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Bile acids are synthesised from cholesterol in the
liver and secreted in bile after conjugation. Assessing the liver’s capacity to remove circulating bile acids
gives an indication of liver function and perfusion.
Its use in detection of hepatobiliary disease and
acute liver damage in dogs, as well as portosystemic vascular anomalies (PSVA) in dogs and cats, has been described across various studies. 2,3,4 Understanding
the limitations of an endogenous challenge help in the interpretation of unusual test results; e.g. higher pre- prandial concentrations. One should also be aware of test vulnerability factors including meal type and size, enteric disease and intestinal motility.5Lastly, one should also bear in mind the possible effects of concurrent administration of ursodeoxycholic acid, as well as
the spurious increase in bile acids seen in Maltese terriers.6,7Fasting ammonia or the ammonia tolerance test serves as possible alternatives to detect hepatic dysfunction and PSVAs. It is less commonly used due to complexities in sample handling.
Protein C is a vitamin K-dependent protein, synthesised in the liver with a short plasma half-life. It serves as
an indicator of portal blood flow. It may be used to differentiate PSVA from microvascular dysplasia (MVD), as both disorders may result in increased bile acids.8Low protein C activity (< 70%) is a characteristic finding in dogs with clinical signs of PSVA. In contrast, dogs with MVD typically have protein C values > 70%. Protein C deficiency, however, may also be seen in patients with vitamin K deficiency, sepsis, SIRS, and DIC.9
The decision to investigate is difficult in asymptomatic animals. If no drug history (including nutraceuticals) is found, persistent increase of two-months duration or progression within this period is generally an indication for further testing. The speed at which investigation takes place may further be influenced by the
patient’s signalment, in conjunction with known breed predispositions.
Investigation is recommended when clinical signs
are present, especially if the signs are specific to
hepatic disease. Again, history, physical examination
and signalment are all critical in establishing the
cause of the increased enzymes. Based on clinical
signs, extra-hepatic disease should be investigated
if indicated. These include intestinal, respiratory and cardiovascular disease, which generally results in
mild to moderate increase in transaminase activity if present. Endocrinopathies, e.g. hyperthyroidism in cats, hypothyroidism and hyperadrenocorticism in dogs should be considered in the presence of appropriate clinicopathological abnormalities. Investigation of primary hepatic disease is indicated if hepatic enzymes remain persistently increased despite addressing extra-hepatic disorders.
Investigation of primary liver disease may involve assessment of hepatic function, imaging and +/- histopathology. Ultrasound is a commonly used modality to image the liver, although scintigraphy and computed tomography are generally thought to be more sensitive for detection of PSVAs. However, histopathology is often required for definitive diagnosis, prognosis and to dictate ongoing management.
Cases References
1. Cocker S, Richter K. Hepatobiliary disease. In: [edited by] Stephen J. Ettinger, Edward C. Feldman. Textbook Of Veterinary Internal Medicine: Diseases of the Dog and Cat. Philadelphia: W.B. Saunders Co. 2017: pp.1611-1621
2. Center SA, Manwarren T, Slater MR, Wilentz E. Evaluation of twelve-hour preprandial and two-hour postprandial serum bile acids concentrations for diagnosis of hepatobiliary disease in dogs. J Am Vet Med Assoc. 1991;199:217-26. 3. Turgut K, Demir C, Ok M, Ciftçi K. Pre- and postprandial total serum bile acid concentration following acute liver damage in dogs. Zentralbl Veterinarmed A. 1997;44:25-9.
4. Dirksen K, Burgener IA, Rothuizen J, van den Ingh TSGAM, Penning LC, Spee B, Fieten H. Sensitivity and Specificity of Plasma ALT, ALP, and Bile Acids for Hepatitis in Labrador Retrievers. J Vet Intern Med. 2017;31:1017-1027. doi: 10.1111/ jvim.14716.
5. Center SA, Randolph JF, Warner KL. Influence of Oral Ursodeoxycholic Acid on Serum and Urine Bile Acid Concentrations in Clinically Normal Dogs. ACVIM 2004.
6. Tisdall PL, Hunt GB, Tsoukalas G, Malik R. Post-prandial serum bile acid concentrations and ammonia tolerance in Maltese dogs with and without hepatic vascular anomalies. Aust Vet J. 1995; 72:121-6.
7. Abraham LA, Charles JA, Holloway SA. Effect of oral ursodeoxycholic acid on bile acids tolerance tests in healthy dogs. Aust Vet J. 2004;82:157-60.
8. Toulza O, Center SA, Brooks MB, Erb HN, Warner KL, Deal W. Evaluation of plasma protein C activity for detection of hepatobiliary disease and portosystemic shunting in dogs. J Am Vet Med Assoc. 2006 Dec 1;229:1761-71.
9. de Laforcade AM1, Rozanski EA, Freeman LM, Li W. Serial evaluation of protein C and antithrombin in dogs with sepsis. J Vet Intern Med 2008;22:26-30.
10. Twedt DC. Abnormal Liver Enzymes: A Practical Clinical Approach. Col-
orado State University; [Last accessed 05 June 2018]. Canine/Feline Liver
& Pancreatic Disease. Available from: b718031aa9dedaf57e23d719d8e90353b799.pdf.
Figure 1: Approach to Increased Liver Enzymes10
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