Presentation Description / Summary: Glucocorticoid-type Vacuolar Hepatopathy is the most common histologic lesion identified in the canine liver. Histologic assessment includes severity scoring and desigation of degenerative change. Chronic progressive degenerative G-VH can evolve cirrhosis. Causal associaitons with G-VH include exposure to glucocorticoids, progestins,nutritional supplements contaminated with endocrine tissue, certain drugs (i.e., d-Penicillamine), breed related metabolic proclivities, and a wide spectrum of chronic illnesses. Chronic G-VH also associates with gallbladder mucocele syndrome, risk for dysplastic hepatic foci and hepatocellular carcinoma, may be mistaken for hepatocutaneous hepatopathy, and often associates with necroinflammatory liver disesae.. In some dogs, moderate-to-severe G-VH causes depletion of GSH and GSH:GSSG ratio. Details from several studies will be illustrated and discussed, elucidating propriety for administration of bioavailable SAMe as a supportive therapy. However, SAMe cannot reduce VH lesions nor glycogen accumulation.. A diagnostic strategy is presented to best investigate causal factors and risks associated with G-VH.
Learning Objectives:
Increase their skill in interpreting histologic grading/description of the G-VH lesion and recognize overlapping syndromes.
Know how to prioritize abdominal ultrasound imaging, adrenal function assessments, hepatic aspiration cytology, and liver biopsy in dealing with this disorder.
Realize the oxidative impact of this lesion and why bioavailable SAMe is recommended as supportive care, and acknowledged that SAMe will not rectify the G-VH lesion.
