What To Do About Fluctuating Liver Enzyme Levels

Liver enzymes are proteins the liver produces. The amount of these proteins in your blood is a good indication of your liver’s overall health. But elevated liver enzyme levels do not always mean serious liver damage or disease.

Sometimes, factors such as hormonal changes or reactions to medications can cause temporarily elevated liver enzyme levels. Elevated levels caused by these factors will generally return to normal in about 2 to 4 weeks without treatment.

Your liver makes proteins called liver enzymes that help your body perform necessary functions. For instance, liver enzymes help your body:

• fight infections
• make coagulation proteins that are necessary for blood clotting
• break down the food you eat
• break down toxins

Your liver makes several liver enzymes, including:

• Aspartate transaminase (AST)
• Alkaline phosphatase (ALP)
• Alanine transaminase (ALT)
• Gamma-glutamyl transferase (GGT)

These liver enzyme levels are a good indicator of how well your liver is functioning. A liver panel test checks liver enzyme levels in your blood.

A healthcare professional might order this test as part of routine blood work, as a way to monitor you if you’re at risk for liver disease, or as a diagnostic test if you have symptoms of liver disease or liver damage.

There are many reasons liver enzyme levels can change. Some causes are temporary and will resolve on their own. Other causes are more serious and will require medical treatment.

Temporary causes of changes in liver enzyme levels include:

• Hormones: Fluctuations in your liver levels can occur during your menstrual cycle and pregnancy.
• Certain medications: Some medications, including acetaminophen, antibiotics, and some cholesterol-lowering medications, can elevate your liver enzyme levels.
• Herbal supplements: Supplements such as iron, vitamin A, comfrey, and chaparral can elevate liver enzyme levels.
• Alcohol: Heavy drinking can raise your liver enzyme levels.

Causes of elevated liver enzyme levels that are more likely to be chronic include:

• Fatty liver disease: Heavy alcohol use, obesity, and a range of other factors can cause fatty liver disease. No matter the cause, fatty liver disease raises your liver enzyme levels.
• Hemochromatosis: Hemochromatosis is a rare condition that occurs when your body builds up too much iron. Elevated liver enzyme levels can be a symptom of the condition.
• All types of hepatitis: Any type of hepatitis, including hepatitis A, hepatitis B, hepatitis C, autoimmune hepatitis, and alcoholic hepatitis, causes liver inflammation and elevated liver enzymes.
• Cirrhosis: Cirrhosis is chronic liver damage. This damage causes elevated levels of liver enzymes.
• Liver cancer: Cancer that impacts your liver will also affect your liver enzyme levels.
• Hemolysis: Hemolysis is a type of anemia that occurs when your red blood cells are destroyed. It’s sometimes seen with alcohol-related liver diseases, and it can cause changes to liver enzyme levels.
• Thyroid disease: Hyperthyroidism can sometimes cause high levels of liver enzymes.
• Metabolic syndrome: Metabolic syndrome is a term that refers to a group of conditions that raise your risk of diabetes, heart disease, and stroke. These conditions include high blood pressure, high cholesterol, high blood sugar, and carrying excess weight around your midsection. People with metabolic syndrome may also have elevated liver levels.

The exact threshold for what is considered an elevated level or a typical level depends on your age, gender, health goals, and the values used by the specific lab. You can see some standard thresholds below.

• AST: under 36 U/L
• ALP: between 20 and 140 U/L
• ALT: under 25 U/L for women or under 33 U/L for men
• GGT: between 5 and 40 U/L

A liver function test might also measure:

• Albumin: between 35 and 50 U/L
• Bilirubin: between 0. 1 and 1.2 mg/dl

These values are not enzymes, but they’re also important chemicals made by your liver.

A liver function test is a standard blood draw. It can be done during a regular office visit. You don’t generally need any special preparation before a liver function test, although a doctor might ask you to fast for 12 to 24 hours before the blood draw. You can read more about liver function tests here.

The treatment for elevated liver enzymes depends on the cause. In many cases, liver enzyme levels return to normal on their own within about a month. You might need to switch medications, stop taking a supplement, or cut back on drinking if you drink, but you will not need a treatment plan.

In other cases, your doctor might need to treat the condition that’s raising your liver enzyme levels. They might order more tests, such as imaging tests, to get a better look at your liver or blood tests. They might also order a liver biopsy. Depending on your results, you might be referred to a specialist. Treatment will depend on your final diagnosis.

If you’re concerned your liver enzyme levels might be elevated, you might consider making some lifestyle changes at home, such as:

• reducing or eliminating alcohol from your diet
• being cautious about the medications and supplements you take
• staying active, including exercising regularly
• trying to add liver-friendly foods to your diet
• maintaining a moderate weight

Liver enzyme levels are an important indication of your liver’s health. When your enzyme levels are too high, it can be a symptom of liver damage or disease.

Some causes of elevated liver levels, such as hormonal changes or certain medications, are temporary and might resolve without treatment. Other causes are more serious and can include conditions such as cirrhosis, hepatitis C, and liver cancer.

Treatment for high liver enzyme levels depends on the cause.

Special Considerations in Interpreting Liver Function Tests

DAVID E. JOHNSTON, M.D.

A number of pitfalls can be encountered in the interpretation of common blood liver function tests. These tests can be normal in patients with chronic hepatitis or cirrhosis. The normal range for aminotransferase levels is slightly higher in males, nonwhites and obese persons. Severe alcoholic hepatitis is sometimes confused with cholecystitis or cholangitis. Conversely, patients who present soon after passing common bile duct stones can be misdiagnosed with acute hepatitis because aminotransferase levels often rise immediately, but alkaline phosphatase and γ-glutamyltransferase levels do not become elevated for several days. Asymptomatic patients with isolated, mild elevation of either the unconjugated bilirubin or the γ-glutamyltransferase value usually do not have liver disease and generally do not require extensive evaluation. Overall hepatic function can be assessed by applying the values for albumin, bilirubin and prothrombin time in the modified Child-Turcotte grading system.

The commonly used liver function tests (LFTs) primarily assess liver injury rather than hepatic function. Indeed, these blood tests may reflect problems arising outside the liver, such as hemolysis (elevated bilirubin level) or bone disease (elevated alkaline phosphatase [AP] level).

Abnormal LFTs often, but not always, indicate that something is wrong with the liver, and they can provide clues to the nature of the problem. However, normal LFTs do not always mean that the liver is normal. Patients with cirrhosis and bleeding esophageal varices can have normal LFTs. Of the routine LFTs, only serum albumin, bilirubin and prothrombin time (PT) provide useful information on how well the liver is functioning.

The general subject of LFTs^1,2 and the differential diagnosis of abnormal LFTs in asymptomatic patients^3–5 have been well reviewed. This article discusses some common pitfalls in the interpretation of LFTs. Hints for interpreting these tests are presented in Table 1.

Situation	Comments
Mildly elevated ALT level (less than 1.5 times normal)	ALT value could be normal for gender, ethnicity or body mass index.
	Consider muscle injury or myopathy.
Alcoholic hepatitis	Laboratory values can appear cholestatic, and symptoms can mimic cholecystitis.
	Minimal elevations of AST and ALT often occur.
AST level greater than 500 U per L	The AST elevation is unlikely to result from alcohol intake alone.
	In a heavy drinker, consider acetaminophen toxicity.
Common bile duct stone	Condition can simulate acute hepatitis
	AST and ALT become elevated immediately, but elevation of AP and GGT is delayed.
Isolated elevation of GGT level	This situation may be induced by alcohol and aromatic medications, usually with no actual liver disease.
Isolated elevation of AP level (asymptomatic patient with normal GGT level)	Consider bone growth or injury, or primary biliary cirrhosis.
	AP level rises in late pregnancy.
Isolated elevation of unconjugated bilirubin level	Consider Gilbert syndrome or hemolysis.
Low albumin level	Low albumin is most often caused by acute or chronic inflammation, urinary loss, severe malnutrition or liver disease; it is sometimes caused by gastrointestinal loss (e.g., colitis or some uncommon small bowel disease).
	Normal values are lower in pregnancy.
Blood ammonia level	Blood ammonia values are not necessarily elevated in patients with hepatic encephalopathy.
	Determination of blood ammonia levels is most useful in patients with altered mental status of new onset or unknown origin.

Markers of Hepatocellular Injury

The most commonly used markers of hepatocyte injury are aspartate aminotransferase (AST, formerly serum glutamic-oxaloacetic transaminase [SGOT]) and alanine aminotransferase (ALT, formerly serum glutamate-pyruvate transaminase [SGPT]). While ALT is cytosolic, AST has both cytosolic and mitochondrial forms.

Hepatocyte necrosis in acute hepatitis, toxic injury or ischemic injury results in the leakage of enzymes into the circulation. However, in chronic liver diseases such as hepatitis C and cirrhosis, the serum ALT level correlates only moderately well with liver inflammation. In hepatitis C, liver cell death occurs by apoptosis (programmed cell death) as well as by necrosis. Hepatocytes dying by apoptosis presumably synthesize less AST and ALT as they wither away. This probably explains why at least one third of patients infected with hepatitis C virus have persistently normal serum ALT levels despite the presence of inflammation on liver biopsy.^6,7 Patients with cirrhosis often have normal or only slightly elevated serum AST and ALT levels. Thus, AST and ALT lack some sensitivity in detecting chronic liver injury. Of course, AST and ALT levels tend to be higher in cirrhotic patients with continuing inflammation or necrosis than in those without continuing liver injury.

As markers of hepatocellular injury, AST and ALT also lack some specificity because they are found in skeletal muscle. Levels of these aminotransferases can rise to several times normal after severe muscular exertion or other muscle injury, as in polymyositis,⁸ or in the presence of hypothyroidism, which can cause mild muscle injury and the release of aminotransferases. In fact, AST and ALT were once used in the diagnosis of myocardial infarction.

Slight AST or ALT elevations (within 1. 5 times the upper limits of normal) do not necessarily indicate liver disease. Part of this ambiguity has to do with the fact that unlike the values in many other biochemical tests, serum AST and ALT levels do not follow a normal bell-shaped distribution in the population.⁹ Instead, AST and ALT values have a skewed distribution characterized by a long “tail” at the high end of the scale (Figure 1).⁵ For example, the mean values for ALT are very similar from one population to another, but the degree to which the distribution is skewed varies by gender and ethnicity. The ALT distributions in males and nonwhites (i.e., blacks and Hispanics) tend to have a larger tail at the high end, so that more values fall above the upper limits of normal set for the average population.^10,11

AST and ALT values are higher in obese patients, probably because these persons commonly have fatty livers.¹² ALT levels have been noted to decline with weight loss. ¹³ Depending on the physician’s point of view, the upper limits of normal for AST and ALT levels could be set higher for more obese persons.

Rare individuals have chronically elevated AST levels because of a defect in clearance of the enzyme from the circulation.¹⁴ For both AST and ALT, the average values and upper limits of normal in patients undergoing renal dialysis are about one half of those found in the general population.¹⁵ Mild elevations of ALT or AST in asymptomatic patients can be evaluated efficiently by considering alcohol abuse, hepatitis B, hepatitis C and several other possible diagnoses (Table 2).⁵

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Various liver diseases are associated with typical ranges of AST and ALT levels (Figure 2). ALT levels often rise to several thousand units per liter in patients with acute viral hepatitis. The highest ALT levels—often more than 10,000 U per L—are usually found in patients with acute toxic injury subsequent to, for example, acetaminophen overdose or acute ischemic insult to the liver. AST and ALT levels usually fall rapidly after an acute insult.

Lactate dehydrogenase (LDH) is less specific than AST and ALT as a marker of hepatocyte injury. However, it is worth noting that LDH is disproportionately elevated after an ischemic liver injury.¹⁶

It is especially important to remember that in patients with acute alcoholic hepatitis, the serum AST level is almost never greater than 500 U per L and the serum ALT value is almost never greater than 300 U per L. The reasons for these limits on AST and ALT elevations are not well understood. In typical viral or toxic liver injury, the serum ALT level rises more than the AST value, reflecting the relative amounts of these enzymes in hepatocytes. However, in alcoholic hepatitis, the ratio of AST to ALT is greater than 1 in 90 percent of patients and is usually greater than 2. ¹⁷ The higher the AST-to-ALT ratio, the greater the likelihood that alcohol is contributing to the abnormal LFTs. In the absence of alcohol intake, an increased AST-to-ALT ratio is often found in patients with cirrhosis.

The elevated AST-to-ALT ratio in alcoholic liver disease results in part from the depletion of vitamin B₆ (pyridoxine) in chronic alcoholics.¹⁸ ALT and AST both use pyridoxine as a coenzyme, but the synthesis of ALT is more strongly inhibited by pyridoxine deficiency than is the synthesis of AST. Alcohol also causes mitochondrial injury, which releases the mitochondrial isoenzyme of AST.

Patients with alcoholic hepatitis can present with jaundice, abdominal pain, fever and a minimally elevated AST value, thereby leading to a misdiagnosis of cholecystitis. This is a potentially fatal mistake given the high surgical mortality rate in patients with alcoholic hepatitis.¹⁹

Markers of Cholestasis

Cholestasis (lack of bile flow) results from the blockage of bile ducts or from a disease that impairs bile formation in the liver itself. AP and γ-glutamyltransferase (GGT) levels typically rise to several times the normal level after several days of bile duct obstruction or intrahepatic cholestasis. The highest liver AP elevations—often greater than 1,000 U per L, or more than six times the normal value—are found in diffuse infiltrative diseases of the liver such as infiltrating tumors and fungal infections.

Diagnostic confusion can occur when a patient presents within a few hours after acute bile duct obstruction from a gallstone. In this situation, AST and ALT levels often reach 500 U per L or more in the first hours and then decline, whereas AP and GGT levels can take several days to rise.

Both AP and GGT levels are elevated in about 90 percent of patients with cholestasis.²⁰ The elevation of GGT alone, with no other LFT abnormalities, often results from enzyme induction by alcohol or aromatic medications in the absence of liver disease. The GGT level is often elevated in persons who take three or more alcoholic drinks (45 g of ethanol or more) per day. ²¹ Thus, GGT is a useful marker for immoderate alcohol intake. Phenobarbital, phenytoin (Dilantin) and other aromatic drugs typically cause GGT elevations of about twice normal. A mildly elevated GGT level is a typical finding in patients taking anticonvulsants and by itself does not necessarily indicate liver disease.^22,23

Serum AP originates mostly from liver and bone, which produce slightly different forms of the enzyme. The serum AP level rises during the third trimester of pregnancy because of a form of the enzyme produced in the placenta. When serum AP originates from bone, clues to bone disease are often present, such as recent fracture, bone pain or Paget’s disease of the bone (often found in the elderly). Like the GGT value, the AP level can become mildly elevated in patients who are taking phenytoin.^22,23

If the origin of an elevated serum AP level is in doubt, the isoenzymes of AP can be separated by electrophoresis. However, this process is expensive and usually unnecessary because an elevated liver AP value is usually accompanied by an elevated GGT level, an elevated 5′-nucleotidase level and other LFT abnormalities.

In one study,²⁴ isolated AP elevations were evaluated in an unselected group of patients at a Veterans Affairs hospital. Most mild AP elevations (less than 1.5 times normal) resolved within six months, and almost all greater elevations had an evident cause that was found on routine clinical evaluation.

Persistently elevated liver AP values in asymptomatic patients, especially women, can be caused by primary biliary cirrhosis, which is a chronic inflammatory disorder of the small bile ducts. Serum antimitochondrial antibody is positive in almost all of these patients.

Indicators of How Well the Liver Functions

BILIRUBIN

Bilirubin results from the enzymatic breakdown of heme. Unconjugated bilirubin is conjugated with glucuronic acid in hepatocytes to increase its water solubility and is then rapidly transported into bile. The serum conjugated bilirubin level does not become elevated until the liver has lost at least one half of its excretory capacity. Thus, a patient could have obstruction of either the left or right hepatic duct without a rise in the bilirubin level.

Because the secretion of conjugated bilirubin into bile is very rapid in comparison with the conjugation step, healthy persons have almost no detectable conjugated bilirubin in their blood. Liver disease mainly impairs the secretion of conjugated bilirubin into bile. As a result, conjugated bilirubin is rapidly filtered into the urine, where it can be detected by a dipstick test. The finding of bilirubin in urine is a particularly sensitive indicator of the presence of an increased serum conjugated bilirubin level.

In many healthy persons, the serum unconjugated bilirubin is mildly elevated to a concentration of 2 to 3 mg per dL (34 to 51 μmol per L) or slightly higher, especially after a 24-hour fast. If this is the only LFT abnormality and the conjugated bilirubin level and complete blood count are normal, the diagnosis is usually assumed to be Gilbert syndrome, and no further evaluation is required. Gilbert syndrome was recently shown to be related to a variety of partial defects in uridine diphosphate-glucuronosyl transferase, the enzyme that conjugates bilirubin.²⁵

Mild hemolysis, such as that caused by hereditary spherocytosis and other disorders, can also result in elevated unconjugated bilirubin values, but hemolysis is not usually present if the hematocrit and blood smear are normal. The presence of hemolysis can be confirmed by testing other markers, such as haptoglobin, or by measuring the reticulocyte count.

Severe defects in bilirubin transport and conjugation can lead to markedly elevated unconjugated bilirubin levels, which can cause serious neurologic damage (kernicterus) in infants. However, no serious form of liver disease in adults causes elevation of unconjugated bilirubin levels in the blood without also causing elevation of conjugated bilirubin values.

When a patient has prolonged, severe biliary obstruction followed by the restoration of bile flow, the serum bilirubin level often declines rapidly for several days and then slowly returns to normal over a period of weeks. The slow phase of bilirubin clearance results from the presence of delta-bilirubin, a form of bilirubin chemically attached to serum albumin.²⁶ Because albumin has a half-life of three weeks, delta-bilirubin clears much more slowly than bilirubin-glucuronide. Clinical laboratories can measure delta-bilirubin concentrations, but such measurements are usually unnecessary if the physician is aware of the delta-bilirubin phenomenon.

ALBUMIN

Although the serum albumin level can serve as an index of liver synthetic capacity, several factors make albumin concentrations difficult to interpret.²⁷ The liver can synthesize albumin at twice the healthy basal rate and thus partially compensate for decreased synthetic capacity or increased albumin losses. Albumin has a plasma half-life of three weeks; therefore, serum albumin concentrations change slowly in response to alterations in synthesis. Furthermore, because two thirds of the amount of body albumin is located in the extravascular, extracellular space, changes in distribution can alter the serum concentration.

In practice, patients with low serum albumin concentrations and no other LFT abnormalities are likely to have a nonhepatic cause for low albumin, such as proteinuria or an acute or chronic inflammatory state. Albumin synthesis is immediately and severely depressed in inflammatory states such as burns, trauma and sepsis, and it is commonly depressed in patients with active rheumatic disorders or severe end-stage malnutrition. In addition, normal albumin values are lower in pregnancy.

PROTHROMBIN TIME

The liver synthesizes blood clotting factors II, V, VII, IX and X. The prothrombin time (PT) does not become abnormal until more than 80 percent of liver synthetic capacity is lost. This makes PT a relatively insensitive marker of liver dysfunction. However, abnormal PT prolongation may be a sign of serious liver dysfunction. Because factor VII has a short half-life of only about six hours, it is sensitive to rapid changes in liver synthetic function. Thus, PT is very useful for following liver function in patients with acute liver failure.

An elevated PT can result from a vitamin K deficiency. This deficiency usually occurs in patients with chronic cholestasis or fat malabsorption from disease of the pancreas or small bowel. A trial of vitamin K injections (e.g., 5 mg per day administered subcutaneously for three days) is the most practical way to exclude vitamin K deficiency in such patients. The PT should improve within a few days.

BLOOD AMMONIA

Measurement of the blood ammonia concentration is not always useful in patients with known or suspected hepatic encephalopathy. Ammonia contributes to hepatic encephalopathy; however, ammonia concentrations are much higher in the brain than in the blood and therefore do not correlate well.²⁸ Furthermore, ammonia is not the only waste product responsible for encephalopathy. Thus, blood ammonia concentrations show only a mediocre correlation with the level of mental status in patients with liver disease. It is not unusual for the blood ammonia concentration to be normal in a patient who is in a coma from hepatic encephalopathy.

Blood ammonia levels are best measured in arterial blood because venous concentrations can be elevated as a result of muscle metabolism of amino acids. Blood ammonia concentrations are most useful in evaluating patients with stupor or coma of unknown origin. It is not necessary to evaluate blood ammonia levels routinely in patients with known chronic liver disease who are responding to therapy as expected.

Grading Liver Function by Child-Turcotte Class

In communicating among themselves, many physicians use the Child-Turcotte class as modified by Pugh, often termed the “Child class,” to convey information about overall liver function and prognosis (Table 3).²⁹ This grading system can be used to predict overall life expectancy and surgical mortality in patients with cirrhosis and other liver diseases.³⁰

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For elective general abdominal surgery, perioperative mortality is in the neighborhood of several percent for patients who fall into the Child class A, 10 to 20 percent for those in class B and approximately 50 percent for those in class C.³¹ These percentages must be balanced by prognostic considerations when transplantation becomes an option. The presence of cirrhosis by itself is not an indication for liver transplantation, and transplantation is rarely performed in patients who fall into Child class A. For example, the 10-year survival rate is as high as 80 percent in patients with hepatitis C and cirrhosis who have Child class A liver function and no variceal bleeding.³² However, once patients with any type of liver disease fall into the Child-Turcotte class B or class C category, survival is significantly reduced and transplantation should be considered.

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When choosing where to perform Enzymes in Moscow and other cities of Russia, do not forget that the cost, methods and terms of performing studies in regional medical offices may differ

Tissues of various organs differ in the spectrum of enzymatic activity. With inflammation or other damaging effects, the components of the cellular content in an increased amount enter the surrounding space and blood. If hepatitis or pancreatitis is suspected, a biochemical blood test for liver or pancreatic enzymes (ALT/AST/GGT and amylase/lipase, respectively) provides laboratory evidence in favor of the proposed diagnosis. Most enzymes do not have strict specificity – the data obtained are always subject to a comprehensive analysis by the attending physician, taking into account the anamnesis, clinical symptoms, and the results of other studies.

Test for alpha-amylase (diastase)

Method of determination
Enzymatic colorimetric (IFCC recommended).

Test material
Blood serum

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Synonyms: Diastasis; Serum amylase; Serum amylase. α-Amylase; AMY; AML; diastase; 1;4-β-D-glucanohydralase; Serum amylase; blood amylase.

Brief description of the analyte Alpha-amylase

Alpha-amylase belongs to the group of enzymes that break down dietary carbohydrates such as starch, glycogen into dextrins, maltose and glucose. This enzyme is produced mainly in the salivary glands and pancreas, then it enters the oral cavity or the lumen of the duodenum, respectively, and participates in the breakdown of food carbohydrates. In the blood serum, pancreatic (P-type) and salivary (S-type) amylase isoenzymes are isolated (see also test No. 12 Alpha-Amylase pancreatic). Usually, persistently low serum alpha-amylase activity is significantly increased in acute pancreatitis or inflammation of the salivary glands. The ovaries, fallopian tubes, small and large intestines, liver, and mammary glands during lactation have a significantly lower amylase activity.

What is the purpose of determining the concentration of alpha-amylase in the blood serum

The study of the level of alpha-amylase is used mainly for the diagnosis and monitoring of the treatment of acute pancreatitis, differentiation of pancreatitis from other acute abdominal disorders, as well as in the diagnosis of other types of pancreatic pathology .

Under what conditions is the concentration of alpha-amylase increased

In acute pancreatitis, after 2-12 hours from the onset of an attack, a transient increase in the activity of blood alpha-amylase is observed. Usually in acute pancreatitis, alpha-amylase activity is 4-6 times higher than the reference values, while the maximum values ​​are reached after 12-72 hours. Alpha-amylase levels return to normal on the third or fourth day. The magnitude of the increase in alpha-amylase is not directly related to the severity of the process in the pancreas. However, the higher the increase, the higher the likelihood of acute pancreatitis.

Up to 20% of cases of acute pancreatitis can occur with a normal level of serum amylase, parallel determination of lipase (test No. 23) increases the likelihood of its detection. In particular, serum amylase may be normal in acute pancreatitis associated with hyperlipemia. Serum amylase is excreted in the urine, therefore, an increase in amylase values ​​in the blood serum is also reflected in an increase in the content of amylase in the urine (see test No. than serum amylase activity, the increase in values ​​persists for a longer period after an attack.However, the diagnostic value of determining serum amylase activity is higher.

Under certain pathological conditions, amylase (usually S-type) can form complexes with immunoglobulins A and G and other high molecular weight plasma proteins (macroamylasemia). These complexes do not pass through the glomerular membrane. In this case, although the content of amylase in the blood serum increases, the normal activity of the enzyme is determined in the urine. A discrepancy between the levels of serum and urinary amylase activity is also observed in renal failure. In chronic pancreatitis without exacerbation, serum amylase activity is usually at a subnormal level. Exacerbations of chronic pancreatitis are accompanied by slight increases in serum alpha-amylase levels.

Some diseases not related to the pancreas may also be accompanied by hyperamylasemia. These include chronic renal failure (decreased clearance of serum amylase), any kind of damage to the salivary glands, diseases of the biliary tract, as a result of primary or secondary involvement of the pancreas.