hepatitis%20-%20viral
HEPATITIS - VIRAL
The majority of acute viral hepatitis infections are asymptomatic or they can cause an anicteric illness that may not be diagnosed as hepatitis.
Hepatitis A generally causes minor illness in childhood with >80% of infections being asymptomatic but more likely to produce clinical symptoms in adults. 
Hepatitis B, C, and D may also be asymptomatic.
Hepatitis A is predominantly transmitted through oral-fecal route.
Hepatitis B is transmitted through perinatal, percutaneous, or sexual routes or close person-to-person contact via open cuts and sores.
Hepatitis C infections are transmitted through perinatal, percutaneous, or sexual routes, blood transfusions, or organ transplants.
Hepatitis D's route of transmission is sexual or percutaneous, especially IV drug use.
Hepatitis E is transmitted primarily through contaminated drinking water and oral-fecal transmission.

History

Important points in the clinical history of patients with suspected viral hepatitis

  • Contacts with jaundiced patients
  • IV drug use
  • History of blood transfusion
  • Surgery or hospitalizations
  • Family history of chronic liver disease
  • Occupation
  • Food and water sources

Laboratory Tests

Serological Tests for Viral Hepatitis

Hepatitis A
  • Anti-hepatitis A virus IgM has high sensitivity and specificity and is a marker of acute infection
    • This test remains positive for ≥6 months

Hepatitis B

  • Usually characterized by the presence of hepatitis B surface antigen (HBsAg) which suggests infectivity
    • Anti-HBs is produced following a resolved infection and is the only HBV antibody marker present after immunization
  • Anti-HBc (anti-core antibody) is the 1st antibody to appear in the serum and is a marker of natural immunity
    • Presence of anti-HBc IgM is diagnostic for acute hepatitis B virus (HBV) infection but may occur during a flare of chronic hepatitis B
    • Its presence indicates an immune response against HBV within liver cells and is a specific marker of acute hepatitis B infection
  • Hepatitis B e antigen (HBeAg) is a marker of active viral replication
    • This may be negative at the time that the patient is evaluated for acute hepatitis B since viral replication may have already ceased
  • Patients with chronic hepatitis B should also be tested for co-infection with hepatitis C virus (HCV), hepatitis D virus (HDV) and human immunodeficiency virus (HIV), if they are at risk for these infections
  • Depending on local health services, the following groups should be tested for chronic HBV infection:
    • Persons born in hyperendemic areas, men who have sex with men (MSM), IV drug users, dialysis patients, HIV-positive individuals, pregnant women and family members, household members and sexual contacts of HBV-infected persons, blood or organ donors, healthcare workers, patients needing chemotherapy
      • Individuals who are seronegative should be vaccinated against HBV
      • HBsAg-positive patients should be evaluated to assess progression of liver disease and need for antiviral therapy
      • Anti-HBs-positive patients have developed natural immunity and do not need to be vaccinated
Hepatitis C
  • Anti-HCV antibodies are the first-line diagnostic test
  • Acute hepatitis C cannot be reliably diagnosed by antibody tests since these often do not become positive until 3 months after infection
    • If the clinical suspicion is high, the patient should be tested for HCV RNA to establish the diagnosis
    • HCV RNA is used to determine acute or chronic infection
  • Chronic hepatitis C should be confirmed with anti-HCV antibodies and HCV RNA
  • Recombinant immunoblot assay (RIBA) may be used to establish the cause of a positive anti-HCV test in a person with undetectable HCV RNA
    • A negative RIBA indicates that a positive anti-HCV immunoassay result showed a false-positive result and no further testing is necessary
    • A positive RIBA and ≥2 subsequent tests in which HCV RNA cannot be detected suggest that HCV infection has resolved and no further testing is indicated
    • A positive anti-HCV and negative HCV RNA indicate no active HCV infection but should have HCV RNA retesting after 3 months to document recovery 
  • HCV RNA quantitative testing to determine baseline viral load is recommended before starting antiviral therapy
    • End of therapy is indicated by undetectable HCV RNA in a sensitive assay (<15 IU/mL) 12 and 24 weeks after therapy
  • HCV genotype, including subtyping of genotype 1a/1b, should be determined, if possible, in all HCV-infected persons prior to treatment to determine type and duration of therapy and chances of response; predominant genotypes in Asia are:
    • Genotypes 1b and 2: East Asia (China, Taiwan, South Korea, Japan)  
    • Genotype 3: South Asia (India and Pakistan)
      • Genotype 3 is considered difficult to treat and is associated with a poor prognosis  
    • Genotypes 1 and 6: Southeast Asia (Vietnam, Cambodia, Laos, Indonesia, Myanmar, Malaysia, Philippines, Thailand) 
  • Liver biopsy may be done if it is thought that the results will influence clinical decision, but biopsy is not mandatory to start therapy in patients with genotypes 2 and 3
    • Liver biopsy may be obtained to provide prognostic information
  • Depending on local health services, the following groups should be tested for chronic HCV infection:
    • Persons who have in the recent or remote past used illicit IV drugs
    • Persons with conditions associated with high prevalence of HCV infection 
      • Positive HIV, hemophiliacs who received clotting factor prior to 1987, history of hemodialysis, persons who received blood/blood products or organ transplants prior to 1995, children born to HCV-infected mothers, healthcare workers after needle stick injury or mucosal exposure to HCV-positive blood, current sexual partners of HCV-infected persons
Hepatitis D
  • Confirmed by positive anti-HDV antibody or HDV RNA test
  • Hepatitis D occurs as a co-infection with Hepatitis B

Hepatitis E

  • IgM anti-HEV, IgG anti-HEV and hepatitis E virus (HEV) RNA indicate acute hepatitis E infection
    • HEV RNA is detected from serum and stool of infected patients by PCR

Other lab tests that are recommended in patients suspected to have viral hepatitis:

  • Liver function tests (LFTs)
    • Aspartate aminotransferase (AST) and alanine aminotransferase (ALT)
    •  Serum bilirubin, alkaline phosphatase (ALP)
  • PT, international normalized ratio (INR)
  • Noninvasive tests such as the aminotransferase/platelet ratio index (APRI) or FIB4 may be used to assess the degree of hepatic fibrosis when resources are limited prior to initiating HCV therapy
    • Transient elastography may be an option for patients with contraindications to liver biopsy

Evaluation

Hepatitis A and E

Features of Hepatic Decompensation
  • Mental dullness, hepatic encephalopathy, bilateral asterixis, ascites, clinical deterioration
  • Serum bilirubin >2.5x upper limit of normal, PT is 3 sec longer than control or INR >1.5

Acute Hepatitis B

  • History and physical exam
  • Measure HBeAg, anti-HBe, HBV DNA and ALT and perform liver ultrasound
  • Complete blood count (CBC), PT, serum albumin to determine severity
  • Screen for hepatocellular carcinoma (HCC) in high-risk patients every 6-12 months using ultrasound and
    alpha-fetoprotein
If patient meets criteria for chronic hepatitis B:
  • Liver biopsy to grade stage of liver disease as chronic hepatitis B may evolve to cirrhosis and hepatocellular cancer
Hepatitis C

Consequences of HCV Infection
  • 55-85% of patients who acquire acute hepatitis C will remain HCV infected
    • 5-20% of these patients may develop cirrhosis over the next 20-25 years
    • HCV-related cirrhosis is associated with risk of developing end-stage liver disease (30% risk over 10 years) as well as HCC
  • In patients with persistent infection, the evolution to cirrhosis is the primary concern
    • Usually occurs ≥20 years after initial infection and occurs more often in patients at older ages (especially men), those who drink >50 g of alcohol/day, those who are obese or have substantial hepatic steatosis and in those with HIV infection
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