Serum (blood sample collected to a Plain tube
)
ALT is specific for hepatocytes. In viral hepatitis and other forms of liver disease associated with hepatic necrosis, serum ALT is elevated even before the clinical signs and symptoms of the disease appear. Although both AST and ALT elevate in the presence of any form of liver cell injury, ALT is the more liver-specific marker. Serum elevations of ALT are rarely observed in conditions other than parenchymal liver disease. Also, ALT elevation persists longer than AST elevation.
REFERENCE LIMITS
<40 U/L
Elevation of ALT is seen in parenchymal liver diseases characterized by destruction of hepatocytes. Values are typically at least 10 times above the normal range. Levels may reach values as high as 100 times the upper reference limit, although 20- to 50-fold elevations are most frequently encountered. In infectious hepatitis and other inflammatory conditions affecting the liver, ALT is characteristically as high as or higher than AST.
ALT:AST ratio, which normally and in other condition is less than 1, becomes >1 in liver parenchymal injury.
Serum (blood sample collected to a Plain tube
)
Albumin constitutes 55% to 65% of total plasma protein. It maintains oncotic pressure, and is involved in the transport and storage of a wide variety of ligands, such as calcium bilirubin. Hypoalbuminemia can be caused by impaired synthesis due either to liver disease (primary) or low protein intake/ malabsorption of amino acids (secondary), increased renal excretion (eg, nephrotic syndrome), and increased catabolism as a result of tissue damage and inflammation.
REFERENCE LIMITS
3.5 - 5.3 g/dL
When the serum albumin values fall below 2.0 g/dL, edema is usually present. Hyperalbuminemia is of little diagnostic significance except in the case of dehydration.
Serum (blood sample collected to a Plain tube
)
The clinically significant origins of ALP include; liver, bone osteoblasts, small intestinal mucosa, proximal convoluted tubules of the kidney, and placenta. The clinically significant origins of ALP include; liver, bone osteoblasts, small intestinal mucosa, proximal convoluted tubules of the kidney, and placenta. The liver isoform mainly contributes to the ALP activity observed in the serum in a healthy adult.
A rise in the ALP occurs with all forms of cholestasis, particularly with obstructive jaundice. It is also elevated in diseases of the skeletal system, such as Paget disease, hyperparathyroidism, rickets, and osteomalacia, as well as with fractures and malignant tumors. A considerable rise in the ALP observed in children is due to the physiological increase in osteoblast activity in growing bone.
REFERENCE LIMITS
Males
0 - 14 days : 83-248 U/L
15 days to <1 year : 122-469 U/L
1 to <10 years : 142-335 U/L
10 to <13 years : 129-417 U/L
13 to <15 years : 116-468 U/L
15 to <17 years : 82-331 U/L
17 to <19 years : 55-149 U/L
⋝19 years : 40-129 U/L
Females
0 - 14 days : 83-248 U/L
15 days to <1 year : 122-469 U/L
1 to <10 years : 142-335 U/L
10 to <13 years : 129-417 U/L
13 to <15 years : 57-254 U/L
15 to <17 years : 50-117 U/L
⋝17 years : 35-104 U/L
Pregnant females : average ALP levels typically mount to about 2-3 times its pregestational value
Increases in serum ALP activity commonly originate from liver and/or bone. Consequently, serum ALP measurements are of particular interest in the investigation of hepatobiliary diseases and bone diseases associated with increased osteoblastic activity.
Any form of biliary tree obstruction induces the synthesis of ALP by hepatocytes. The increase is more notable (>4-fold the upper reference limit) in extrahepatic obstruction (eg, by stone, by cancer of the head of the pancreas) than in intrahepatic obstruction. Serum enzyme activities may reach 10 to 12 times the URL and usually return to baseline on surgical removal of the obstruction. A similar increase is seen in patients with advanced primary liver cancer or widespread secondary hepatic metastases.
Liver diseases that principally affect parenchymal cells, such as infectious hepatitis, typically show only a moderate (<3-fold) rise in the ALP levels. Intestinal ALP isoenzyme is normally cleared by the hepatocytes, thus often increases in patients with liver cirrhosis.
Serum (blood sample collected to a Plain tube
)
Amylase is produced primarily by the exocrine pancreas. Amylases also are produced by the salivary glands, small intestine mucosa, ovaries, placenta, liver, and fallopian tubes. Pancreatic and salivary isoenzymes contribute to the serum amylase activity.
REFERENCE LIMITS
⋜1 month : 0-6 U/L
1 - 6 months : 1-17 U/L
7 - 12 months : 6-44 U/L
1 - 3 years : 8-79 U/L
4 - 17 years : 21-110 U/L
⋝18 years : 28-100 U/L
In acute pancreatitis, a transient rise in serum amylase activity occurs within 2 to 12 hours of onset and the levels typically return to normal by the 3rd or 4th day. Serum amylase levels peak around 12 to 72 hours from the onset typically by 4-6-fold rise. The magnitude of the elevation of serum enzyme activity is not related to the severity of pancreatic involvement. Normalization is not necessarily a sign of resolution. If acute pancreatitis is associated with hyperlipidemia, serum amylase activity may be spuriously normal due to analytical interference by lipids.
Because it is produced by several organs, amylase is not a specific indicator of pancreatic function. Elevated levels also may also be seen in nonpancreatic pathologies such as mumps, salivary duct obstruction, ectopic pregnancy, and intestinal obstruction/infarction.
CAUTIONS
Amylase results may be elevated in patients with macroamylase. Macroamylase refers to a high-molecular weight form of amylase due to amylase complexing with a larger moleculae such as immunoglobulin. Amylase being a small molecule, serum amylase is normally cleared by renal excretion. Due to the large size of macroamylase-complex, it is not excreted in urine. As a result, the serum amylase is elevated in the presence of macroamylase in absence of any pancreatic or other pathology. Serum lipase and urinary amylase, can be used in differentiating the presence of macroamylase.
Serum (blood sample collected to a Plain tube
)
AST is found in high concentrations in liver, heart, skeletal muscle, kidney, and red blood cells (RBC). It has 2 isoforms; cytoplasmic and mitochondrial. The cytoplasmic isoform is mainly released into blood in mild tissue injury, while severe tissue damage results in more mitochondrial isoform being released. High levels of AST can be found in cases such as myocardial infarction and acute liver disease. Slight to moderate elevation of AST is seen in muscular dystrophy, dermatomyositis, acute pancreatitis, and crush injury to muscles.
REFERENCE LIMITS
<35 U/L
Elevated AST values are seen in parenchymal liver diseases characterized by destruction of hepatocytes, typically rising above >10-fold of UNL. In infectious hepatitis and other inflammatory conditions affecting the liver, ALT is characteristically as high as or higher than AST. AST levels are usually elevated before clinical signs and symptoms of disease appear. 5-10 fold elevations of both AST and ALT occur in patients with primary or metastatic carcinoma of the liver, with AST usually being higher than ALT, but levels are often normal in the early stages of malignant infiltration of the liver. Elevated AST values may also be seen in disorders affecting the heart, skeletal muscle, and kidney.
ALT:AST ratio, which normally and in other conditions is less than 1, becomes >1 in liver parenchymal injury.
CAUTIONS
Haemolysis of the blood sample results in spurious elevation of AST levels.
Rifai N, Horvath AR, Wittwer CT, eds: Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 6th ed. Elsevier; 2018