HEPATITIS
I. Definition
A. Hepatitis refers to an inflammation of the liver that can be caused by many drugs and toxic agents, as well as by viruses.
B. Common forms of viral hepatitis are as follows:
1. Hepatitis A virus (HAV)
2. Hepatitis B virus (HBV)
3. Hepatitis C virus (HCV/non-A non-B virus)
4. Hepatitis D virus (delta agent)
5. Hepatitis E virus (HEV/enterically transmitted or epidemic non-A non-B virus)
6. Hepatitis G virus (HGV)
C. Hepatitis A, C, D, E, and G are all RNA viruses. Hepatitis B is the only DNA virus.
D. All types of hepatitis produce similar illnesses.
II. Etiology
A. HAV: usually is spread by fecal-oral route, including contaminated food sources, water, and shellfish; spread by the parenteral route is rare.
1. Spread is enhanced by crowding and by poor sanitation.
2. Maximum infectivity occurs 2 weeks prior to clinical illness.
3. Blood and stools are infectious during a 2- to 6-week incubation period.
4. Mortality rate is low, and fulminant hepatitis A is uncommon.
B. HBV: blood-borne virus that is present in saliva, semen, and vaginal secretions
1. Transmission
a. Sex
b. Contaminated blood and blood products
d. Perinatal
e. Body piercing
f. Tattooing
g. Recreational cocaine
2. Approximately 500 million chronic carriers worldwide
3. Chronic carrier state is responsible for much of the world’s liver cirrhosis.
4. Coinfection, superinfection, or chronic infection with HDV markedly increases mortality and morbidity of HBV.
C. HCV: blood-borne virus
1. In many patients, the source of infection is uncertain.
2. Approximately 50% of cases are related to IV drug abuse.
3. Although HCV causes approximately 90% of posttransfusion hepatitis, only 4% of HCV cases are related to blood transfusion.
4. In all, 40% to 60% of patients with posttransfusion hepatitis develop chronic hepatitis C that leads to cirrhosis in 20% to 40% of cases.
5. Risk of sexual and perinatal transmission is small.
6. Six genotypes with several subtypes have been identified. Genotypes 2 and 3 are more sensitive to antiviral treatment. Genotype 1, which usually results in cirrhosis, is more difficult to treat.
D. HDV: defective RNA virus that causes hepatitis only when accompanied by HBV infection (as shown by hepatitis B surface antigen [HBsAg])
1. Combined infection has a worse prognosis than HBV alone, along with an increased incidence of fulminant hepatitis.
E. HEV: fecal-oral route primarily seen in less developed countries (e.g., India, Mexico, Burma, Algeria, Afghanistan)
1. Incubation period is 2 to 9 weeks (mean, 6 weeks).
2. Clinical disease is similar to HAV except it is more severe.
3. Mortality rate is 1% to 2% in general population and 10% to 20% in pregnant women—significantly higher than HAV.
F. HGV: recently identified virus that is transmitted percutaneously and may cause mild acute hepatitis and chronic viremia lasting as long as 9 years.
1. HGV has been detected in 50% of IV drug abusers and in 20% of hemophiliac patients.
2. Diagnostic tests are not currently available.
III. Risk factors
A. Health care providers/other occupational risks; positive needlestick
B. Hemodialysis patients
C. Recipients of blood and/or blood products
D. IV drug users
E. Sexually active homosexual males or those with multiple heterosexual partners
F. Household exposure
G. Intimate exposure
H. Persons in underdeveloped countries
J. Tattooing
IV. Subjective findings (extremely variable)
A. Prodromal phase
1. Malaise, myalgia, arthralgia, easy fatigue
2. Upper respiratory symptoms (nasal discharge, pharyngitis)
3. Anorexia, nausea, and vomiting are common.
4. Diarrhea or constipation may occur.
5. Aversion to smoking (HBV)
6. Skin rashes, arthritis, or serum sickness may be seen early in HBV.
7. Fever usually less than 103.1° F (39.5° C) (more common in HAV)
8. Mild, constant abdominal pain in the right upper quadrant or epigastrium that is often aggravated by exertion
B. Icteric phase
1. Clinical jaundice occurs after 5 to 10 days but may occur at the same time as the initial symptoms.
2. Most patients never develop clinical icterus.
3. Intensification of prodromal symptoms usually occurs with the onset of jaundice; this is generally followed by progressive improvement.
4. Dark urine/clay-colored stools
5. Patient may be asymptomatic.
V. Physical findings
A. Jaundice
B. Tender hepatomegaly
C. Splenomegaly
D. Posterior cervical lymphadenopathy (rare)
E. Rash (HBV)
F. Arthritis (rare)
G. Examination findings may be normal.
VI. Laboratory findings
A. WBC count is normal or may be low.
B. Urinalysis—Proteinuria is common; bilirubinuria may occur prior to jaundice.
C. Greatly increased alanine transaminase (ALT) and aspartate transaminase (AST) levels (more than 500 international units/L; normal, 0 to 35 international units/L)
D. Increased bilirubin and alkaline phosphatase levels; may remain elevated after ALT and AST have normalized
E. Prothrombin time (PT) and glucose level are usually normal; increased PT or decreased glucose level indicates severe liver damage.
VII. Diagnosis
A. Hepatitis A
1. Immunoglobulin (Ig)M anti-HAV: excellent diagnostic test
a. First laboratory test ordered with acute illness with increased ALT and AST
b. IgM occurs during the first week of clinical disease.
d. Positive interpretation: HAV infection within the preceding 6 months
e. Negative interpretation: no HAV infection within the preceding 12 months
2. IgG anti-HAV
a. IgG peaks after 1 month; peak level may persist for years.
b. Presence of IgG
i. Indicates previous exposure and noninfectivity
ii. Confers lifelong immunity
c. Negative interpretation: no previous HAV infection
B. Hepatitis B
1. Detection of HBsAg or anti–HBc IgM (IgM antibody to hepatitis B core antigen). HBsAg is often detected in patients with acute HBV infection and is detectable in the serum of patients with active viral replication. Anti–HBc IgM can facilitate differentiation of acute from chronic HBV.
2. Anti-HBc is very useful as a serologic marker of acute hepatitis during a gap when patients have cleared HBsAg, but anti-HBs (antibody to hepatitis B surface antigen) cannot be detected.
3. Anti-HBs
a. Appears
i. After clearance of HBsAg
ii. After successful hepatitis vaccination
b. Appearance of anti-HBs and disappearance of HBsAg indicate the following:
i. Recovery from HBV
ii. Noninfectivity
iii. Protection from recurrent infection
C. Hepatitis C
1. Anti-HCV (anti–hepatitis C virus antibody)
a. First-line test when diagnosis is suspected
b. Highly sensitive—If negative, infection is unlikely.
c. Specificity depends on the situation—If positive in a person with risk factors and elevated liver enzymes, specificity is high.
d. Positive anti-HCV—Hepatitis C infection is present until it is proved otherwise.
2. Standard enzyme-linked immunosorbent assay (ELISA) cannot isolate the virus; therefore, problems with false-positive results have been reported. Sensitivity and specificity are low.
3. A second-generation recombinant immunoblot assay (RIBA II) avoids these problems. This test identifies antibodies to four specific viral antigens (c100-3, c33c, c22-3, 5-1-1). At least two of the four antibodies must be present if results are to be considered positive.
a. “Confirmatory” test for hepatitis C
b. Rarely needed in clinical practice
c. A positive anti-HCV no longer needs to be confirmed by RIBA.
D. Hepatitis D
1. Diagnosis is made by detection of anti-HDV (anti–hepatitis D virus antibody).
2. Remember that HDV can occur as a coinfection or as a superinfection with HBV.
E. Hepatitis E: Diagnosis is made by detection of anti-HEV (anti–hepatitis E virus antibody) in the serum.
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