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Chapter 25: Hepatitis, Viral

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    AMA Citation
    Hepatitis, Viral. In: Wells BG, DiPiro JT, Schwinghammer TL, DiPiro CV. Wells B.G., DiPiro J.T., Schwinghammer T.L., DiPiro C.V. Eds. Barbara G. Wells, et al.eds. Pharmacotherapy Quick Guide New York, NY: McGraw-Hill; . http://accesspharmacy.mhmedical.com/content.aspx?bookid=2177&sectionid=165472369. Accessed October 19, 2018.
    MLA Citation
    . "Hepatitis, Viral." Pharmacotherapy Quick Guide Wells BG, DiPiro JT, Schwinghammer TL, DiPiro CV. Wells B.G., DiPiro J.T., Schwinghammer T.L., DiPiro C.V. Eds. Barbara G. Wells, et al. New York, NY: McGraw-Hill, , http://accesspharmacy.mhmedical.com/content.aspx?bookid=2177&sectionid=165472369.

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INTRODUCTION

  • Viral hepatitis refers to the clinically important hepatotropic viruses responsible for hepatitis A (HAV), hepatitis B (HBV), delta hepatitis, hepatitis C (HCV), and hepatitis E.

HEPATITIS A

  • HAV infection usually produces a self-limited disease and acute viral infection, with a low fatality rate, and confers lifelong immunity.

  • HAV infection primarily occurs through transmission by the fecal-oral route, person-to-person, or by ingestion of contaminated food or water. The incidence of HAV correlates directly with low socioeconomic status, poor sanitary conditions, and overcrowding. Rates of HAV infection have increased among international travelers, injection drug users, and men who have sex with men.

  • The disease exhibits three phases: incubation (averaging 28 days, range 15–50 days), acute hepatitis (generally lasting 2 months), and convalescence. Nearly all individuals will have clinical resolution within 6 months of the infection, and a majority will have done so by 2 months. HAV does not lead to chronic infections.

  • The clinical presentation of HAV infection is given in Table 25–1. Children younger than 6 years are typically asymptomatic.

  • The diagnosis of acute HAV infection is based on clinical criteria of acute onset of fatigue, abdominal pain, loss of appetite, intermittent nausea and vomiting, jaundice or elevated serum aminotransferase levels, and serologic testing for immunoglobulin (Ig) M anti-HAV.

TABLE 25–1Clinical Presentation of Acute Hepatitis A
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TABLE 25–1 Clinical Presentation of Acute Hepatitis A

Signs and symptoms

  • The preicteric phase brings nonspecific influenza-like symptoms consisting of anorexia, nausea, fatigue, and malaise.

  • Abrupt onset of anorexia, nausea, vomiting, malaise, fever, headache, and right upper quadrant abdominal pain with acute illness.

  • Icteric hepatitis is generally accompanied by dark urine, alcoholic (lightcolored) stools, and worsening of systemic symptoms.

  • Pruritus is often a major complaint of icteric patients.

Physical examination

  • Icteric sclera, skin, and secretions

  • Mild weight loss of 2–5 kg

  • Hepatomegaly

Laboratory tests

  • Positive-serum Ig M anti–HAV

  • Mild elevations of serum bilirubin, γ-globulin, and hepatic transaminase (ALT and AST) values to about twice normal in acute anicteric disease

  • Elevations of alkaline phosphatase, γ-glutamyl transferase, and total bilirubin in patients with cholestatic illness

(ALT, alanine transaminase; AST, aspartate transaminase; HAV, hepatitis A virus; Ig, immunoglobulin.)

TREATMENT

  • Goals of Treatment: Complete clinical resolution, including reducing complications, normalization of liver function, and reductioning infectivity and transmission. No specific treatment options exist for HAV. Management of HAV infection is primarily supportive. Steroid use is not recommended.

PREVENTION

  • The spread of HAV can be best controlled by avoiding exposure. The most important measures to avoid exposure include good handwashing techniques and good personal hygiene practices.

  • The current vaccination strategy in the United States includes vaccinating all children at 1 year of age. Groups who should receive HAV vaccine are shown in Table 25–2.

  • Three inactivated virus vaccines are currently licensed in the ...

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