Zinc-responsive dermatosis are a relatively uncommon scaling skin disorder caused by frank zinc deficiency, zinc malabsorption, or improper zinc utilization.
Zinc is important in a multitude of biological functions, including regulation of the immune response, modulation of keratogenesis and wound healing, maintenance of normal reproductive function, and acuity of taste and smell.
There are a number of clinical presentations in dogs:
- Syndrome I - seen almost exclusively in northern breed dogs (i.e. Siberian Husky and Alaskan Malamute), characterized as an inherited impairment in the absorption or metabolism of zinc
- Syndrome II - rapidly growing large-breed puppies consuming a high phytate diet, zinc-deficient diet, or diet supplemented with components that may inhibit zinc absorption.
As well, a number of hereditary zinc deficiencies have been reported including nasal hyperkeratosis has been reported in Golden retrievers and congenital follicular parakeratosis in Rottweiler and Siberian Husky dogs.
Zince deficiency has also been reported in zinc-deficient commercial diets.
Both syndromes manifest clinically with mucocutaneous junction and pressure point erythema, scaling, crusting, alopecia, pyoderma and lichenification that primarily affect the head.
In severe cases, anorexia, lethargy, retarded growth, suppurative paronychia, distal limb pyoderma, and peripheral lymphadenopathy are evident. Skin lesions include generalized erythematous-crusted papules, often pruritic, accompanied by hyperkeratosis, erythema and swelling of footpads. Visual deformities such as corneal vacuoles are also reported
Diagnosis is based on histological examination of affected skin, demonstration of reduced zinc levels in blood (normal = 0.8–2.0 ppm) and response to therapy. The demonstration of low zinc concentrations in serum and hair have only a corroborative value in the diagnosis of zinc-responsive dermatosis in dogs and must be correlated with response to therapy in order to obtain a diagnosis.
A differential diagnosis would include lethal acrodermatitis which has been reported in Staffordshire Bull terriers, as well as demodectic mange, vitamin A–responsive dermatosis, erythema multiforme, lupus erythematosus and Malassezia dermatitis.
Treatment is usually successful with zinc and retinoid supplementation. Zinc can be given as a daily oral supplement as zinc gluconate (10 mg/kg/day orally), and in severe cases, an intravenous injection of zinc sulfate (10 mg/kg) may be required. Treatment should be continued for one month to determine response to treatment, and the daily dosage should be increased by 50% if the initial dosage is not effective.
Additional therapy includes antimicrobial therapy if indicated and frequent bathing with keratolytic shampoos, such as sulfur and salicylic acid, may be beneficial.
Syndrome 1 has a fair prognosis, although an underlying heritable susceptibility suggests that affected individuals not breed. Syndrome 2 has an excellent prognosis.
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