Liver: steroid hepatopathy

Jump to... Pathogenesis Diagnosis Treatment Prevention Sequelae Sources

• Cause : exogenous glucocorticoids, hyperadrenocorticism.
• Signs : asymptomatic, elevation in liver enzymes or very occasionally hepatic failure.
• Diagnosis : history of glucocorticoid use, signs, histopathology.
• Prognosis : very good; reversible on removal of excess steroid.

Pathogenesis

Top

• Excessive steroid, either through exogenous administration or secondary to hyperadrenocorticism .
• Individual variation in response, different potencies of glucocorticoids, and route of exposure influence changes in hepatic morphology, clinicopathologic features, and clinical signs.

• Exogenous steroid administration.
• Hyperadrenocorticism .

• Excess glycogen accumulation in hepatocytes.

• Depends on dose, route of exposure and potency of glucocorticoid.

Diagnosis

Top

• Asymptomatic.
• Those of steroid administration (polydipsia/polyuria, polyphagia, weight gain, skin changes).
• Those of hyperadrenocorticism.
• Occasionally may show evidence of hepatic dysfunction.

• Asymptomatic.
• Polydipsia/polyuria.
• Polyphagia.
• Weight gain.
• Skin and haircoat changes.

• Asymptomatic.
• Polydipsia/polyuria.
• Polyphagia.
• Obesity.
• Skin and haircoat changes.
• Signs of liver dysfunction.
• Hepatomealy.
• Jaundice.

• Usually not required.
• Excess glycogen in hepatocytes.

Biochemistry

• Increased ALP  and GGT  as these enzymes are induced by steroids and subsequent released from sinusoidal and canalicular membranes. Initially a liver-ALP isoenzyme predominates, but this is replaced (within a week) by a glucocorticoid-ALP isoenzyme.
• Little clinical use of measuring individual ALP isoenzymes.
• Mild increases in ALT   and AST .
• Liver enzymes increase by 1-2 days if glucocorticoids given intravenously, and by 1-2 weeks if given orally.
• May be mild to moderate elevations in bile acids .
• Other biochemical alterations seen in hyperadrenocorticism (elevated cholesterol  and glucose  , reduced BUN  ).

Ultrasonography

• Diffuse of multifocal parencymal hyperechogenicity .
• Variable appearance of hypoechoic nodules.
• Hepatomegaly.

• Clinical history of excess steroids coincident with histopathological evidence of excess glycogen and in hepatocytes.

• Diffusely swollen liver.

• Glycogen accumulation in hepatocytes.
• This accumulates firstly in zone 1, but thereafter predominantly in zone 3 resulting in typical ballooning degeneration.

• Inflammatory hepatopathies.

Treatment

Top

• Specific treatment is not usually indicated.
• Withdraw exogenous steroids.
• Treat hyperadrenocorticism .
• Very occasionally other supportive therapies if in hepatic failure.

• Improved hepatic function.

Prevention

Top

• Avoid the use of glucocorticoids or use at lowest dose when possible.

Sequelae

Top

• Good - reversible on elimination of excess steroids.
• Hepatocellular glycogen slowly diminishes over time.

• Resolution of clinical symptoms of hepatic disease. Hepatic histopathology resolves - time scale depends on degree of damage.

Sources

Top

• Recent references from PubMed.
• Center S A, Warner K L, McCabe J, Foureman P, Hoffmann W E & Erb H N (2005) Evaluation of the influence of S-adenosylmethionine on systemic and hepatic effects of prednisolone in dogs. Am J Vet Res 66 (2), 330-341 PubMed.
• Rutgers H C, Batt R M, Vaillant C & Riley J E (1995) Subcellular pathologic features of glucocortcoid-induced hepatopathy in dogs. Am J Vet Res 56 (7), 898-907 PubMed.

• Scherk M A & Center S A (2005) Toxic, Metabolic, Infectious, and Neoplastic Liver Diseases. In: Textbook of Veterinary Internal Medicine. 6th edn. Eds: S J Ettinger & E C Feldman. Philadelphia: W B Saunders. pp 1464-1477.

• Nick Bexfield BVetMed DSAM DipECVIM-CA MRCVS RCVS Diplomate and European Specialist in Small Animal Medicine , The Queen's Veterinary School Hospital, University of Cambridge, Madingley Road, Cambridge CB3 OES, UK.

Back to top
© Copyright Vetstream

CANIS DIS01096

---