Subject: pediatrics

Topic: chronic hepatitis

Mohammd thawabta

Introduction:

Viral hepatitis is one of the most common causes of liver disease in the
pediatric population. Approximately 10% to 20% of North American
children have naturally acquired antibodies to hepatitis A, and up to 10%
of children at high risk in North America (such as the urban poor) have
been infected with hepatitis B virus. The prevalence of hepatitis C in
North American children 5 to 14 years of age is 0.2% to 0.4%.
Hepatitis viruses A and B cause acute liver disease, often with jaundice
and constitutional symptoms. Hepatitis B and C cause chronic liver
disease that rarely evolves rapidly enough to produce morbidity in
childhood; the major concern is the risk for development of cirrhosis and
liver cancer. Fulminant hepatitis occurs in a small proportion of children
infected with hepatitis A or B viruses. In Europe and Asia, delta hepatitis
also may cause fulminant hepatitis in children with hepatitis B, but this
virus occurs rarely in the United States. Hepatitis E virus causes epidemic
disease in the developing world, but is rare in the United States.
Although hepatitis G virus has been reported in US children, particularly
those who have received blood transfusions, to date no evidence
suggests that it causes acute or chronic liver injury.
Research in the field of viral hepatitis in North America should focus on
the three major hepatitis viruses, A, B, and C. Research should focus on
the epidemiology, pathogenesis, transmission, natural history, role of
the host immune response, and, in the case of hepatitis C, development
of an effective vaccine. Effective, safe antiviral therapies for hepatitis B
and C viruses are needed urgently. In addition, modern molecular
virology techniques should be used to investigate the role of as yet
unknown viruses in fulminant hepatitis and in inflammatory liver
diseases for which viral causes have been proposed, for example, biliary
atresia.
Viral hepatitis Can be chronic and acute , Depend on the causative
agent, and the tendency of chronicity of these infections.

Hepatitis A:

Pathogenesis:
HAV infection is transmitted via the fecal-oral route, and viral replication
occurs in the liver, leading to hepatic injury. The entire liver exhibits
necrosis, which is most marked in the centrilobular areas, as well as
increased cellularity in the portal areas. The regional lymph nodes and
spleen may become enlarged. Liver injury is represented in 3 ways:
* Direct cellular injury that elevates serum liver enzyme levels
* Cholestasis that causes jaundice and hyperbilirubinemia
* Inadequate liver function that lowers serum albumin levels and
prolongs the prothrombin time (PT).

Etiology:
Hepatitis A is caused by HAV, a positive-sense, single-stranded,
nonenveloped RNA virus that belongs to the Picornaviridae family and
the Hepatovirus genus. After fecal-oral transmission, the virus is then
excreted into the bile. Its concentration is highest in the stool, especially
during the 2 weeks preceding the onset of jaundice. This correlates with
the period of peak infectivity. Children and adults can be assumed to be
noninfectious 1 week after the appearance of jaundice.
Common-source outbreaks from contaminated food or water may
occur. HAV is concentrated in filter-feeding shellfish, which may thrive
close to sewage outlets, and widespread outbreaks can occur from a
single contaminated source, such as uncooked vegetables that are
distributed to restaurants or grocery stores. Statistically, eating out is
actually less risky than home cooking.
Childcare centers may be sources of outbreaks from contaminated
changing tables. These outbreaks may not be identified until an adult
contact has a recognizable HAV infection, because young children are
often asymptomatic or have anicteric illnesses.
Nosocomial outbreaks have occurred because of HAV shedding.
Outbreaks of HAV infection have been increasingly reported among illicit
drug users. International travel is another risk factor for HAV infection.
Vertical transmission of HAV (ie, from mother to neonate) and
transmission by means of blood transfusion are extremely rare. Sexual
transmission is possible, especially between homosexual men. Spread of
HAV from nonhuman primates to humans has been reported.
Epidemiology:

In developing countries, infection is highly endemic; nearly 100% of the

population in some countries has serologic evidence of past HAV disease
during childhood.
In a surveillance study of 1156 HAV cases from 6 sites in the United
States’ Emerging Infections Program, from 2005 through 2007, the
majority of infections were due to international travel or exposure to
travelers. Many of the cases that implicated travel or contact with
travelers as a risk factor involved travel to Mexico.

Prognosis:

The prognosis is excellent. In most patients, HAV infection is self-limited,

and complete recovery occurs. In fact, many cases are asymptomatic.
Except in the setting of fulminant hepatitis, sequelae are rare. Fulminant
hepatitis due to HAV is uncommon and has a case-fatality rate of 0.4%.
Relapsing HAV infection occurs in approximately 10% of patients 1-4
months after the initial episode and results in full recovery.
Chronic active hepatitis, which can be seen in hepatitis B virus (HBV) or
hepatitis C virus (HCV) infection, does not occur in HAV infection. A
chronic carrier state is not seen with HAV infection.

Clinical presentations:

*History: The incubation period from the time of exposure to hepatitis A

virus (HAV) to the appearance of symptoms is around 28 days (range 2
weeks to 6 months). The patient’s initial symptoms during the
prodromal period include low-grade fever, nausea, vomiting, decreased
appetite, and abdominal pain. Older children and adults are more likely
to report pain in the right upper quadrant.
Diarrhea may occur in young children, whereas constipation is more
common in adults. If present, jaundice, dark urine, and light-colored
stool develop several days to a week after the onset of systemic
symptoms. Anicteric infections are common in young children.
*Physical examinations:The general appearance is that of mild-to-
moderate illness. A patient who appears severely ill is likely to have
hepatitis of another cause or an atypical course. Mild hepatomegaly and
right upper quadrant tenderness may be present. Clinical jaundice is
present in two thirds of symptomatic patients. Splenomegaly may occur
in 10-20% of patients.
*Complications:Complications are few. Fulminant hepatitis with massive
hepatic necrosis and liver failure due to HAV infection is rare. Cholestatic
hepatitis occurs in a small percentage of patients. It is identified by
persistent hyperbilirubinemia, pruritus, and constitutional symptoms
that last for 12-16 weeks in the absence of biliary obstruction on
sonograms.

Diagnosis:

*Liver function test:Liver inflammation during hepatitis A virus (HAV)

infection can be identified by elevations in (ALT), (AST), and gamma-
glutamyltranspeptidase (GGTP; also known as gamma
glutamyltransferase[GGT]) levels. Increases in ALT and AST levels are
seen most consistently, and the values are usually 4-100 times the
normal levels. Elevations in ALT and AST levels may precede the onset of
symptoms by a week or more and usually peak within 3-10 days after
onset of clinical illness.
Serum bilirubin levels, although elevated, usually remain below 10
mg/dL and peak after 1-2 weeks of illness. Prolongation of
the prothrombin time (PT) and a significant decrease in
the albumin level suggest a more severe course.
*Serologic tests: Specific antibody tests for HAV confirm infection. Anti-
HAV immunoglobulin M (IgM) is present at the onset of symptoms, and
its level remains high for 4-8 weeks. It usually disappears by 4-6 months,
but occasionally it persists for a longer period.
Anti-HAV immunoglobulin G (IgG) becomes detectable shortly after the
IgM titer appears and usually increases as the IgM level decreases. IgG
persists for life and provides ongoing immunity against reinfection
*Ultrasound: Ultrasonography of the liver may be helpful when
cholelithiasis is a consideration. However, imaging studies are generally
not necessary. The history and physical examination and laboratory
findings are used to establish the diagnosis in most cases of HAV
infection.
*Histologic findings: Histologic findings are similar to those in other
forms of acute viral hepatitis and include inflammatory cell infiltration,
hepatocellular necrosis, and liver cell regeneration.
Liver biopsy is not indicated, because of the self-limited nature of HAV
infection and the absence of a chronic infectious state.

Management:
*Supportive care:Inpatient care is not needed for most patients with
HAV infection. Some patients may require hospitalization for
intravenous (IV) rehydration. Once emesis subsides and the patient can
tolerate oral fluids, discharge is appropriate. In the rare case of
fulminant hepatitis, transfer to a facility with pediatric subspecialty care
is indicated.
Follow-up liver enzyme studies should be performed at monthly
intervals until levels normalize. If elevations persist for longer than 3
months, complications or additional diagnoses should be considered.
Medications that have known liver toxicity should be avoided
*Immunization: Pre-exposure prophylaxis with HAV vaccine is
recommended for persons aged 1 year or older who are traveling to
countries where HAV infection is endemic. If the trip is shorter than 2
weeks, or if the patient is younger than 1 year, IG should be given. If the
trip is longer than 3 months, a larger dose of IG (0.06 mL/kg) is needed
for those who cannot receive the vaccine. Repeat dosing is
recommended if the trip lasts longer than 5 months.

*Postexposure prophylaxis: Postexposure prophylaxis consists of the

administration of HAV vaccine (preferred if the patient is >1 y and < 40 y)
or immune globulin (IG) to contacts as soon as possible, but no later
than 2 weeks after exposure. IG is given as an intramuscular injection of
0.02 mL/kg. It is 80-90% effective in preventing HAV infection by means
of passive immunity.
Candidates for postexposure prophylaxis include household and sexual
contacts of infected patients, contacts in childcare centers during
outbreaks, and, if the patient is a food handler, others who work at the
same establishment. Information regarding administration of hepatitis A
vaccine after exposure (either alone or in addition to IG) is currently
available.
*prevention: General prevention measures consist of good personal
hygiene, handwashing, ingestion of safe drinking water, and proper
sanitation. Prevention specific to hepatitis A infection includes the use of
IG and HAV vaccine.
Hepatitis B:

HBV is a DNA virus in the Hepadnaviridae family. The virus is responsible

for 40% of hepatitis cases in the United States. Seven major genotypes
of HBV are recognized, with different geographic distributions. The
genotypes are thought to affect disease progression, but their role in
response to treatment is not as clear as in hepatitis C. The genome of
HBV is a partially double-stranded, circular DNA molecule of 3200
nucleotides that encodes the following:
* The precore/core region of a nucleocapsid core protein (hepatitis B
core antigen [HBcAg]) and a precore protein (hepatitis B e antigen
[HBeAg]: HBcAg is retained in the infected hepatocyte; HBeAg is
secreted into blood and is essential for the establishment of persistent
infection
* Envelope glycoprotein (ie, hepatitis B surface antigen [HBsAg]), which
may be produced and secreted into the blood in massive amounts:
Blood HBsAg is immunogenic and can be visualized as spheres or tubules
*A DNA polymerase with reverse transcriptase activity: Genomic
replication takes place through an intermediate RNA known as
pregenomic RNA. In this process, mutant viral genomes are frequently
generated
* HBV-X protein: This acts as a transcriptional transactivator for many
viral and host genes through interaction with various transcription
factors. HBV-X is required for viral infectivity and may have a role in the
causation of hepatocellular carcinoma by regulating p53 degradation
and expression
HBV is a double-stranded DNA virus of the Hepadnaviridae family. HBV is
a hepatotropic virus that replicates in the liver and causes hepatic
damage and dysfunction. HBV is transmitted by percutaneous or
permucosal exposure to infectious body fluids, by sexual contact with an
infected person, and by perinatal transmission from an infected mother
to her infant. Persons with chronic HBV infection are predisposed to
chronic liver disease and have a greater than 200-fold increased risk of
hepatocellular carcinoma.
Fulminant hepatic failure occurs in approximately 0.1-0.5% of patients
and is believed to be caused by massive immune-mediated lysis of
infected hepatocytes. Various extrahepatic manifestations (eg, urticarial
rashes, arthralgia, arthritis) are associated with acute clinical and
subclinical HBV infection, as well as multiple immune-complex disorders
such as Gianotti-Crosti syndrome (papularacrodermatitis), necrotizing
vasculitis, and hypocomplementemic glomerulonephritis. HBV is
associated with 20% of membranous nephropathy cases in children.
Essential mixed cryoglobulinemia, pulmonary hemorrhage related to
vasculitis, acute pericarditis, polyserositis, and Henoch-Schönlein
purpura have been reported in association with HBV infection.
The adaptive immune response is thought to be responsible for viral
clearance and disease pathogenesis during HBV infection. The humoral
antibody response contributes to the clearance of circulating virus
particles and the prevention of viral spread within the host while the
cellular immune response eliminates infected cells.Persistent HBV
infection is characterized by a weak immune response due to inefficient
CD4+ T cell (helper T cell) priming early in the infection and subsequent
development of a quantitatively and qualitatively ineffective CD8+ T
(cytotoxic T cell) cell response.

Etiology:

HBV is transmitted by percutaneous or permucosal exposure to

infectious body fluids, by sexual contact with an infected person. It is
also transmitted by perinatal transmission from an infected mother to
her infant.
The virus is present in all body fluids, except stool. Blood and body fluids
are the primary vehicles of transmission; the virus may also spread by
contact with body secretions, such as saliva, sweat, tears, breast milk,
semen, and pathologic effusions.
Modes of transmission are the same as for the human
immunodeficiency virus (HIV), but HBV is 50-100 times more infectious.
Unlike HIV, HBV can survive outside the body for at least 7 days. During
that time, the virus can still cause infection if it enters the body of a
person who is not infected.
Common modes of transmission in developing countries are as follows:
* Perinatal (from mother to baby at birth)
* Early childhood infections (inapparent infection through close
interpersonal contact with infected household contacts)
* Unsafe injection practices
* Blood transfusions
* Sexual contact
In many developed countries (eg, those in Western Europe and North
America), patterns of transmission are different from those mentioned
above. Today, most infections in these countries are transmitted during
young adulthood by sexual activity and injecting drug use. HBV is a major
infectious occupational hazard of health workers.
HBV is not spread by contaminated food or water and cannot be spread
casually in the workplace.
Epidemiology:
HBV infects more than 350 million people worldwide. Approximately 5%
of the world's population has chronic HBV infection and it is the leading
cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma
worldwide. Each year, an estimated 500,000 people die of cirrhosis and
hepatocellular carcinoma caused by chronic infection and an additional
40,000 people die of acute hepatitis B. An estimated 500,000-1,000,000
persons die annually from HBV-related liver disease.
The distribution of HBV infection widely varies throughout the world. In
some regions, over 10% of the population is positive for hepatitis B
surface antigen (HBsAg), which indicates active infection. Countries are
classified as having low endemic rates (< 2% of the population has the
antibody to HBsAg), intermediate endemic rates (2-8% positive for
HBsAg), or high endemic rates (>8% positive for HBsAg).

Prognosis:
Among patients with acute hepatitis B, 90% have a favorable
course and recover completely. Patients of advanced age and
those with serious underlying medical disorders, such as
congestive heart failure, severe anemia, and diabetes mellitus,
may have a prolonged course and are more likely to have severe
hepatitis.Although fatality rates for most cases of hepatitis B are
low, patients ill enough to be hospitalized for acute hepatitis B
have a 1% fatality rate.In patients with persistent infection, 10-30%
develop chronic hepatitis. Of patients with chronic hepatitis, 20-
50% of patients progress to cirrhosis, and approximately 10% of
those who progress to cirrhosis may develop hepatocellular
carcinoma.Approximately 2,000-4,000 persons in the United
States die each year of HBV-related conditions. Most deaths are
attributed to cirrhosis and primary hepatocellular carcinoma, and a
smaller proportion of patients die of fulminant hepatitis. HBV-
infected individuals are also at increased risk of death from onliver
causes such as non-Hodgkin lymphoma and circulatory diseases.
Clinical presentation:

1) Acute:

-Anorexia
- Nausea
- Malaise, vomiting
-Arthralgias, myalgias
- Headache, photophobia,
-Pharyngitis, cough, coryza,
-Jaundice, dark urine, clay-colored or light stools, and abdominal pain.

2) Chronic:

Chronic hepatitis is symptomatic, and affected individuals have

biochemical or serologic evidence of continuing or relapsing hepatic
disease for longer than 6 months, with histologically documented liver
inflammation. The clinical features vary. The common symptoms include
fatigue, loss of appetite, and occasional bouts of mild jaundice.
Fulminant hepatitis occurs in 1-2% of persons with acute disease and has
a case-fatality ratio of 63-93%. It may present as jaundice,
encephalopathy, and fetor hepaticus. Life-threatening extrahepatic
complications include coagulopathy, renal failure, adult respiratory
distress syndrome, electrolyte and acid-base disturbances, and sepsis.
Without liver transplantation, the overall mortality ranges from 25-90%.
Consider hepatitis D virus infection if a patient who is a carrier of chronic
hepatitis B presents with recurrent acute hepatitis or sudden fulminant
hepatitis.

Rare complications:

-Pancreatitis
- Myocarditis
- Atypical pneumonia
- Aplastic anemia
- Transverse myelitis
- Peripheral neuropathy

Diagnosis:

*Liver function test:Elevations of alanine aminotransferase (ALT)

and aspartate aminotransferase (AST) levels are hallmarks of acute
hepatitis. Values as high as 1000-2000 IU/L are typical, with ALT values
higher than AST values. In patients with hepatitis, increases
in bilirubin levels often lag behind increases in aminotransferase levels.
The prothrombin time is the best indicator of prognosis. Alpha-
fetoprotein levels as high as 8000 ng/mL may also be seen.
Because the symptoms of acute HBV infection and the laboratory
indicators of hepatocellular dysfunction are indistinguishable from those
of other forms of viral hepatitis, definitive diagnosis depends on
serologic testing for HBV infection.
*Serological test: HBV serologic testing can be confusing and requires
multiple tests for antigens (Ag) and antibody (Ab) responses in order to
accurately diagnose the stage of infection.
HBV surface antigen (HBsAg) appears before the onset of symptoms,
peaks during overt disease, and then declines to undetectable levels in
3-6 months. Acute HBV infection is characterized by the presence of
HBsAg in the serum.
Hepatitis B e antigen HBeAg, HBV DNA, and DNA polymerase appear in
the serum soon after HBsAg, and all signify active viral replication.
Measuring HBV DNA with quantitative DNA polymerase chain reaction
(PCR) is ideal for monitoring disease progression and effect of treatment.
Immunoglobulin M (IgM) anti-HBc becomes detectable in serum shortly
before the onset of symptoms, concurrent with the onset of elevation of
serum aminotransferases. Over months, the IgM antibody is replaced by
immunoglobulin G (IgG) anti-HBc. Detection of IgM HBcAb is diagnostic
of acute HBV infection, but total HBcAb is not helpful since IgG
antibodies to HBcAg may persist for life.
IgG anti-HBs does not rise until the acute disease is over and is usually
not detectable for a few weeks to several months after the
disappearance of HBsAg. Anti-HBs may persist for life, conferring
protection; this is the basis for current vaccination strategies using
noninfectious HBsAg. Hepatitis B surface antibody (HBsAb), but not
hepatitis B core antibody (HBcAb), is detected in persons who have
received the hepatitis B vaccine. The coexistence of HBsAg and HBsAb
has been reported in approximately 25% of individuals who are HBsAg
positive.
The carrier state is defined by the presence of HBsAg in the serum for 6
months or longer after its initial detection.
The presence of HBsAg alone does not necessarily indicate replication of
complete virions, and patients may be asymptomatic and without liver
damage. Chronic replication of HBV virions is characterized by
persistence of circulating HBsAg, HBeAg, and HBV DNA, usually with anti-
HBc and, occasionally, with anti-HBs. In these patients, progressive liver
damage may occur.
During convalescence, HBsAg and HBeAg are cleared, and IgG antibodies
to HBsAg, HBcAg, and HBeAg develop.

Management:

*Vaccination: The American Academy of Pediatrics recommends that

the hepatitis B vaccine should be administered within the first 24 hours
to all newborn infants with a birth weight of greater than or equal to
2000 g.
*Medications:

- Tenofuvir.
- Interferon alpha-2b.
- Lumivudine.
- adefovir.
- Enticavir.
- Telbivudine.

Hepatitis C:

Pathophysiology:
Hepatitis C virus is a member of the Flaviviridae family of RNA-containing
viruses. Thus, it is not integrated into the host genome.
Although the liver is the primary target of infection, studies to better
define the steps of hepatitis C virus infection are greatly hampered by
the lack of a suitable animal model for such studies (the only animal
known to be susceptible to hepatitis C virus is the chimpanzee). A tissue-
culture system using recombinant DNA technology was recently
developed and has advanced the scientific knowledge base considerably,
including early forays into vaccine development.
The primary immune response to hepatitis C virus is mounted by
cytotoxic T lymphocytes. Unfortunately, this process fails to eradicate
infection in most people; in fact, it may contribute to liver inflammation
and, ultimately, tissue necrosis.
The ability of hepatitis C virus to escape immune surveillance is the
subject of much speculation. One likely means of viral persistence relies
on the presence of closely related but heterogeneous populations of
viral genomes. Further studies of these quasi-species enable
classification of several genotypes and subtypes, which may have clinical
implications.

Etiology:

Direct percutaneous exposure is the primary means of transmission.

Blood transfusions are another means of transmission.
Historically, most hepatitis C virus infections result from blood
transfusions. The risk of transfusion-borne hepatitis C virus began to
decline in 1986, when surrogate-marker screening of blood donors
started. Further declines were noted after the introduction of hepatitis C
virus–directed antibody screening in 1990 (first generation) and 1992
(second generation). The current risk of transfusion-derived hepatitis C
virus is estimated to be 1 case in every 100,000 units transfused.
Currently, the use of injected drugs is the most important epidemiologic
risk factor, probably accounting for around 50% of both acute and
chronic infections. Other parenteral routes may be involved.
Hemodialysis is a possible cause of hepatitis C virus infection. Health
care employees may be accidentally exposed. Tattooing, body piercing,
and acupuncture with unsterile equipment are possible routes of
infection.
The risk of sexual transmission appears to be low, even among
individuals with multiple sex partners. However, the presence of
coexisting sexually transmitted diseases (eg, human immunodeficiency
virus [HIV] infection) appears to increase the risk.
Vertical transmission may occur. Perinatal transmission is possible and
affects an estimated 5% of babies born to mothers with hepatitis C virus
infection. The risk is higher for babies born to mothers who are co-
infected with hepatitis C virus and HIV or hepatitis B virus.

Epidemiology:

An estimated 30,000 new hepatitis C infections occur annually in the

United States, although only 25-30% are diagnosed. Since the 1980s,
acute infections have declined by more than 80%. Nearly 4 million
Americans, or about 2% of the US population, are infected with hepatitis
C virus. Although the worldwide prevalence varies considerably by
geographic region, more than 3% of the global population is infected.

Prognosis:

Acute fulminant hepatitis C virus infection is rare, but more than 80% of
acutely infected individuals develop chronic hepatitis. Most patients
chronically infected with hepatitis C virus remain asymptomatic and do
not have significant liver disease. The prognosis is guarded for those who
have hepatitis C virus–related complications such as hepatocellular
carcinoma and liver failure.In more than 20% of adults with chronic
infection, progression to cirrhosis occurs an average of 20 years after
initial infection. Cirrhosis poses a secondary risk of portal hypertension,
liver failure, and other complications. Hepatitis C is now the leading
reason for liver transplantation in the United States. In 1-5% of patients,
most of whom have underlying cirrhosis, hepatocellular carcinoma (HCC)
is diagnosed an average of 30 years after initial hepatitis C virus
infection. Annually, hepatitis C virus infection accounts for 8,000-10,000
deaths in the United States.
Complications:

1) Intrahepatic:
* Fulminant hepatitis (rare)
* Cirrhosis, which may result in portal hypertension and liver failure
* Hepatocellular carcinoma

2) Extrahepatic:

* Porphyria cutaneatarda
* Sialadenitis resembling Sjögren syndrome
* Mooren corneal ulcers, a form of chronic ulcerative keratitis
* Type II cryoglobulinemia
* Membranoproliferative glomerulonephritis
* Non-Hodgkin lymphoma

Diagnosis:

*HCV testing:Hepatitis C virus–directed antibodies may be detected.

Antibody screening using enzyme immunoassay (EIA) is inexpensive and
reliable; generally, this is the screening test of choice for diagnosis.
Recombinant immunoassay (RIBA) can then be used to confirm positive
EIA results.
The US Food and Drug Administration (FDA) has approved OraQuick HCV
Rapid Antibody Test, which uses a venipuncture whole blood sample and
provides results in approximately 20 minutes. The test can be used for
persons at risk for hepatitis or for those with signs or symptoms of
hepatitis.Hepatitis C virus RNA may be detected with the polymerase
chain reaction (PCR) test. Several FDA-approved test kits that can be
used for blood product screening or diagnostic testing are currently
available. (Kits are not usually approved for both uses.) Hepatitis C virus
RNA is usually detectable within 1-2 weeks of exposure. Quantitative
assays are available, but hepatitis C viral load has not been definitively
shown to be useful in predicting outcome (unlike HIV viral load). It may
be useful in predicting risk of recurrence in transplant recipients.PCR
testing is useful to confirm positive EIA results in the setting of
indeterminate RIBA test results and to distinguish between resolved and
chronic HCV infection in patients with positive EIA and RIBA results.
*other viral serological tests:
1. Hepatitis A virus immunoglobulin M (IgM) and immunoglobulin G
(IgG)
 2. Hepatitis B virus surface antigen and antibody, core antibody
3. Cytomegalovirus (CMV) IgM and IgG (and/or CMV in urine
cultures)
4. Epstein-Barr virus IgM and IgG
5. HIV IgG enzyme-linked immunoassay (ELISA)
*Liver biopsy:Liver biopsy is generally not used to diagnose hepatitis C
virus. However, it is the most accurate method of evaluating the extent
of hepatitis C virus–related liver disease. Liver biopsy is recommended
for all patients before they start antiviral therapy.

Management:

Prevention:
For individuals exposed to hepatitis C virus (HCV), passive immunization
is not recommended. No vaccine has been developed for hepatitis C
virus. People with HCV should be vaccinated against hepatitis A and B
virus to prevent worsening of liver disease. Household contacts of
children with HCV should be vaccinated against hepatitis A virus.
Discourage users of intravenous drugs from sharing needles. Adhere to
universal precautions. Breastfeeding is not contraindicated for mothers
with HCV infection. There is no need to bar children with HCV infection
from attending daycare.
Infected patients with multiple partners should use barrier protection
during sex. No special precautions are needed for monogamous
relationships.Instruct the patient not to share personal care articles such
as toothbrushes or razors.Blood, organ, or sperm donation from patients
with hepatitis C virus infection is not permitted.

Long term monitoring:

Long-term monitoring is essential in patients with chronic HCV infection
because the risk of liver cancer is high, even in sustained virologic
responders. The prothrombin time is useful for assessing liver function.
The serum alpha-fetoprotein assay is a potential screening test for HCC.
Ultrasonography is potentially useful to monitor for hepatitis C virus–
related complications such as portal hypertension and HCC.

Medications:
1) Direct antiviral therapy:
-Sofosbuvir
-Ledipasvir

2) Other antiviral therapy:

-Ribavirin
- Interferon alpha

Reference:

Kaplan Textbook
Medscape.com
Emedicine.com
Wikipedia.com
NCBI.