GGT (gamma glutamyl transferase)

DESCRIPTION:
g-GT is an enzyme that catalyzes the transfer of a glutamic acid residue released by hydrolysis to an amino acid or peptide. In the body, it occurs predominantly bound to cell membranes. It is most abundant in the brush border of the epithelial cells of the proximal tubules of the kidney, prostate, pancreas, liver, small intestine epithelium and brain. An increase in the catalytic concentration of g-GT is the most sensitive indicator of liver damage, and is especially pronounced if the damage is caused by alcohol. It is a good indicator in the differential diagnosis of hepatocellular and obstructive jaundice. gamma-GT is a microsomal enzyme, so it is induced (increased enzyme synthesis) by some drugs. Alcohol, barbiturates, antiepileptics and contraceptives have the most pronounced influence on the synthesis of gamma-GT.

DETERMINATION:
The determination method is the photometric kinetic method according to the IFCC. The sample for analysis is serum. The stability of the sample is 3 days if stored at 2°C – 8°C, 8 hours at 15°C to 25°C, one month at -20°C. They have an anticoagulant effect on enzyme activity.

CLINICAL SIGNIFICANCE:
1) Physiological changes in the catalytic concentration of gamma-glutamyltransferase The values of gamma-glutamyltransferase activity in the serum remain normal during a normal pregnancy. In newborns, the values in the serum are increased, and in childhood they decrease to the values as in adults. 2) Pathological changes in the catalytic concentration of gamma-glutamyltransferase A) Increased values of the catalytic concentration of gamma-glutamyltransferase in: Liver diseases: Acute hepatitis / Acute pancreatitis / Alcoholism / Liver cirrhosis / Crohn’s disease / Therapy with hepatotoxic drugs / Carcinoma of the bile duct / Cholelithiasis / Lipoid nephrosis / Cancer metastases in the liver / Biliary tract obstruction / Liver damage associated with infectious mononucleosis and with ulcerative colitis / Increase in parallel with the increase in serum triglycerides in secondary hyperlipidemia after carbohydrate intake and primary hyperlipidemia of the hereditary type / Cardiac arrest / Taking barbiturates Pancreatic diseases: Acute pancreatitis / Diabetes mellitus (some cases) / Pancreatic carcinoma / Chronic pancreatitis (some cases) Kidney diseases: Renal carcinoma (some cases) / Nephrosis / Rejections of a transplanted kidney Heart diseases: Myocardial infarction / Congestive decompensation of the heart due to anoxic liver damage Brain diseases: In some tumors Enzyme induction: Taking barbiturates / Taking phenytoin

RISK FACTORS:
Reduced values:
Start of the reaction with the sample and start of the reaction with the reagent: Citrates, EDTA, Fluoride, Oxalates. Heparin (start of reaction with sample) Hemoglobin concentration > 3.0 g/L
Increased values:
Alcoholism

EFFECT OF DRUGS:
Reduced values:
cefotaxime
Increased values:
barbiturates, cytostatics, phenytoin, glutamate, streptokinase

RESULT:
The reference interval depends on age, gender and work method. The reference interval is displayed on each validated result.