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Hepatitis A

and Hepatitis C
Overview of viral hepatitis
Definition of
Viral hepatitis

Acute viral hepatitis is


diffuse liver inflammation
caused by specific
hepatotropic viruses that
have diverse modes of
transmission and
epidemiologies.
Etiology of Viral hepatitis
At least 5 specific viruses appear to be responsible:
• Hepatitis A (HAV)
• Hepatitis B (HBV)
• Hepatitis C (HCV)
• Hepatitis D (HDV)
• Hepatitis E (HEV)
Other viruses (eg, Epstein-Barr virus, yellow fever virus,
cytomegalovirus) can also cause acute viral hepatitis but less commonly.
Characteristics of hepatitis viruses
Symptoms and Signs of Acute Viral
Hepatitis
Some manifestations of acute hepatitis are virus-specific but in
general, acute infection tends to develop in predictable phases:
• Incubation period: The virus multiplies and spreads without
causing symptoms.
• Prodromal (pre-icteric) phase: Nonspecific symptoms occur;
they include profound anorexia, malaise, nausea and vomiting,
and often fever or right upper quadrant abdominal pain. Urticaria
and arthralgias occasionally occur, especially in HBV infection.
• Icteric phase: After 3 to 10 days, the urine darkens, followed by
jaundice. Systemic symptoms often regress, and patients feel
better despite worsening jaundice. The liver is usually enlarged
and tender, but the edge of the liver remains soft and smooth.
Mild splenomegaly occurs in 15 to 20% of patients. Jaundice
usually peaks within 1 to 2 weeks.
• Recovery phase: During this 2- to 4-week period, jaundice fades.
Appetite usually returns after the first week of symptoms. Acute viral
hepatitis usually resolves spontaneously 4 to 8 weeks after
symptom onset.
Simplified diagnostic approach to possible acute viral hepatitis
Jaundice or clinical suspicion of acute viral hepatitis

Obtain liver function test

Normal AST
Marked elevation in ALT and AST; No marked elevation in ALP and ALT

Not acute viral


Possible viral hepatitis hepatitis

Determine severity Determine the cause

Encephalopathy or prolongation
of INR
Viral serologic testing

anti-HAV IgM HBsAg Anti-HCV


Present Absent
Positive Positive Positive
Fulminant
Acute fulminant
hepatitis
hepatitis Hepatitis A Hepatitis B Hepatitis C
unlikely
Hepatitis A infection
Hepatitis A
• Hepatitis A virus (HAV) is a single-stranded RNA picornavirus.
• It is the most common cause of acute viral hepatitis
• HAV spreads primarily by fecal-oral contact and thus may
occur in areas of poor hygiene. Eating contaminated raw
shellfish is sometimes responsible. Sporadic cases are also
common, usually as a result of person-to-person contact.
• Fecal shedding of the virus occurs before symptoms develop
and usually ceases a few days after symptoms begin; thus,
infectivity often has already ceased when hepatitis becomes
clinically evident.
• HAV has no known chronic carrier state and does not
cause chronic hepatitis or cirrhosis
Symptoms and signs of hepatitis A
• In children < 6 years old, 70% of hepatitis A infections are asymptomatic,
and in children with symptoms, jaundice is rare.
• In contrast, most older children and adults have typical manifestations of
viral hepatitis, including anorexia, malaise, fever, nausea, and vomiting;
jaundice occurs in over 70%.
• Manifestations typically resolve after about 2 months, but in some
patients, symptoms continue or recur for up to 6 months.
• Some patients have prolonged cholestasis (cholestatic hepatitis) due to
hepatitis A; cholestatic hepatitis is characterized by marked jaundice with
pruritus, continued fever, weight loss, diarrhea, and malaise.
• Fulminant hepatitis rarely occurs.
Diagnostic tests for HAV
• CBC: leukopenia, relative lymphocytosis, elevated ESR
• Biochemical blood test: hyperbilirubinemia, increase in ALT
and AST.
• Serological test: determine in blood serum anti-HAV-IgM and
anti-HAV-IgG
• PCR: HAV RNA in blood serum
Management of Hepatitis A
• No treatments attenuate acute viral hepatitis, including hepatitis A.
• Alcohol should be avoided because it can increase liver damage.
Restrictions on diet or activity, including commonly prescribed bed
rest, have no scientific basis.
• For cholestatic hepatitis, cholestyramine 8 g orally once or twice a
day can relieve itching.
• Recovery from acute hepatitis A is usually complete.
• Viral hepatitis should be reported to the local or state health
department.
Prevention of hepatitis A
1. Good personal hygiene helps prevent fecal-oral
transmission of hepatitis A.
2. Vaccination:
• Hepatitis A (HepA) vaccines are available(inactivated virus
vaccine)
• HepA vaccine is a routine childhood vaccination.
• Should be considered for patients with chronic Hepatitis B or C.
3. Immediate protection can be provided by immune serum globulin
if this is given soon after exposure to the virus.
Hepatitis C Infection
Hepatitis C
• Hepatitis C virus (HCV) is a single-stranded RNA
flavivirus that causes acute viral hepatitis and is a
common cause of chronic viral hepatitis.
• Six major HCV subtypes exist with varying amino
acid sequences (genotypes); these subtypes vary
geographically and in virulence and response to
therapy.
Transmission of hepatitis C
• Infection is most commonly transmitted through blood, primarily
when parenteral drug users share needles, but also through
sharing vessels for intranasal drug use, or tattoos or body piercing
with nonsterile equipment.
• Sexual transmission and vertical transmission of hepatitis C from
mother to infant are relatively rare.
• Transmission of hepatitis C through blood transfusion has become
very rare since the advent of screening tests for donated blood.
• Some sporadic cases occur in patients without apparent risk
factors.
Acute Hepatitis C
Symptoms and signs of acute Hepatitis C
• Hepatitis C may be asymptomatic during the acute infection.
• Most individuals are unaware of when they become infected and are
identified only when they develop chronic liver disease
• Its severity often fluctuates, sometimes with recrudescent hepatitis
and roller-coaster aminotransferase levels for many years or even
decades.
• Fulminant hepatitis is extremely rare.
Diagnosis of Acute Hepatitis C
• Complete blood count
• Biochemical blood test - bilirubin, ALT, AST.
• Serological test - determine in blood serum anti-HCV antibodies.
• PCR - HCV RNA in blood serum
In hepatitis C, serum anti-HCV represents chronic, past, or acute
infection; the antibody is not protective.
• If the anti-HCV test is positive, HCV RNA is measured to distinguish
active from past hepatitis C infection.
Serological markers of HCV

Marker Acute HCV Chronic HCV Prior HCV


Infection Infection Infection*

Anti-HCV + + +

HCV RNA + + −

* Patients have had HCV infection and spontaneously


recovered or been successfully treated.
Treatment of acute hepatitis C
• There are a number of highly effective direct-acting antiviral
drugs (DAAs) for hepatitis C that may decrease the likelihood of
developing chronic infection.
• Current recommendations are to start treatment after the initial
diagnosis of acute HCV, without waiting for spontaneous resolution.
• Alcohol and hepatotoxic drugs (eg, acetaminophen) should be
avoided because it can increase liver damage. Restrictions on diet or
activity, including commonly prescribed bed rest, have no scientific
basis.
• Viral hepatitis should be reported to the local or state health
department.
Chronic Hepatitis C
Chronic Hepatitis C
• Hepatitis lasting > 6 months is generally defined as chronic hepatitis.
• Among the 6 major genotypes of hepatitis C virus (HCV), genotype 1
is more common than genotypes 2, 3, 4, 5, and 6 and it accounts for
70 to 80% of cases of chronic hepatitis C .
• Acute hepatitis C becomes chronic in about 75% of patients.
• Chronic hepatitis C progresses to cirrhosis in 20 to 30% of patients;
cirrhosis often takes decades to appear.
• Hepatocellular carcinoma can result from HCV-induced cirrhosis but
results only rarely from chronic infection without cirrhosis (unlike
in chronic HBV infection).
Symptoms and signs of chronic Hepatitis C
• Many patients are asymptomatic and do not have jaundice,
although some have malaise, anorexia, fatigue, and nonspecific
upper abdominal discomfort.
• Often, the first findings are signs of cirrhosis (eg, splenomegaly,
spider nevi, palmar erythema) or complications of cirrhosis
(eg, portal hypertension, ascites, encephalopathy).
Diagnosis of Acute Hepatitis C
The diagnosis of chronic hepatitis C is suspected in patients with any
of the following:

• Suggestive symptoms and signs


• Incidentally noted elevations in aminotransferase levels
• Previously diagnosed acute hepatitis
Actions of the therapist (GP) in case of suspected disease
Mandatory laboratory tests:
• Clinical blood test;
• biochemical analysis of blood: glucose, total cholesterol, total and direct
bilirubin, ALT, AST, total protein, alkaline phosphatase albumin;
• INR, prothrombin according to Quick;
• blood test for HIV, syphilis, hepatitis B and C.
Mandatory instrumental examinations:
• Ultrasound of the abdominal organs: liver; spleen; determination of the
diameter of the portal and splenic veins; presence/absence of free fluid;
Specialist consultations
• Gastroenterologist. Diagnosis is confirmed by finding positive anti-HCV and
positive HCV RNA ≥ 6 months after initial infection
• Infectionist.
• HCV genotype is determined before treatment because
genotype influences the course, duration, and success of
treatment.
Treatment of chronic hepatitis C
• For chronic hepatitis C, treatment is recommended for all patients,
except those with a short life expectancy due to comorbid conditions
that cannot be remediated by HCV therapy, liver transplantation, or
another directed therapy.
• The goal of treatment is permanent elimination of HCV RNA (ie, SVR),
which is associated with permanent normalization of
aminotransferase levels and cessation of histologic progression.
• Treatment results are more favorable in patients with less fibrosis
than in patients with cirrhosis.
Treatment of chronic hepatitis C
Antivirals:
• Currently, interferon-based treatment regimens are no longer used,
and ribavirin is no longer considered first-line and is used only in
certain alternative regimens.
• Instead, all patients are treated with direct-acting antivirals (DAAs)
that affect specific HCV targets, such as proteases or polymerases.
Liver treansplantation:
• Decompensated cirrhosis due to hepatitis C is the most common
indication for liver transplantation in the
Test for evidence of chronic or prior hepatitis B:
Hepatitis B reactivation resulting in liver failure and death has been
reported during or after HCV treatment with DAAs.
DAA Combination Therapies for the Treatment of HCV
Drug Genotype Duration of Treatment

Sofosbuvir/Ledipasvir 1, 4, 5, 6 8–24 weeks depending on patient population

Sofosbuvir/Velpatasvir 1–6 12 weeks

Glecaprevir/Pibrentasvir 1–6 8–16 weeks depending on patient population

Elbasvir/Grazoprevir 1, 4 12–16 weeks depending on patient population

Sofosbuvir/Velpatasvir/Voxilaprevir 1–6 12 weeks


Prevention of hepatitis A
• Patients should be advised to avoid high-risk behavior (eg,
sharing needles to inject drugs, getting tattoos and body
piercings).
• Blood and other body fluids (eg, saliva, semen) are
considered infectious.
• Posttransfusion infection is minimized by avoiding
unnecessary transfusions and screening all donors for
hepatitis B and C.
• No product exists for immunoprophylaxis of HCV. The
propensity of HCV for changing its genome hampers
vaccine development
Thank you

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