Vitamins and Minerals for Integumentary Disease in Animals

Naturally occurring and synthetic compounds with vitamin A activity include retinol, retinoic acid, and retinol derivatives or analogues. At the molecular level, retinoids are important in regulation of proliferation, growth, differentiation, and maintenance of epithelial tissues. Retinoids also affect proteases, biosynthesis of mucopolysaccharides, prostaglandins, cellular adhesion, cellular communication, and immunity. They prevent tumor promotion by inhibition of ornithine decarboxylase, a key enzyme for cell proliferation and differentiation. Vitamin A (1,000 U/kg) has been used for follicular keratosis in cats. However, the retinoids used most commonly are isotretinoin (13-cis-retinoic acid) and etretinate (no longer available but replaced with acitretin, a metabolically active metabolite of etretinate).

Isotretinoin is indicated for Schnauzer comedone syndrome, ichthyosis, feline acne, sebaceous adenitis, epitheliotropic lymphoma, keratoacanthoma, and sebaceous gland hyperplasias and adenomas. The dosage is 1–3 mg/kg, PO, every 24 hours. Adverse effects include conjunctivitis, mucocutaneous drying, alopecia, pruritus, hyperactivity, vomiting, and diarrhea. In dogs, blood chemistry abnormalities not normally associated with clinical disease include plasma cholesterol concentration, triglycerides concentration, ALT activity, AST activity, and alkaline phosphatase activity. Rarely, keratoconjunctivitis sicca may develop in dogs. Conjunctivitis, anorexia, diarrhea, and vomiting are the major adverse effects in cats. All retinoids are potent teratogens, and teratogenicity may persist for up to 2 years after treatment with etretinate because the half-life is approximately 100 days. Skeletal abnormalities that may be evident with long-term treatment, including premature closure of the epiphyses in growing animals, cortical hyperostosis, periosteal calcification, and long-bone demineralization, are less common with etretinate than with isotretinoin. Monitoring during long-term treatment should include complete physical examination and serum biochemical analysis at monthly intervals for the first 3–4 months and then every 4–6 months.

Zinc is an important factor of many enzyme systems and is necessary for maintenance of growth, metabolism, normal reproduction, and hormonal regulation. It is essential for keratinization and immune function. Zinc supplementation is administered in cases of insufficient intestinal absorption, including deficiency syndrome I (Siberian Huskies and Alaskan Malamutes) and syndrome II (rapidly growing dogs on zinc-deficient diets). Dietary deficiency may be either absolute or relative—diets high in phytates or minerals may inhibit zinc absorption. For syndrome I, zinc supplementation is administered as 1 mg of elemental zinc/kg, PO, every 24 hours (zinc sulfate 10 mg/kg, zinc gluconate 5 mg/kg, or zinc methionine 1.7 mg/kg). Supplementation is typically lifelong. If the response is insufficient after 4 weeks, the dose should be increased by 50%. Low-dose corticosteroids may also enhance zinc absorption via induction of metallothionein in some nonresponsive cases. Animals with syndrome II normally respond to correction of the diet with resolution within 2–6 weeks, although supplementation speeds this process.

Hereditary zinc deficiency associated with deficient intestinal absorption has also been reported in Friesian, Danish Black Pied, and Shorthorn cattle. There is a rapid response to zinc oxide (0.5 g, PO, every 24 hours) or zinc sulfate (2 g, PO, every 7 days). Response to zinc supplementation is usually rapid (a few days) except for cases of achromotrichia, which requires several weeks for resolution.

• Also see pet health content regarding drugs used to treat skin disorders.