Gamma Glutamyl Transferase

The γ-GT (synonyms: γ-GT (gamma-GT); γ-glutamyltranspeptidase (γ-GTP); gamma-glutamyl transferase, GGT) is a liver enzyme that has been measured as a standard part of routine clinical practice for many years to check liver function. It belongs to a group of peptidases that carry out the transfer of amino acids from one peptide to another and thus act as amino acid transferases. Together with direct bilirubin, it is one of the cholestasis-indicating enzymes. The measurable activity of gamma-GT originates primarily from the hepatobiliary system (liver and bile ducts).

The procedure

Material needed

Interfering factors

  • Avoid hemolysis! Decrease in γ-GT in the presence of severe hemolysis.

Normal values

Age Female Male
Adult up to 39 U/L up to 66 U/L
13-17 years up to 38 U/L up to 52 U/L
7-12 years up to 19 U/L up to 19 U/L

Indications

  • Screening for liver and biliary tract diseases
  • Differential diagnosis and follow-up of liver and biliary tract diseases.
  • Control of chronic alcoholism in combination with other laboratory parameters.
  • Assessment of the risk for cardiovascular disease.

Interpretation

Interpretation of very strongly elevated values

Interpretation of strongly elevated (to elevated) values.

  • Chronic active hepatitis
  • Cirrhosis of the liver (advanced or end stage of various liver diseases that destroy the liver structure)
  • Primary liver tumors and liver metastases (malignant tumor settlement (metastasis, daughter tumor) in the liver).
  • Steatosis hepatis (fatty liver)
  • Acute and chronic pancreatitis
  • Acute renal insufficiency (kidney weakness),
  • Nephrotic syndrome – collective term for symptoms that occur in various diseases of the glomerulus (renal corpuscles); symptoms include: Proteinuria (excretion of protein in the urine) with a protein loss of more than 1 g/m²/body surface per day; hypoproteinemia, peripheral edema due to hypalbuminemia of < 2.5 g/dl in serum, hyperlipoproteinemia (lipid metabolism disorder).
  • Chronic and acute circulatory disorders of the liver, e.g., chronic right heart failure (right heart weakness), portal vein thrombosis (vascular disease in which a blood clot (thrombus) has formed in the portal vein of the liver)
  • Diabetes mellitus – in up to 57% of diabetics, especially those with vascular disease, mildly elevated γ-GT levels are present without clinical signs of liver disease
  • Brain tumor, cerebral hemorrhage – slight γ-GT increases may occur.
  • Infectious mononucleosis (synonyms: Pfeiffer’s glandular fever; Pfeiffer’s glandular fever; mononucleosis; mononucleosis infectiosa; monocytangina; Pfeiffer’s disease).
  • Myocardial infarction (heart attack) – in circa 50% of patients, a γ-GT rise is measured with maximum in the 2nd week
  • Chronic alcohol abuse (alcohol abuse).
  • Ingestion of medications – e.g., phenytoin, phenobarbital, thyrostatic agents, anabolic steroids, thiazide diuretics, meprobamate, phenothiazines, azathioprine, ifosfamide, streptokinase, diethylpentamide, aminopyrine, MAO inhibitors, tuberculostatics, antirheumatic agents.
  • Exposure to chemicals – e.g., chlorinated hydrocarbons, vinyl chloride, trichloroethylene.

Other notes

  • Gamma-GT is membrane bound and liver specific.
  • The half-life is 3-4 days.

Gamma-GT around cardiovascular disease

The γ-GT level an indicator of cardiovascular disease such as coronary heart disease (CHD), heart failure (heart failure) or apoplexy (stroke).Although the relationship between alcohol consumption and cardiovascular disease has been the subject of countless studies, there have been few studies that have investigated or given significance to a relationship between elevated γ-GT and heart disease or apoplexy.The study by the group of researchers led by Hanno Ulmer, Professor of Medical Statistics at the Medical University of Innsbruck, and his colleagues at the University of Ulm is considered evident. The study is based on an analysis of nearly 164,000 Austrians (89,000 women and 75,000 men), conducted between 1985 and 2001 in Vorarlberg and collected, documented and evaluated by the Working Group for Preventive and Social Medicine. Men with elevated γ-GT (γ-GT > 28 U/I) had a 28 percent increased risk of dying from cardiovascular disease, men with severely elevated γ-GT (γ-GT > 56 U/I) even had a 64 percent increased risk In women, the risk was increased by 35 percent (γ-GT > 18 U/I) and by 51 percent (γ-GT > 36 U/I), respectively. Elevated γ-GT in younger individuals represented an even higher risk constellation than in older individuals. Men with elevated γ-GT showed increased mortality from chronic coronary artery disease (coronary artery disease), heart failure (heart failure), ischemic and hemorrhagic insults (cerebral stroke). No statistically significant effect was seen in acute coronary disease (e.g., myocardial infarction/ heart attack) or other forms of heart disease. Women with elevated γ-GT showed an increased risk for all forms of heart disease. This association was not statistically significant for deaths from cerebrovascular accidents. The γ-GT was shown to be a statistically independent risk factor. Even the inclusion of age, sex, smoking, blood pressure, cholesterol, triglycerides, glucose, and social status did not change this assessment. Elevated γ-GT was a relatively strong risk factor when compared with established risk factors and ranked 3rd in terms of risk after smoking and hypertension (high blood pressure) but ahead of elevated blood glucose, cholesterol, and triglycerides. The study results showed a dose-response relationship between γ-GT and cardiovascular causes of death. The pattern (the higher the γ-GT, the higher the mortality/sterility rate) was consistent across the different subtypes of cardiovascular disease. Men with a γ-GT greater than 55 U/l had a 1.6-fold higher mortality risk (risk of death) than those with low levels below 14 U/l, whereas women with more than 35 U/l had a 1.5-fold higher mortality risk than those with levels below 9 U/l. The γ-GT appears to be directly involved in the mechanism of atherosclerosis development. For example, it had been found in cerebral, coronary, and carotid plaques (vessel wall deposits in the carotid artery) and would trigger oxidative processes there.

Further evidence

  • The γ-GT is membrane bound:
    • Mild liver damage → γ-GT ↑
    • Moderate liver damage → cytoplasmic ALT (GPT) ↑ and AST (GOT) ↑
    • Severe liver damage → mitochondrial GLDH ↑ and AST (GOT) ↑
  • The γ-GT is not only liver-specific but also bile duct-specific:
    • Sensitive indicator in disorders of the liver (proportional to liver damage) and bile duct system.
    • High values can be detected in cholestasis and alcoholic hepatitis
  • Because GLDH is localized exclusively intramitochondrially, this parameter is a significant indicator for estimating hepatocellular death or liver damage.
  • To determine liver function, aspartate aminotransferase (AST, GOT), alanine aminotransferase (ALT, GPT), gamma-glutamyl transferase (gamma-GT), alkaline phosphatase (AP), and bilirubin should always be measured as well.
  • Detect more than 95% of all liver diseases by simultaneous determination of AST, ALT and γ-GT.