Steroid hepatopathy in dogs

Hepatic Lipidosis Most common form of severe liver disease in cats. Most often seen in obese cats suddenly subjected to dietary deprivation. May also be associated with diabetes mellitus, drug injury and toxicity. Thedisease seems to result from the sudden mobilisation of the bodies fat stores which quickly overwhelms the liver's ability to process the raw fat into useful nutrients. The fat accumulates in the liver rapidly and causes acute liver failure. The end result is a swollen, greasy liver which is fragile and yellow to see. The cats present with complete lack of appetite and many signs of acute liver failure. Treatment is based on the provision of a highly nutritious diet to provide the energy required to run the body, stop the ongoing mobilisation of the fat stores, and drive the liver to decrease the fatty accumulation in the liver. Treatment is difficult and a long process.

Zycortal® (Dechra Veterinary Products) is indicated for replacement therapy for mineralocorticoid deficiency in dogs with primary hypoadrenocorticism.  Zycortal contains desoxycortone pivalate (DOCP) – an aldosterone analogue with purely mineralocorticoid effect.  Zycortal is available as a prolonged-release suspension for subcutaneous injection and the dosing interval is approximately 25 days.  The exact dose to be given and the interval between treatments depend on the dog’s clinical response as well as sodium and potassium levels.  A glucocorticoid (. prednisolone) is also needed daily to replace the missing cortisol.  To obtain a Monitoring and Dose Adjustment Flowchart, or for further advice, contact Dechra by e-mailing technical@.

Dogs are particularly susceptible to development of glucocorticoid-induced hepatopathy, but the mechanisms are not well understood. We investigated the pathogenesis of glucocorticoid hepatopathy by examining sequential morphologic and biochemical changes in the liver of dogs during steroid administration. Six adult Beagles were given prednisolone acetate (4mg/kg of body weight, once daily for 24 days IM). Serum samples and percutaneous liver biopsy specimens were obtained before the start of the study (treatment day [TD] 0) and at TD 5, 10, 15, and 25. There were significant (P < ) and progressive increases in serum activities of alkaline phosphatase, gamma-glutamyltransferase, and alanine transaminase. Light microscopic changes in liver biopsy specimens included progressive hepatocellular swelling and vacuolation. Electron microscopy revealed glycogen accumulation, peripheral displacement of organelles, and prominent dilatation of bile canaliculi, compared with findings at TD 0. Liver biopsy specimens taken at TD 25 had significantly (P < ) increased activities of the plasma membrane enzymes, alkaline phosphatase and gamma-glutamyltransferase, and 5'-nucleotidase was significantly (P < ) decreased. Subcellular fractionation on reorientating sucrose density gradients revealed high-density peaks of alkaline phosphatase and gamma-glutamyltransferase, compatible with a specific increase in the biliary canalicular component of the enzyme activities. Neutral alpha-glucosidase activity was shifted to the denser fractions, indicative of an increase in the proportion of rough to smooth endoplasmic reticulum and consistent with enhanced synthesis of plasma membrane proteins. There also was evidence for progressive increase in fragility of intracellular organelles, particularly lysosomes. These findings indicate that glucocorticoid hepatopathy in dogs is associated with progressive alterations not only to the plasma membrane, but also to other subcellular organelles.

Steroid hepatopathy in dogs

steroid hepatopathy in dogs

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