Hepatitis C virus (HCV) accounts for approximately 20% resembles other forms of acute viral hepatitis with onset of malaise, nausea, and right upper quadrant pain followed by of cases of acute hepatitis, 70% of chronic hepatitis, and 30% of end-stage liver disease in the United States. The acute dark urine and jaundice. The mean incubation period to onset of symptoms is 7 weeks (range, 3-20 weeks). How-infection has an incubation period of 7 weeks (range, 4-20 weeks) and is symptomatic and icteric in only one third of ever, long before onset of symptoms, viral markers of infection appear: HCV RNA becomes detectable in serum within patients. Serum aminotransferase levels generally increase greater than 10-fold elevated and as symptoms and signs re-1 to 2 weeks of exposure (Fig. ) and increases to levels of 10 6 to 10 8 genomes/mL. After several weeks, serum alanine solve decrease into the normal range. Antibody to HCV is usually but not always present at the time of onset of symp-aminotransferase (ALT) levels begin to increase and shortly thereafter, clinical symptoms appear. The severity of the toms. HCV RNA appears in the serum early during the incubation period, increases in titer and peaks at the time of symp-acute illness is variable; virtually all infected patients have a transient elevation in ALT, and peak levels are greater than toms, and then disappears in resolving disease. Importantly, 85% of patients with acute HCV infection develop chronic 10-fold elevated in more than 80% of patients. Yet, only a third of patients develop jaundice or symptoms; in the infection. In these patients, HCV RNA remains present and in approximately two thirds of patients, aminotransferases remainder, the disease is anicteric and subclinical. If clinically apparent, the illness generally lasts for 2 to 12 weeks. remain elevated in the range of 1.5-to 10-fold the upper limit of normal. The course of chronic hepatitis C is variable. Acute hepatitis C can result in fulminant hepatitis, but this is rare. In cases of acute, self-limited disease, HCV RNA Probably fewer than 20% of patients have symptoms and they are usually intermittent, vague, and nonspecific, largely being becomes undetectable within a few weeks of onset of symptoms and aminotransferase levels return to normal. malaise and easy fatiguability. A small percentage of patients develop extrahepatic manifestations of hepatitis C, including
CHRONIC HEPATITIS C cryoglobulinemia and glomerulonephritis. It is estimated that 20% to 30% of patients with chronic hepatitis C develop
Unfortunately, acute, self-limited hepatitis is not the most cirrhosis, but the process is generally slow and insidious. common course of acute HCV infection. In the majority of Once cirrhosis develops, symptoms are more common and patients, symptoms of acute hepatitis resolve, but ALT levels the signs of end-stage liver disease can appear with jaundice, often remain elevated and HCV RNA persists (Fig. ). 2-5,8-10 weakness, wasting, and gastrointestinal bleeding. Patients Indeed, a propensity to chronicity is the most distinguishing with cirrhosis are also at risk for developing hepatocellular characteristic of hepatitis C, occurring in at least 85% of carcinoma. Thus, this important liver disease has protean patients with acute HCV infection. The factors that lead to manifestations but is often insidious and can lead to endchronicity in hepatitis C are not well defined. The quasispestage liver disease despite the presence of few symptoms and cies nature of HCV and the tendency of the envelope gene signs of illness. (HEPATOLOGY 1997;26(Suppl 1):15S-20S.)
The hepatitis C virus (HCV) is an important cause of both acute and chronic hepatitis. As with all diseases, the clinical course of hepatitis C is variable-there is no single typical course or natural history of disease, but rather a broad clinical spectrum of disease presentations and outcomes.