This disease is uncommon in dogs and rare in cats. The cause is unknown, but the strong predisposition of certain canine breeds to develop the disease suggests that genetics plays a role. The proposed pathogenesis includes cell-mediated immunologic destruction of the sebaceous gland; a primary cornification disorder of the glandular duct, resulting in obstruction and secondary inflammation of the gland; an anatomic defect of the sebaceous gland, leading to lipid leakage and a foreign body reaction; or an abnormal lipid metabolism, leading to glandular destruction. Predisposed canine breeds include Standard Poodles, Akitas, Samoyeds, and Vizlas; however, various other breeds can be affected. Lesions typically affect the pinnae, forehead, face, and dorsal trunk and are characterized by alopecia and adherent scales that cast hair shafts. The severity and characteristics of clinical signs vary among breeds. Pruritus is variable and mostly associated with secondary bacterial infection. Histopathologic findings include diffuse absence of sebaceous glands, granulomatous to pyogranulomatous inflammation at the site of previous glands, and follicular keratosis. Currently, the most efficacious therapy for sebaceous adenitis is oral cyclosporine (5 mg/kg, sid). Oral vitamin A or synthetic retinoids (eg, iso-tretinoin or acitretin) may be efficacious in some cases. The combination of tetracycline and niacinamide is an option for milder cases or when owners are concerned about costs and/or adverse effects associated with cyclosporine or retinoids. Palliative therapy for all cases includes keratolytic shampoos followed with an emollient rinse and omega-3 and omega-6 fatty acids. To help soften the adherent scales, a mixture of propylene glycol and water can be sprayed on the animal's coat and allowed to act for 2–3 hr before bathing with a medicated shampoo.
Last full review/revision July 2011 by Sheila Torres, DVM, PhD, DACVD; Scott A. Dee, DVM, MS, PhD, DACVM