Hepatitis virus B will be used as a model here. After an incubation period, acute viral hepatitis most often begins with some combination of GI tract symptoms, fever, chills, and malaise, lasting 4-7 days. During this phase there is no clinical jaundice. Leukopenia with a relative lymphocytosis is common, and there may be a few atypical lymphocytes. Hemoglobin values and platelet counts usually are normal. Liver function tests reflect acute hepatocellular damage, with AST and ALT values more than 10 times the upper reference limit and usually more than 20 times the upper limit. ALP is usually elevated; values typically are less than 3 times the upper reference limit, but some patients may have elevation even higher than 5 times the upper limit. Lactic dehydrogenase (LDH) is usually less than 3 times normal. Serum bilirubin values begin climbing toward the end of this initial phase. The next development is visible jaundice; during this period, clinical symptoms tend to subside. The serum bilirubin level continues to rise for a time, then slowly falls. Both conjugated and unconjugated fractions are increased. The ALP level often begins to fall shortly after clinical icterus begins. The AST level begins to decrease about 1-2 weeks after it reaches its peak. A convalescent phase eventually ensues, with return of all test values to normal, beginning with the ALP. Some patients continue to manifest a low-grade hepatitis (chronic persistent or chronic active), reflected by variable and intermittent AST abnormalities (usually mild or moderate in degree) with or without ALP elevation. The majority of patients (75%-80%) never develop jaundice during viral hepatitis; this condition is known as “anicteric hepatitis.” In such situations, function tests reveal mild to moderate acute hepatocellular damage with a minimal obstructive component.

The textbook picture of AST more than 20 times (especially when over 25 times) the upper reference range limit (see the box), an ALT level greater than or equal to AST; with ALP mildly elevated and GGT mildly or moderately elevated, is strongly suggestive of hepatitis virus hepatitis. Other liver disorders that may be associated with an AST level over 20 times the upper reference limit include a small minority of patients with drug-induced liver injury (especially acetaminophen overdose), active alcoholic cirrhosis, a few cases (2%) of infectious mononucleosis, and some cases of severe liver passive congestion, as well as a few patients with early “atypical” extrahepatic obstruction. In addition, there are nonhepatic etiologies for markedly elevated AST, such as acute myocardial infarct and severe skeletal muscle injury. The patient may not be seen until the early convalescent phase, or the patient may have a mild anicteric episode. If so, the AST level may have decreased to less than 20 times the upper reference limit, and the differential diagnosis includes a wide variety of conditions, such as subsiding hepatitis, chronic hepatitis, alcoholic and active cirrhosis, infectious mononucleosis or cytomegalovirus infection, liver congestion, drug-induced liver dysfunction, liver space-occupying lesions, and severe fatty liver.

Chronic hepatitis is usually associated with AST values less than 20 times the upper reference limit and usually less than 10 times the upper limit. However, one study reported that about 15% of persons with the category of chronic hepatitis known as “chronic active hepatitis” had AST values at some time greater than 20 times the upper reference limit.