Blood biochemistry: bile acid

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Sections available in full article Overview, Uses, Sampling, Source of test material, Quantity of test material, Sample collection technique, Quality control, Test (s), Methodologies, Availability, Technique (intrinsic) limitations, Technician (extrinsic) limitations, Result data, Normal (reference) values, Abnormal values, Errors and Artifacts, Sources, Publications, Vetstream contributor(s),
Contributors Dr Kathleen P Freeman DVM MS PhD MRCVS
Synonyms Bile salts

Overview

  • Cholic and chenodeoxycholic acids (primary bile acids) synthesized in liver from cholesterol   →   conjugated with taurine (preferred) or glycine and excreted in bile as their sodium salts (bile salts).
  • Discharged at time of eating to small intestine where they assist in fat digestion.
  • Only 2-5% of total bile acids are lost in faces each day - remainder resorbed, pass to the liver where extracted and re-excreted (enteropathic circulation).
  • Small proportion reach general circulation - it is these that are measured.
  • Sensitive indicator of liver function and of integrity of liver, biliary and intestinal circulation.

Uses

Alone

  • Liver function.
    Post-prandial bile acid concentration reported to have the highest sensitivity of any single test for the diagnosis of feline liver disease. 
  • Portosystemic shunt  Portosystemic shunt  .

Result data

Normal (reference) values

Normal
  • Fasting reference range: 0-10 umol/l.
  • Post-prandial reference range: <15 umol/l.
  • Specificity of post-prandial TSBA using cut-off >15 umol/l = 89%.
  • Using cutoff >20 umol/l for fasting and post-prandial TSBA specificity = 100%.
  • Sensitivity of fasting TSBA using cut-off of >5 umol/l = 83%.
  • Sensitivity of post-prandial TSBA using cut-off >15 umol/l = 82%.
  • Sensitivity of pre- and post-prandial TSBA decrease if cut-off value >20 umol/l (59% and 74%).
  • Abnormal TSBA are specific and sensitive indicator of hepatic dysfunction but do not discriminate the underlying type of hepatobiliary disease.

Abnormal values

Increased (bile acids)
  • Impaired liver function  Liver: acute disease  , eg toxins, infection.
  • Biliary obstruction.
  • Portosystemic shunt  Portosystemic shunt  .
  • Slight to moderate increase (usually <50 umol/l) commonly seen in:
    • Hyperthyroidism  Hyperthyroidism  .
    • Hyperadrenocorticism  Hyperadrenocorticism  .
    • Excessive steroid therapy  Prednisolone  .
    • Diabetes mellitus  Diabetes mellitus  .
    • Cardiac disease  Congestive heart failure  .

Decreased (bile acid)

  • May be undetectable in serum of normal animals in random blood samples.
    Need multiple subnormal [bile acid] to diagnosis pathologically low [bile acid].
  • Severe intestinal obstruction  Intestine: obstruction  .
  • Malabsorption (<1 umol/l).

Errors and Artifacts

  • Post-prandial TSBA <pre-prandial TSBA, or lack of expected rise in post-prandial TSBA, may occur if there has been:
    • Decreased gastric emptying.
    • Altered intestinal transit time.
    • Ileal disease resulting in lack of absorption of bile acids.
    • Incomplete/lack of stimulation of gall bladder emptying.
    • Small intestinal bacterial overgrowth resulting in bacterial deconjugation of bile acids and decreased ileal absorption.
  • May see pre-prandial TSBA >post-prandial TSBA:
    • Interdigestive gall bladder contraction has occurred during fasting.

Sources

Publications

Refereed papers

  • Center S A, Erb H N & Joseph S A (1995) Measurement of Serum Bile and Concentrations for Diagnosis of Hepatobiliary Disease in Cats. JAVMA 207, 1048-1054.
  • Sutherland R J (1989) Biochemical evaluation of the hepatobiliary system in Dogs and Cats. Vet Clin North Am Small Anim Pract 19 (5), 899-927.
  • Center S A, Bladwin B H, Erb H & Tennant B C (1986) Bile acid concentrations in the diagnosis of hepatobiliary disease in the cat. JAVMA 189 (8), 891-896.
  • Center S A, Bladwin B H, King J M & Tennant B C (1983) Hematologic and biochemical abnormalities associated with induced extrahepatic bile duct obstruction in the cat. Am J Vet Res 44 (10), 1822-1829.

Other sources of information

  • Ettinger S J & Feldman E C (eds) (2000) Textbook of Veterinary Internal Medicine. 5th edn. Philadelphia: W B Saunders & Co.
  • Kaneko J J, Harvey J W & Brass M L (eds) (1997) Clinical Biochemistry of Domestic Animals. 5th edn. Boston: Academic Press.
  • Duncan J R, Prasse K W & Mahaffey E A (1994) Veterinary Laboratory Medicine. Clinical Pathology. 3rd edn. Iowa: Iowa University Press.

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