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Thursday, March 31, 2011

Steroid Hepatopathy

Reversible vacuolar change in hepatocytes in dogs, associated with glucocorticoid treatment, hyperadrenocorticism (iatrogenic or spontaneous), or chronic illnesses in other organ systems; typified by high ALP activity without signs of hepatic insufficiency

Glucocorticoids—cause reversible glycogen accumulation in hepatocytes within 2–3 days after administration; injectable and reposital forms usually induce more severe changes than do oral forms; topical, ocular, cutaneous, and aural administration may also produce an effect
Cell swelling—leads to parenchymal enlargement and hepatomegaly
Response (dogs)—marked individual variation related to the type, route, dosage, duration of treatment, and individual sensitivity; may develop even with low-dose, short-term oral medication
May develop with systemic diseases not related to glucocorticoid exposure or hyperadrenocorticism
Association with significant nonhepatobiliary health problems that involve inflammation—suggests a relationship with stress (endogenous glucocorticoid release) or acute phase reactants

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