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INTRODUCTION

A group of disorders characterized by a chronic inflammatory reaction in the liver for at least 6 months.

OVERVIEW

ETIOLOGY

Hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV, delta agent), drugs (methyldopa, nitrofurantoin, isoniazid, dantrolene), autoimmune hepatitis, Wilson's disease, hemochromatosis, α1-antitrypsin deficiency.

HISTOLOGIC CLASSIFICATION

Chronic hepatitis can be classified by grade and stage. The grade is a histologic assessment of necrosis and inflammatory activity and is based on examination of the liver biopsy. The stage of chronic hepatitis reflects the level of disease progression and is based on the degree of fibrosis (see Table 306-2, p. 2568, HPIM-18).

PRESENTATION

Wide clinical spectrum ranging from asymptomatic serum aminotransferase elevations to apparently acute, even fulminant, hepatitis. Common symptoms include fatigue, malaise, anorexia, low-grade fever; jaundice is frequent in severe disease. Some pts may present with complications of cirrhosis: ascites, variceal bleeding, encephalopathy, coagulopathy, and hypersplenism. In chronic HBV or HCV and autoimmune hepatitis, extrahepatic features may predominate.

CHRONIC HEPATITIS B

Follows up to 1–2% of cases of acute hepatitis B in immunocompetent hosts; more frequent in immunocompromised hosts. Spectrum of disease: asymptomatic antigenemia, chronic hepatitis, cirrhosis, hepatocellular cancer; early phase often associated with continued symptoms of hepatitis, elevated aminotransferase levels, presence in serum of HBeAg and HBV DNA, and presence in liver of replicative form of HBV; later phase in some pts may be associated with clinical and biochemical improvement, disappearance of HBeAg and HBV DNA and appearance of anti-HBeAg in serum, and integration of HBV DNA into host hepatocyte genome. In Mediterranean and European countries as well as in Asia, a frequent variant is characterized by readily detectable HBV DNA, but without HBeAg (anti-HBeAg-reactive). Most of these cases are due to a mutation in the pre-C region of the HBV genome that prevents HBeAg synthesis (may appear during course of chronic wild-type HBV infection as a result of immune pressure and may also account for some cases of fulminant hepatitis B). Chronic hepatitis B ultimately leads to cirrhosis in 25–40% of cases (particularly in pts with HDV superinfection or the pre-C mutation) and hepatocellular carcinoma in many of these pts (particularly when chronic infection is acquired early in life).

EXTRAHEPATIC MANIFESTATIONS (IMMUNE COMPLEX–MEDIATED)

Rash, urticaria, arthritis, polyarteritis nodosa–like vasculitis, polyneuropathy, glomerulonephritis.

TREATMENT Chronic Hepatitis B

There are currently seven approved drugs for the treatment of chronic HBV: interferon α (IFN-α), pegylated interferon (PEG IFN), lamivudine, adefovir dipivoxil, entecavir, telbivudine, and tenofovir (see Table 164-1). Use of IFN-α has been supplanted by PEG-IFN. Table 164-2 summarizes recommendations for treatment of chronic HBV.

TABLE 164-1COMPARISON OF PEGYLATED INTERFERON (PEG IFN), LAMIVUDINE, ADEFOVIR, ENTECAVIR, TELBIVUDINE, AND TENOFOVIR THERAPY FOR ...

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