3.12 Nutritional Related Keratinization Disorders – General Considerations
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General Considerations
- In this section, only canine zinc responsive dermatosis is discussed. Vitamin A responsive dermatosis and fatty-acid deficiencies are also associated with abnormal keratinization and cornification but these diseases are rarer or not well documented in dogs and cats. Interesting, zinc is essential for biosynthesis of fatty acids and is involved in vitamin A metabolism.
- Zinc responsive dermatosis is a keratinization disorder that responds to certain formulations of zinc supplement.
- Two syndromes have been identified. Syndrome I occurs primarily in Siberian huskies and Alaskan malamutes eating a balanced diet and most dogs are less than 2 years of age by the time they develop clinical signs. Syndrome II develops in rapidly growing puppies or young adults eating a diet deficient in zinc or diets with high concentration of calcium, iron and copper, which interfere with zinc metabolism and absorption.
- Erythema, alopecia to hypotrichosis, and tightly adhered scales and crusts develop primarily on the face, but lesions can also affect the elbows and hocks. Footpads can become hyperkeratotic and hyperpigmentation frequently develops in chronic cases. Pruritus and secondary infections are often present and aggravate clinical signs.
- Treatment involves giving zinc sulfate, zinc gluconate or zinc methionine. Ideally, the dose should be based on the amount of elemental zinc in the supplements (i.e. 2-3 mg/kg/day). An oral and short-acting glucocorticoid, such as prednisone/solone, is often added to the treatment regimen for its excellent anti-inflammatory and anti-pruritic effects. Treatment is life-long for dogs with Syndrome I. In dogs with Syndrome II, dietary correction alone may resolve clinical signs in 2-6 weeks but temporary zinc supplementation may also be required in some cases.