Dea Erica

I4061171001

Pembimbing
dr.Amanda Trixie H., Sp.PD
dr. I Ketut Sujana, Sp.PD

Kepaniteraan Klinik Ilmu Penyakit Dalam, SMF-Ilmu Penyakit Dalam

Rumah Sakit Sultan Mohamad Al-Qadrie
2018
Definition
 Hepatitis is a systemic infection affecting the liver
predominantly.
Etiology
 Caused by one of the five viral agents:
1.Hepatitis A virus (HAV)
2.Hepatitis B virus (HBV)
3.Hepatitis C virus (HCV)
4.Hepatitis D virus (HDV)
5.Hepatitis E virus (HEV)
Virology
 Hepatitis B is a DNA virus, hepadnaviruses
(hepatotropic DNA viruses)
 HBV DNA codes for four sets of viral products: S, P, C,
and X.
Serologic & Virologic Markers
1-12 weeks
HBsAg

Infected with Undetectable by 1-2

Virologic markers
Hepatitis B months

Antibody to HBsAg
(Anti-Hbs)
 Anti-HBc
1-2 weeks after
HBsAg

Only serologic on
gap/window period

Infected with HBcAg IgM Anti-HBc

Hepatitis B First 6 months

IgG anti-HBc
Beyond 6 months
 High level of virus
replication

Infected with HBeAg

Hepatitis B (appears with or
shortly)

Circulating virions
and detectable
HBV
 Detectable beyond
HBsAg
6 months

Undetectable or
Anti-HBs
detectable in low

Primarily of IgG
Chronic Hepatitis B Anti-HBc
class

High in serum and

HBV DNA hepatocyte nuclei
(quantitative)

HBeAg Qualitative marker

Pathogenesis
 Inactive hepatitis B carriers with normal liver
histology and function suggests that the virus is not
directly cythopathic.
 Nucleocapsid protein (HBcAg and possibly HBeAg)
present on cell membrane are the viral target antigens
that invites cytolytic T cells to destroy HBV infected
hepatocytes.
 Differences in T cell responsiveness related to
outcomes between those who recover after acute
hepatitis and those who progress to chronic hepatitis.
 Components of innate immune system participate in
early immune response to HBV infection, mediated
largely by Natural Killer (NK) cell.
Epidemiology
 Percutaneous inoculation has long been recognized as
a major route of hepatitis B transmission.
 HBsAg has been identified in almost every body fluid
from infected persons and some of these, most notably
semen and saliva are infectuos.
Symptoms and Signs
Prodromal Symptoms
(Precede Jaundice by 1- Clinical Jaundice Recovery Phase
2 weeks)
• Anorexia • Prodromal • Constitutional
• Nausea symptoms diminish symptoms disappear
• Vomiting • Mild weight loss • Liver enlargement
• Fatigue • Upper quadrant pain
• Malaise and discomfort
• Athralgia • Splenomegaly
• Myalgia • Cervical adenopathy
• Headache • Spider angiomas
• Photophobia
• Pharyngitis
• Coughing
 Posticteric phase duration is variable, usually 3-4
months in hepatitis B.
 Acute hepatitis-like clinical events in person with
chronic hepatitis B may accompany spontaneous
HBeAg to anti-Hbe spontaneous reactivation or
seroconversion.
Laboratory Features
Serum Aminotransferase

• Aspartate aminotransferase (AST) and alanine aminotransferase

(ALT) (previously SGOT amd SGPT) increase to a variable degree and
precede the rise of bilirubin level.
• Peak levels vary from 400-4000 IU or more. These level usually
reached at the time patient is clinically icteric and diminish during
recovery phase.

Bilirubin

• Jaundice is usually visible in sclera or skin when the serum bilirubin

value is >43 µmol/L (2.5 mg/dL). When jaundice appears, the serum
bilirubin typically rises to levels ranging to 85-340 µmol/L (5-20
mg/dL).
The presence of HBsAg with or without IgM anti-HBc represent HBV
infection. If IgM anti-HBc is present, the HBV infection is considered
acute. If IgM anti-HBc is absent, the HBV infection is considered
chronic.
Prognosis
 In acute hepatitis B, 95-99% of previously healthy
adults have favorable course and recover completely.
 Patients of advanced age and with serious underlying
medical disorders may have prolonged course and
more likely to experience severe hepatitis.
 The case fatality of hepatitis B is very low (~0.1%) but
is increased by advanced age and underlying
debilitating disorders.
Complications and Sequelae
 Most feared complications of viral hepatitis is
fulminant hepatitis (massive hepatic necrosis).
Fulminant hepatitis is seen primarily in hepatitis B, D,
and E.
 Chronic hepatitis is an important late complication of
acute hepatitis B occuring in small proportion of
patients with acute disease but more common in those
who present with chronic infection without having
experienced an acute illness, as occurs typically after
neonatal infection or after infection in
imunosuppressed host.
 The following clinical and laboratory features suggest
progression of acute hepatitis to chronic hepatitis:
1) Lack of complete resolution of clinical symptomps of
anorexia, weight loss, fatigue, and the persistence of
hepatomegaly.
2) The presence of bridging/interface or multilobular
hepatic necrosis on liver biopsy during protracted,
severe acute viral hepatitis.
3) Failure on serum aminotransferase, bilirubin, and
globulin levels to return to normal within 6-12 months
after the acute ilness.
4) The persistence of HBeAg for >3 months or HBsAg for
>6 months after acute hepatitis.
Differential Diagnosis
Aminotransferase

• Aminotransferase elevations can accompany almost any systemic viral infection.

Other rare causes of liver injury confused with viral hepatitis are infections with
Leptospira, Candida, Brucella, Mycobacteria, and Pneumocystis.

Drug

• Complete drug history is particulary important because many drugs and certain
anesthetic agents can produce picture of either acute hepatitis or cholestasis.

Alcoholic Hepatitis

• Serum aminotransferase is low and stigmata of alcoholism. Finding on liver biopsy

of fatty infiltration, a neuthrophilic inflammatory reaction and alcoholic hyaline
would be consistent with alcohol induced rather than viral liver injury.
Symptoms

• Acute hepatitis may present with right upper quadrant

abdominal pain, nausea and vomiting, fever, and icterus, it
is often confused with cholecystitis, common duct stone,
and cholangitis. Patient with acute viral hepatitis may
tolerate surgery poorly.

Elderly

• Viral hepatitis in elderly is often misdiagnosed as

obstructive jaundice resulting from a common duct stone
or carcinoma of pancreas.
Treatment
 In hepatitis B among previously healthy adults who
present with clinically apparent acute hepatitis,
recovery occurs in ~99%.
 Therefore antiviral therapy is not likely to improve the
rate of recovery an is not required.
 In rare instances of severe acute hepatitis B treatment
with a nucleoside analogue (NA) at oral doses used to
treat chronic hepatitis B has been attempted
successfully.
 Most authorities would recommend institution of
antiviral therapy with a nucleoside analogue (entecavir
or tenovir, the most potent and least resistance-prone
agents) for severe acute hepatitis B.
 Treatment should continue until 3 months after
HBsAg seroconversion or 6 months after HBeAg
seroconversion.
 In most cases of typical acute viral hepatitis specific
treatment generally is not necessary. Although
hospitalization may be required for clinically severe
illness, most patients does not require hospital care.
 In fulminant hepatitis, the goal therapy is to support
the patient by maintenance of fluid balance, support
of circulation and respiration, control of bleeding,
correction of hypoglycemia, and treatment of other
complications.
 The main goal of therapy for patients with chronic HBV
infection is to improve survival and quality of life by
preventing disease progression, and consequently HCC
development. Additional goals of antiviral therapy are to
prevent mother to child transmission, hepatitis B
reactivation and the prevention and treatment of HBV-
associated extrahepatic manifestations.
 The likelihood of achieving these goals depends on the
timing of therapy during the natural course of the infection
but also on the stage of the disease and the patients’ age
when treatment is started. Regression of fibrosis and
cirrhosis can be regarded as a further goal of treatment in
patients with established advanced fibrosis or cirrhosis.
 In patients with acute hepatitis B, preventing the risk
of acute or subacute liver failure is the main treatment
goal. Improving the quality of life by shortening the
duration of the disease associated symptoms as well as
lowering the risk of chronicity may be also regarded as
relevant goals of treatment.
Indications for Treatment
Phrophylaxis
 For pre-exposure against hepatitis B in setting of
frequent exposure, three IM (deltoid) inections of
hepatitis B vaccine are recommended at 0, 1, and 6
months.
 For unvaccinated person sustaining an exposure to
HBV, post exposure phrophylaxis with combination of
HBIG (for rapid achievement of high-titer circulating
anti-HBs) and hepatitis B vaccine (for achievement of
long lasting immunity as well as its apparent efficacy
in attenuating clinical illness after exposure) is
recommended.
 For perinatal exposure of infants born to HBsAg-
positive mothers, a single dose of HBIG 0,5 mL, should
be administered IM in the thigh immediately after
birth followed by complete course of three injections
of recombinant hepatitis B vaccine to be started within
the first 12 h of life.
 The precise duration of protection afforded by
hepatitis B vaccine is unknown however 80-90% of
immunocompetent adult vaccines retain protective
level of anti-Hbs for at least 5 years, and 60-80% for 10
years.