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The American College of Veterinary Nutrition<\/strong> (acvn.org<\/a>) and Today\u2019s Veterinary Practice<\/em> are delighted to bring you the Nutrition Notes column, which provides the highest-quality, cutting-edge information on companion animal nutrition, written by the ACVN\u2019s foremost nutrition specialists.<\/p>\n The primary objectives of the ACVN are to:<\/p>\n The ACVN achieves these objectives in many ways, including designating specialists in animal nutrition, providing continuing education through several media, supporting veterinary nutrition residency programs, and offering a wide array of resources related to veterinary nutrition, such as this column.<\/p>\n The influence of nutrition in dermatologic conditions is explained by critical nutrients that affect keratinization, cellular barriers, and turnover, as well as sebum production and composition.<\/p>\n Protein and amino acids provide substrates for keratinization, pigmentation, and hair growth. A substantial portion of daily protein requirements is used for skin and hair production.1<\/sup><\/p>\n Figure 1. This middle-aged domestic shorthair cat displays reddening of the fur, which may prove responsive to increased dietary protein and\/or supplementation with tyrosine or phenylalanine.<\/p><\/div>\n Polyunsaturated fatty acids provide substrate for the production of sebum, which protects the dermis and improves coat quality.a<\/sup><\/p>\n Several vitamins play critical roles in skin health.<\/p>\n Copper serves as a cofactor in enzymatic conversion of tyrosine to melanin. Deficiency can cause changes in pigmentation. Zinc is critical for the transition of nucleated epidermal cells to anucleate squamous cells in the stratum corneum, and deficiency induces parakeratosis. Zinc also participates in essential fatty acid conversion.3<\/sup><\/p>\n Commercial diets conforming to Association of American Feed Control Officials recommendations should be replete in all of the nutrients above. However, several factors could increase the relative risk for deficiencies over time:<\/p>\n Several common dermatologic signs may prove nutritionally responsive (Box 1<\/strong>). The primary cause may not always be identified, but a skin biopsy is often prudent to better characterize the lesion and to decide how best to modify a patient\u2019s diet. Knowledge of characteristic or common clinical conditions informs the possible use of nutritional intervention, and a response to a particular nutritional therapy is often used to confirm a presumptive diagnosis.<\/p>\n Pruritus<\/p>\n Recurrent pyoderma<\/p>\n Dull hair coat<\/p>\n Epidermal scaling<\/p>\n Urticaria<\/p>\n Keratinization disorders<\/p>\n Concurrent gastrointestinal signs<\/p>\n Coat color change<\/p>\n Chronic otitis<\/p>\n Miliary dermatitis (in cats)<\/p>\n Alopecia<\/p>\n<\/div>\n In dogs, zinc-related dermatoses are characterized by parakeratotic hyperkeratosis of the face and feet, with resultant crusts and lesions (Figure 2<\/strong>).10<\/sup> These dermatoses include lethal acrodermatitis in bull terriers and zinc-responsive dermatosis syndromes I and II. Characteristics of these conditions are presented in Box 2<\/strong>.<\/p>\n Figure 2. Zinc-responsive dermatosis syndrome 1 in a young Siberian husky. Courtesy Dr. Dunbar Gram.<\/p><\/div>\n Serum and hair testing are unreliable measures of zinc status, so supplementation of dogs with characteristic lesions, especially in breeds associated with zinc-responsive dermatosis syndrome I, is advised. Zinc gluconate is well tolerated and efficacious, but some clinicians prefer zinc methionine because of increased availability.\u00a0 The relative amount of elemental zinc for different supplements is found in Table 1. Vomiting is the most common, and generally dose-dependent, side effect of zinc supplementation, and several forms may need to be tried at varying doses to assess individual tolerance.<\/p>\n Dermatosis responsive to vitamin A is a rare, presumably heritable, condition of dogs. Lesions are characterized by abnormal cornification, hyperkeratotic plaques, abnormal sebum, epidermal scaling, alopecia, and secondary pyoderma (Figure 3<\/strong>). Biopsy specimens are consistent with orthokeratotic and follicular hyperkeratosis.13<\/sup> Cocker spaniels are the most affected breed, but other breeds are also rarely affected.14<\/sup> Oral retinol (vitamin A) is reported to ameliorate clinical signs, but the optimal dose is unknown (authors have suggested 10,000 IU\/dog q24h or 1000 IU\/kg q24h).4,13<\/sup> Synthetic retinoids have been reported in the treatment of primary keratinization disorders but are unlikely to be necessary in cases of true vitamin A dermatosis; moreover, the side effect profiles of these drugs warrant their use only by those familiar with their administration.<\/p>\n Figure 3. Vitamin A\u2013responsive dermatosis lesions in cocker spaniels. Courtesy UF Veterinary Dermatology.<\/p><\/div>\n This condition, also called migratory necrolytic erythema or superficial necrolytic dermatitis, is diagnosed infrequently in dogs and, very rarely, cats with liver dysfunction, chronic phenobarbital exposure, diabetes mellitus, or pancreatic tumors (such as glucagonomas).4,15,16<\/sup> The syndrome has been reported in older dogs of many breeds, and evidence exists for a possible heritable predisposition in shih tzus.16<\/sup><\/p>\n Elevated alkaline phosphatase and microcytosis are laboratory findings reported in case series, but liver values may be normal. Histologic lesions are unique with parakeratotic hyperkeratosis (\u201cred\u201d layer), pale and edematous keratinocytes in the stratum granulosum and stratum spinosum (\u201cwhite\u201d layer), and stratum basale hyperplasia (\u201cblue\u201d layer). Distribution of lesions is similar to that in zinc dermatoses but of increased severity, and affected animals generally display nonspecific systemic signs (lethargy, inappetence) or risk factors described above (Figure 4<\/strong>). Plasma amino acid levels are often below reference intervals.17<\/sup> Hepatic ultrasonography may reveal diffuse mottling or a reportedly characteristic \u201cSwiss cheese\u201d or \u201choneycomb\u201d appearance. Median survival times with supportive treatments are less than 6 months.16<\/sup><\/p>\n Figure 4. Hepatocutaneous syndrome lesions of the nasal planum and feet with characteristic severe crusts and secondary inflammation. Courtesy UF Veterinary Dermatology.<\/p><\/div>\n Reported treatments include16<\/sup>:<\/p>\n Parenteral amino acid infusions appear to have the greatest effect on the condition, and one report suggested a reduced frequency of administration with concurrent parenteral lipid administration (2.4 g\/kg amino acids + 1.4 g\/kg lipid).18<\/sup> The underlying cause, if identified, should be concurrently managed. High-protein diets should not be given to dogs with hepatic encephalopathy.<\/p>\n This condition is associated with diets high in polyunsaturated fats, such as canned seafood, that are deficient in vitamin E. Affected cats display reluctance to move and pain and are often febrile. Pansteatitis is evident grossly, and ceroid deposits within affected subcutaneous fat are characteristic of this condition (Figure 5<\/strong>).19<\/sup><\/p>\n Figure 5. Nodular pansteatitis of the mesenteric fat (top) and subcutaneous fat (bottom). Courtesy of Mike Schaer, DVM, DACVIM, DACVECC, University of Florida.<\/p><\/div>\n The vitamin E requirement is mildly increased as the polyunsaturated fat concentration of the diet increases (<5 IU per g of marine oil).20<\/sup> Improper food storage, heat processing, or inadequate vitamin E in high-fat diets all increase the risk for the condition, as the degree of fatty acid oxidation is likely correlated to risk.20<\/sup><\/p>\n These disorders are characterized by cutaneous manifestations of food intolerance or food allergy. Adverse reactions to food may also cause gastrointestinal, respiratory, or systemic signs, which are reviewed elsewhere.21,22<\/sup> Owners commonly ascribe dermatologic symptoms to food allergy, but atopic dermatitis (AD; see Nutritional Considerations in Diagnosing and Managing Atopic Dermatitis<\/strong>) is more prevalent. Owners also often insist that dietary modification be made even when a dietary origin of clinical signs is unlikely.<\/p>\n Food intolerance could result from many individual predispositions, but by definition, it is nonimmunologic in origin.22<\/sup> Gastrointestinal signs are most commonly ascribed to food intolerance.<\/p>\n Dermatologic manifestations of food intolerance are presumptively related to dietary compounds that worsen the response to another disease, such as AD. Examples may include38<\/sup>:<\/p>\n Some foods may increase endogenous histamine release via activation of enzymatic pathways of histamine production.<\/p>\n Trials of diets with different primary, even if not novel, ingredients should be sufficient to determine whether food intolerance is responsible for cutaneous signs.<\/p>\n Food allergy is an inappropriate immunologic response to dietary antigens.21<\/sup> Clinical signs may include erythema, epidermal scaling, patchy alopecia, miliary dermatitis (in cats), recurrent pyoderma, and urticaria (Figure 6<\/strong>). Many dogs with food allergy display perianal pruritus.24<\/sup> Concurrent gastrointestinal signs are variably present. Signs are often nonseasonal and unresponsive to immunosuppressive corticosteroids.<\/p>\n\n
\n<\/div>\n<\/div>\nNutrients<\/strong><\/h2>\n
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Clinical Conditions<\/h2>\n
Box 1. Dermatologic Signs That May Respond to Nutritional Management<\/h3>\n
Zinc-Related Dermatoses<\/strong><\/h3>\n
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<\/a><\/p>\nBox 2. Characteristics of Zinc-Related Dermatoses<\/h3>\n
Lethal acrodermatitis of bull terriers11<\/sup><\/h3>\n
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Zinc-responsive dermatosis syndrome I3,10<\/sup><\/h3>\n
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Zinc-responsive dermatosis syndrome 23,12<\/sup><\/h3>\n
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Vitamin A\u2013Responsive Dermatosis<\/strong><\/h3>\n
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<\/a>Hepatocutaneous Syndrome<\/strong><\/h3>\n
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Vitamin E Deficiency in Cats<\/strong><\/h3>\n
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<\/a>Diet-Related Dermatoses<\/strong><\/h3>\n
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