Laboratory testing in viral hepatitis has two jobs. One is to measure the general picture of liver injury — the enzymes, bilirubin and clotting — which shows that hepatitis is present and how severe it is. The other is serology, which identifies the responsible virus.
Prodromal phase
The earliest abnormality is an increase in AST and ALT. These enzymes rise before bilirubin does, but the height of the rise does not correlate with the amount of hepatic damage: a mild illness and a severe one can produce similar numbers.
Icteric phase
The general laboratory findings of icteric acute hepatitis are as follows.
Bilirubin becomes clinically visible as jaundice when the serum concentration reaches about 2.5 mg/dl, and in icteric patients it is mostly in the range of 5-20 mg/dl. A bilirubin above 20 mg/dl correlates with severe disease; in patients with an underlying haemolytic disorder such as G6PD deficiency or sickle cell disease, however, even a value of 30 mg/dl does not correlate with severe liver damage.
Gamma globulin shows a diffuse but mild increase: during the acute phase both IgM and IgG rise, reflecting the immune reaction to the ongoing viral infection. A rise in IgM is most characteristic of HAV infection.
White cells show a transient neutropenia and lymphopenia first, followed by a leukocytosis.
Clotting is a prognostic marker: a severely prolonged prothrombin time indicates severe hepatocellular necrosis and a very bad prognosis, while a mild prolongation may simply reflect the increase in bilirubin and aminotransferases.
Other findings include hypoglycaemia, seen in patients with prolonged nausea and vomiting, poor carbohydrate reserves and poor carbohydrate intake; slight microscopic haematuria and mild proteinuria; and mild steatorrhoea. Serum albumin is mostly in the normal range in uncomplicated acute hepatitis.
The general picture above shows that hepatitis is present and how severe it is, but it cannot say which virus is responsible. That distinction depends on serology.