BASICS
- BAs are cholesterol derivatives made by the liver and secreted via the biliary tree into the small intestine, where they emulsify dietary lipid and enhance its digestion by pancreatic lipases
- Primary functions of BAs:
- Facilitate cholesterol excretion
- Stimulate hepatic bile flow
- Enhance dietary lipid absorption
- During digestion, primary BAs are dehydroxylated by enteric bacteria to secondary BAs
- BAs are reabsorbed from the gastrointestinal tract in the ileum; they are transported back to the liver via portal circulation, where they are extracted by the liver, conjugated, and resecreted. Approximately 90% of the BA pool is concentrated in the enterohepatic circulation, and may be recycled 10–40 times/day
- Under physiologic conditions, equilibrium exists between intestinal absorption, hepatic uptake from the portal circulation, and hepatic secretion of BAs; this is represented and quantified as the SBAs
- Assessment of SBAs in the horse can be performed at any time, as the horse does not store BAs in a gallbladder between meals. Further, SBA concentrations do not display diurnal variation in this species
- Reference range < 12 μmol/L
- Elevated SBA concentration is a sensitive and specific marker of hepatic disease; however, the nature of the lesion cannot be determined by this parameter alone
- The primary BAs are taurocholic, taurochenodeoxycholic, and glycochenodeoxycholic acid; the majority of BAs are conjugated with taurine. Conjugation is required for secretion
- Three general mechanisms increase SBAs:
- Failure of hepatocytes to extract BAs from portal blood
- Biliary stasis
- Portosystemic shunting
- BA accumulation in the skin has been suggested to induce pruritus
- Signs of hepatic dysfunction
- Icterus
- Anorexia, weight loss
- Depression
- Edema
- Hepatic encephalopathy
- Photosensitization
- Colic
- Diarrhea
- Hemolysis (rare, but significant)
- Hemorrhagic diathesis (rare)
- Acute disease
- Theiler's disease
- Hepatic lipidosis
- Tyzzer's disease
- Cholangiohepatitis
- Biliary obstruction
- Cholelithiasis/choledocholithiasis
- Colon displacement
- Parasitic hepatitis
- Toxic hepatopathy (iron, drugs, plants, mycotoxins)
- Viral hepatitis (equine infectious anemia, equine viral arteritis, equine herpesvirus 1)
- Chronic disease
- Pyrrolizidine alkaloid toxicity
- Chronic active hepatitis
- Cholelithiasis
- Neoplasia
- Hepatic abscess
- Congenital disease
- Portosystemic shunt
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS