drugs should be avoided if possible (especially sedatives and hypnotics).
 Alcohol to be avoided for next 6 months.
 Oral contraceptives can be resumed after clinical and biochemical
recovery.
 Antiviraldrugs
 Some evidence suggests efficacy of interferon-a in patients with acute
hepatitis C infection in reducing the rate of chronicity.

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References :
1. Goldman%27sCecil Medicine, 24th Ed 2012
2. Dipiro 9th edition
3. essentials of internal medicine
4. Herifindel , 18E
5. kodakimble 10E
6. harrison’s principles of internal medicine, 20th edition