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Subject 101: Interpretation of lab results – ALAT and ASAT

Interpretation of lab results – ALAT and ASAT

Introduction

In lab reports often values of ASAT and ALAT are reported. Many do know it has something to do with the liver, but what is it actually? What does it reflect and how should the results be interpreted? A short explanation followed by two cases for self-assessment.

 

What is ALAT and ASAT?

ALAT is an abbreviation for an enzyme known as Alanine (Amino)Transaminase. It transfers an amino group from L-alanine to alpha-ketoglutarate, which results in the formation of pyruvate and L-glutamate.

ASAT in an abbreviation for aspartate aminotransferase, an enzyme that catalyzes the reversible reaction Aspartate + α-ketoglutarate ↔ oxaloacetate + glutamate.

ALAT is especially abundant in the liver, much more than ASAT which is also expressed in many other cells, such as erythrocytes, kidney cells and muscle. As such, ALAT is more liver-specific then ASAT.

 

What does it reflect?

Both ALAT and ASAT are measured to quantify liver cell turn-over. In general it is often seen as a reflection of liver health, but these enzymes do not reflect the synthetic capability of the liver. It reflects liver cell turn-over, with an increase in ALAT/ASAT values reflects increased cell turn-over, such is the case in inflammation (due to an infection or due to steatosis hepatis). Since ASAT is also expressed in many other cell types (more than ALAT), an increase in ASAT > ALAT should prompt the clinician to look for cell turnover in other cells than the liver: such as caused by destruction of erythrocytes (hemolysis?) or skeletal muscle (rhabdomyolysis, or necrosis of muscle cells).

Often the ratio of ASAT/ALAT is noted by clinicians. As stated most liver diseases have a lower ASAT and higher ALAT. However, an much higher increase in ASAT compared to ALAT (often more than 2-fold) may be suggestive of alcoholic liver disease. An concomitant increase in gamma-glutamyl-tranferase, (γ-GT) is supportive of that observation (but not exclusive). Very high levels of ASAT and ALAT (x50 or higher) are suggestive of liver failure.

 

When should it be ordered?

Measurement of ALAT/ASAT can be helpful when a clinician is interested in liver cell turn-over (eg to detect a possible liver infection). One may wonder whether it is necessary to measure both ALAT/ASAT as a screening tool. Often only ASAT is determined, as it levels reflect more than liver cells only and a normal ASAT level thus provides more information than ALAT. It is important to remember that one should not order ALAT/ASAT when the function of the liver needs to be studied. Vital function of the liver is the formation of gall, synthesis of clotting factors and formation of urea from ammonia. Thus when the function of the liver needs to be evaluated, one should look for presence of jaundice (either clinically, or by measurement of blood bilirubin levels), but plasma albumin or ammonia (NH4) levels or certain coagulation tests /clotting factors also reflect liver synthetic capability.

Self-assessment

Case 1

A 35-year old female has had an increase in ALAT/ASAT these past two years. She reports some minor diarrhea and abdominal discomfort, but is otherwise in good condition. She does not use any medication and denies use of alcohol or drugs. She has not gone abroad. Physical examination is normal (no jaundice). You get the following lab results:

ALAT 68 U/l                               (<45)

ASAT 46 U/l                               (<40)

MCV 101 fL                                (80-100)

Thrombocytes 457 10e 9/l         (<400)

Bilirubin, ferritin, ceruloplasmin are normal.

Hepatitis B and C were excluded.

Abdominal ultrasound: normal liver, no steatosis.

How would you interpret these results:

  1. Because of increased muscle turn-over
  2. Because of an inflammatory process in the liver
  3. Typical of alcoholism.
  4. Typical of reduced liver synthetic capacity.

 

Case 2

A 55-year old female visits the emergency room because of severe myalgia (muscle-pain) following the flu one week earlier. She has already recovered from the flu, but now has difficulties getting up and walking due to the myalgias. Apart from 2-4 tablets of paracetamol for 2 days she did not use any other medications. Otherwise she is in good condition. She does use moderate amounts of alcohol (1 glass a day) but no drugs. She has not gone abroad. Physical examination demonstrates reduced muscle strength due to pain, but there is no jaundice. You get the following lab results:

ALAT 79 U/l               (<45)

ASAT 249 U/l             (<40)

CRP 4 ng/l                 (<5)

kreatinin 88 umol/l     (40-95)

Bilirubin, hemoglobin, MCV, leukocytes and albumin were all normal.

How would you interpret these results:

  1. Because of increased muscle turn-over
  2. Because of a inflammatory process in the liver
  3. Typical of alcoholism.
  4. Typical of reduced liver synthetic capacity.

Answers

Case 1

How would you interpret these results:

  1. Because of increased muscle turn-over
  2. Because of an inflammatory process in the liver
  3. Typical of alcoholism.
  4. Typical of reduced liver synthetic capacity.

ALAT>ASAT, thus appears to be a liver problem. patient was found to have celiac disease, which also explains the diarrhea and abdominal discomfort. Celiac disease also causes (mild) hepatitis.

 

 

Case 2

How would you interpret these results:

  1. Because of increased muscle turn-over
  2. Because of a inflammatory process in the liver
  3. Typical of alcoholism.
  4. Typical of reduced liver synthetic capacity.

ASAT>>ALAT, thus appears not be liver related. CK (creatinin kinase) was measured and found to be severely elevated (35.000, normal <350), suggestive of rhabdomyolysis after an infection.

G.E. Linthorst

References

  1. Uptodate.com. Arterial blood gases. Wolters Kluwer Health. Updated 25 sep 2014; cited 20 nov 2014. Available here.
  2. Gyton, A.C. and Hall, J.E. Textbook of medical Physiology. Elsevier Saunders. 2006, 11th ed.
  3. Stehouwer, C.D.A., Koopmans, R.P. Meer, van de J. Interne Geneeskunde. Bohn Stafleu van Loghum. 2010, 14th ed.

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