Web Chapter 53 Treatment of hepatic disease incorporates the following general principles: • Address the underlying cause, if known (e.g., withdrawal of a hepatotoxic drug) • Reduce and prevent inflammation • Reduce and prevent copper accumulation, if applicable • Reduce and prevent oxidative damage • Treat complications as needed (e.g., hepatic encephalopathy, coagulopathy, gastric ulceration, fluid/electrolyte disturbances, ascites, and infection/endotoxemia) Vitamin E refers collectively to the antioxidant compounds known as tocopherols and tocotrienols. α-Tocopherol is the most biologically active form of vitamin E. The D stereoisomer is abundant in nature, where it is synthesized by plants. Synthetic vitamin E contains D and L stereoisomers of α-tocopherol (Matthai, 1996). Food sources of vitamin E include vegetable oils, nuts, seeds, and grains. Because the various vitamin E isomers have differing biologic activities, preparations of vitamin E are standardized to international units (IU). One IU is equivalent to the activity of 1 mg of synthetically prepared dl-α-tocopherol. Vitamin E is fat soluble and requires bile and pancreatic juice for maximal intestinal absorption. High dosages of vitamin E may interfere with absorption of other fat-soluble vitamins and may predispose to development of vitamin K–dependent coagulopathy. Vitamin E supplementation traditionally has been thought harmless; however, a recent metaanalysis of vitamin E use in humans with various diseases revealed that supplementation at dosages greater than 150 units/day was associated with increased all-cause mortality. This finding led to recommendations against vitamin E supplementation, particularly at dosages above 400 units/day (Miller et al, 2005). In experimental animal models silymarin has been shown to ameliorate hepatic injury secondary to acetaminophen, carbon tetrachloride, radiation, iron overload, alcohol, cold ischemia, and the death cap mushroom (Amanita phalloides). Indeed, silymarin is so effective at reducing A. phalloides toxicosis by preventing hepatocyte uptake of mushroom toxins in humans and dogs that an intravenous formulation has been developed specifically for the purpose of treating mushroom poisoning in humans (Seeff et al, 2001). In veterinary medicine, clinical trials evaluating efficacy of silymarin in dogs and cats with naturally occurring hepatic disease have not been published. A silybin-phosphatidylcholine complex given to normal cats was found to be safe and demonstrate antioxidant activity (Webb et al, 2012). Dosage recommendations reported in conference proceedings vary, but 20 to 50 mg/kg every 24 hours orally (dogs and cats) commonly is recommended. A veterinary product is now available containing silybin bound to phosphatidylcholine for improved gastrointestinal absorption (Marin, 5 to 10 mg/kg every 24 hours orally).
Hepatic Support Therapy
Antioxidants
Vitamin E
Milk Thistle (Silymarin)
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