Chronic hepatitis is defined as necroinflammation of the liver of more than 3 to 6 months’ duration, demonstrated by persistently elevated serum aminotransferase levels and associated with characteristic histologic findings. The causes of chronic hepatitis include hepatitis B, C, and D viruses (HBV, HCV, and HDV) as well as noninfectious disorders, including nonalcoholic steatohepatitis (NASH), autoimmune hepatitis, hepatitis following medication exposure (such as isoniazid or nitrofurantoin), Wilson's disease, α1-antitrypsin deficiency, and, infrequently, celiac disease. Hepatitis A virus does not cause chronic hepatitis, but hepatitis E virus may rarely lead to chronic hepatitis in immunosuppressed persons or transplant recipients. Chronic hepatitis is characterized on the basis of etiology; grade of portal, periportal, and lobular inflammation (minimal, mild, moderate, or severe); and stage of fibrosis (none, mild, moderate, severe, cirrhosis).
In the absence of advanced cirrhosis, patients are often asymptomatic or have mild, nonspecific symptoms. Infection caused by HBV may be associated with glomerulonephritis and polyarteritis nodosa. HCV is a pathogenetic factor in mixed cryoglobulinemia and membranoproliferative glomerulonephritis and may be related to lichen planus, autoimmune thyroiditis, lymphocytic sialadenitis, idiopathic pulmonary fibrosis, sporadic porphyria cutanea tarda, and monoclonal gammopathies. HCV infection confers a 20% to 30% increased risk of non-Hodgkin's lymphoma and may induce insulin resistance (which in turn increases the risk of hepatic fibrosis); moreover, the risk of type 2 diabetes mellitus is increased in persons with chronic hepatitis C. Hepatic steatosis is a particular feature of infection with HCV genotype 3 and may also occur in patients infected with other HCV genotypes who have risk factors for fatty liver. On the other hand, chronic HCV infection is associated with a decrease in serum cholesterol and low-density lipoprotein levels.