Diagnostic Value of ALKP and GGT in Disease
Learn about the diagnostic value of ALKP and GGT in various diseases as explained by M.R. Fariborzi, a pediatric gastroenterologist from Bushehr Medical University. ALP is found in several tissues such as the liver, bone, intestines, kidney, placenta, and white blood cells. Serum ALP levels vary with age, with isolated increases not always indicating hepatic or biliary disease. Markedly increased ALP levels are associated with conditions like infiltrative liver disorders, while minimal increases can be seen in diseases like Hodgkin's disease and heart failure. The differential diagnosis for increased serum ALP includes factors like pregnancy, familial inheritance, chronic renal failure, blood group types, and vitamin D status.
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Presentation Transcript
DIAGNOSTIC VALUE OF ALKP AND GGT IN DISEASE M.R.Fariborzi pediatric gastroentrologist Bushehr Medical Univercity
ALKALINE PHOSPHATASE They are found in several tissues, including : Canalicular membrane of hepatocyte Bone osteoblasts Brush border of enterocytes in the smallintestine Proximal convoluted tubules of the kidney Placenta White blood cells Activity of ALP is normally demonstrable in serum, with the most likely sources being liver and bone.
The serum level of ALP varies considerably with age. Normal growing children and rapidly growing adolescents, in particular, have elevations of serum ALP of bone origin, with good correlation with the rate of bone growth, which causes influx of enzymes from osteoid tissues. Mean serum ALP activity is higher in males aged 15 50 years of age; levels in females over 60 years equal or exceed those of age-matched males. Half-life is 3 days
REFERENCE RANGE FOR SERUM ALKALINE PHOSPHATASE ACTIVITY IN CHILDREN
An isolated increase in ALP may not indicate hepatic or biliary disease if other liver biochemical tests are normal. Initial management may involve repeating the test, or confirming the hepatic origin with another liver chemistry test such as GGT or 5 NT The extent of the abnormal elevation does not differentiate or discriminate intrahepatic from extrahepatic causes.
Markedly increased ALP levels are seen predominantly with: infiltrative liver disorders (such as primary or metastatic tumor) Amyloid Abscess Lymphoma granulomas Minimal increased ALP levels are seen in : Hodgkin s disease Heart failure Hyperthyroidism Renal cell carcinoma
The differential diagnosis of increased serum ALP in the absence of liver disease includes: Pregnancy Familial inheritance (an autosomal dominant pattern in the absence of bone or hepatic diseases) Chronic renal failure Blood group types B or O (particularly after a fatty meal) Transient hyperphosphatemia of infancy (often exceeding 10 ULN for the laboratory, with return to normal levels within 8 to 12 weeks) Vit D deficiency and hypervitaminosis D
Macro-APLS, formed by the complexing of ALP from liver or bone with immunoglobulin, are demonstrated as slow-moving forms on electrophoresis, but their significance is uncertain.
A low serum ALP level is seen in: Zinc deficiency (as acrodermatitis enteropathica and Crohn disease) Wilson disease with hemolysis (fulminant presentation) Hypothyroidism Congenital hypophosphatasia Pernicious anemia Sever hepatic insufficiency Children recoverng from sever enteritis Malnutrition Celiac Post CPR transfusion
EVALUATION OF ELEVATED SERUM ALKALINE PHOSPHATASE
GAMMA-GLUTAMYLTRANSFERASE The microsomal enzyme GGT catalyzes the transfer of gamma- glutamyl groups from peptides such as glutathione to other amino acids. The enzyme is present in the cell membranes of multiple organs, including: Kidney Pancreas Liver Spleen Brain Breast Small intestine However, GGT does not increase in serum of patients with bone disease or children with active bone growth.
GGT is helpful in confirming the hepatic origin of elevated serum ALP. The newborn may have very high levels of GGT, up to five to 8 ULN for adults . In premature infants in the first few days of life, the values of GGT may be even higher than in the full-term infant. Serum values then decline rapidly in both the full-term and premature infant and reach adult normal levels by 6 to 9 months of age .
REFERENCE NORMAL VALUES FOR SERUM GAMMA- GLUTAMYLTRANSFERASE BY PATIENT AGE
ELEVATED GGT IN: Hepatobiliary disease Alcoholism Chronic obstructive airways disease Diabetes mellitus Hyperthyroidism Exocrine pancreatic diseases Myocardial infarction Renal failure
ELEVATED GGT IN: Drug: Anticonvulsants ( such as phenobarbital and phenytoin , carbamazepine) Cimetidine Furosemide Heparin Isotretinoin Methotrexate OCP Valproic acid may not induce an increase in serum GGT, except in cases of true hepatotoxicity, making this biochemical test a good candidate for monitoring for liver injury during therapy with this anticonvulsant
In up to 90% of cases of primary liver disease, elevated serum GGT is found, and hence it is not of great value in differential diagnosis. Serum GGT was most elevated in all children with: biliary atresia sclerosing cholangitis paucity of intrahepatic bile ducts (Alagille syndrome) cholestatic patients with 1-antitrypsin deficiency The presence of increased serum GGT in both intrahepatic and extrahepatic cholestasis is variable and cannot be used to differentiate between them.
PFIC: elevated serum GGT in PFIC type 3 normal to low serum GGT levels in PFIC type 1 (Byler disease) and type 2 A normal or low GGT with preserved normal liver structure also occurs in infants with benign recurrent intrahepatic cholestasis with a good long-term prognosis.
While measurement of serum GGT provide a sensitive indicator of the presence or absence of hepatobiliary disease, the usefulness of this assay is limited by its lack of specificity.
