Sebaceous adenitis is an inflammatory dermatosis affecting the sebaceous glands resulting in destruction of the glands and resultant scarring.  It was initially described in 1987 by Drs. Rosser and Dunstan in the Standard Poodle. It has since been documented in more than 50 breeds, including the Airedale, Maltese, Havanese, St. Bernard, Toy & Miniature Poodle, Bernese Mountain Dog, Irish Setter, Collie, Samoyed, Golden Retriever, German Shepherd, English Springer Spaniel, Viszla, Doberman Pinscher, Basset Hound, Old English Sheepdog, Scottish Terrier, Akita, Miniature Pinscher, Chow Chow, Dachshund, Weimaraner, Lhasa Apso, Dalmatian and mixed breeds. The disease has also been reported in rabbits, cats and humans.

The etiology of the disease is unknown with theories including a possible defect in keratinization which destroys the sebaceous duct and glands, a defect in epidermal or sebaceous lipids, an autoimmune or hypersensitivity reaction, or an infectious cause, although no agents have ever been isolated. Research indicates a hereditary predisposition in the Standard Poodle and possibly the Golden Retriever, Samoyed and Akita.

Clinical signs
The clinical signs of SA can occur between the ages of 1-3 in the Standard Poodle, but may occur even older, as late as 8 years of age, with males and females affected equally. The patients are usually nonpruritic unless a secondary bacterial pyoderma is present. Affected long-haired breeds may present with a dry, often symmetrical seborrhea beginning on the dorsal midline, lateral pinnae, bridge of the nose, and tops of the feet. The groomer may comment that the dog's feet seem more "sensitive" when he/she is groomed. A tightly adherent gray/silver scale on the hair shafts and skin is present along with a thinned hair coat with brittle stubs.

Unfortunately, the dog could have been bred over several years before showing clinical signs of the disease, producing clinically affected offspring. At this point, the only reliable diagnosis is a skin biopsy obtained from a clinically affected area, preferably the dorsal cervical and lumbar areas.

Diagnosis
The differential diagnosis of SA includes hypothyroidism (as the scaling and alopecia are often symmetrical), bacterial pyoderma, demodicosis and idiopathic seborrhea. As mentioned above, the most reliable method of diagnosis is the skin biopsy submitted in 10 percent formalin. Unfortunately, a normal biopsy reading dose not rule out SA. If the affected areas are not biopsied, a false negative result will occur resulting in a "normal" skin biopsy reading. However at this point, a skin biopsy is all we have to diagnose SA. Other noninvasive methods of diagnosing the disease include the qualitative and quantitative measurement of skin lipids which is still investigational. Early stages of SA in a skin biopsy indicate inflammation of the sebaceous glands or duct, late stages show scarring (fibrosis) where glands used to be accompanied by hyperkeratosis.

Treatment
Therapy ranges from topicals such as baby oil, propylene glycol or other emollients to oral natural and/or synthetic Vitamin A, fatty acids and cyclosporine. Antibiotics may be needed for any secondary bacterial pyoderma.

Therapies that have proven not to be helpful include ketoconazole, zinc supplementation, and steroids. When using one of the topicals mentioned above, the patient is bathed in a keratolytic shampoo, rinsed and towel dried. Then the emollient of choice is massaged into the skin and allowed to stay on for 15-30 minutes. The keratolytic shampoo or detergent is then reapplied onto the oiled dog to solubilize the oil and the entire mixture is rinsed off. This is usually repeated at weekly intervals until a successful response is noted, then used as needed.