GGT (formerly gamma-glutamyltranspeptidase) is located mainly in liver cells, to a lesser extent in kidney, and in much smaller quantities in biliary tract epithelium, intestine, heart, brain, pancreas, and spleen. Some GGT activity seems to reside in capillary endothelial cells. The serum GGT level is increased in the newborn but declines to adult levels by age 4 months. One report found that obese persons could have GGT values up to 50% higher than nonobese persons. By far the most common cause of serum GGT elevation is active liver disease. GGT is affected by both acute liver cell damage and biliary tract obstruction. In biliary tract obstruction and space-occupying lesions of the liver, GGT was found by some investigators to have the same sensitivity as ALP (with a few cases of metastatic tumor to liver abnormal by GGT but not by ALP and vice versa) and is reported to be more sensitive than ALP by other investigators. Overall sensitivity for metastatic liver tumor is said to be about 88% (literature range, 45%-100%) compared to about 80% for ALP. In acute liver cell injury, GGT levels are elevated with approximately the same frequency as the AST. Therefore, GGT has overall better sensitivity than either ALP or AST in liver disease. GGT levels are elevated in about 90% of patients with infectious mononucleosis (Epstein-Barr virus) and about 75% with cytomegalovirus infection, presumably due to liver involvement from these viruses.

GGT levels are not significantly affected by “normal” alcoholic beverage intake in most cases. In heavy drinkers and chronic alcoholics, GGT levels are reported to be elevated in about 70%-75% of patients (literature range, 63%-80%). Determining the GGT level has been advocated as a screening procedure for alcoholism.

GGT levels may become elevated in several conditions other than liver disease (see the box).

About 5%-30% of patients with acute myocardial infarction develop elevated GGT levels. This is usually attributed to proliferation of capillaries and fibroblasts in granulation tissue. The increase is usually reported 7-14 days after infarction. However, a few investigators found the elevation soon after infarction, and it is unclear how many cases are actually due to liver passive congestion rather than infarct healing. The GGT level may be transiently increased by extensive reparative processes anywhere in the body.

GGT levels are usually not increased in bone disease, childhood or adolescence, and pregnancy, three nonhepatic conditions that are associated with increased ALP levels. GGT has therefore been used to help differentiate liver from nonliver origin when ALP levels are increased. However, the possible nonhepatic sources for GGT must be kept in mind.