Pathology Associates Of Lexington, P.A.

GGT/GGTP blood test

This is one of the liver function tests (LFTs). Yet the parameter is not specific to liver; it is said that some 30% of cases with elevated GGT are negative for liver disease. Screening panels sometimes pick up isolated GGT elevations in apparently healthy persons; it is said that workups of such rarely detect a true disease.

GGT stands for gamma glutamyltransferase, a specific transferase enzyme protein (previously called a "transpeptidase"...gamma glutamyltranspeptidase [GGTP]...now considered to be more appropriately called a "transferase"¹). GGT & GGTP = synonyms. Sometimes also referred to as "gamma GT" or just "GT". The protein is predominantly located in cell membranes. It is the most sensitive LFT for detecting intrahepatic or posthepatic biliary obstruction; GGT rises earlier & persists longer than others. Liver, kidney, and prostate parenchymal cells have high levels of GGT. GGT elevations that are liver-derived come from increased enzyme production and not from cell destruction.

If alkaline phosphatase (AP) is elevated & GGT normal, then the AP elevation is likely of bone or placental origin. If both AP & GGT are proportionately elevated, investigation of the biliary tree is needed. If tree is negative for general or focal dilation, AP/GGT elevation may be cholestatic or due to an "infiltrative process. And if GGT is solely elevated or discordantly higher than AP, there also may be an "induction elevation" of GGT (as with alcohol or medications)...which could be superimposed on some microscopic ductal problems. So, liver biopsy would seek to rule out any cannalicular or ductular cholestatsis or ductular injury/inflammation [LMC-03-7710].

Diseases in which GGT may be normal:

acute biliary obstruction...AP & GGT take about 24 hours to begin rising.
chronic alcoholism (only elevated in about 75%)...CDT is a reference-lab test for alcohol abuse.
inactive states or phases of chronic liver disease
high alkaline phosphatase and normal GGT suggest bone disease but does not ALWAYS indicate absence of liver disease.
normal in pure skeletal muscle diseases and pure bone diseases.

Diseases associated with low GGT levels:

some cases of treatments to reduce high triglycerides also decrease the GGT.
levels fall (but not necessarily below normal) after meals.
hypothyroidism.
hypothalamic malfunction.
low levels of serum magnesium.

Diseases associated with elevated GGT levels:

acute biliary obstruction...takes about 24 hours after obstructive onset to start rising.
especially if the CBC has an MCV of 100 or more, may reflect increased chronic consumption of alcohol.
when LFT group has both elevated GGT and alkaline phosphatase ( the two "biliary markers") clearly elevated but one is much more so elevated, think of drug induced cholestasis especially if the GGT is disproportionately high.
drugs, medications, and alcohol can induce hepatocytes to maintain mildly elevated to very high elevations of GGT...there is "injury to microsomal structures" so that glutathione levels are depleted² unless enzyme productive capacity is increased, causing proliferative expansion of the quantity of those structures (histologically called hepatocyte "induction cell change").
congestive heart failure.
excessive magnesium ingestion.
post-radiation reflection of tumor-cell injury in radiated malignancies.
prostate infarcts or cancer...not sensitive at all for cancer.
active destructive renal disease...as with infarcts.
as a rule, only moderate elevations (2-5x normal) in uncomplicated viral hepatitis, fatty liver, usual-dose medications (NSAIDs, etc.) .
high elevations (5-15x normal) most common when considerable metastatic tumor in liver, or acute and chronic pancreatitis, or malignant extrahepatic obstruction.

References:

Burtis CA & Ashwood ER, Tietz Textbook of Clinical Chemistry, 3rd Edition, 1999.
McKenna and Keffer, The Handbook of Clin. Path., 2nd Ed. (EBS's office)
hepatic lab tests, Practice Guidelines, National Academy of Clinical Biochemistry (NACB), USA.

(posted 5 January 2005; latest addition 2 May 2005)