In-depth Information on Canine Sebaceous Adenitis
Sebaceous adenitis is an inflammatory disease of the sebaceous (oil) glands leading to the destruction of the glands. Vizlas, Akitas, poodles and Samoyeds are predisposed and the exact pathogenesis has not been established. It seems to be a genetically inherited defect and young dogs are usually affected.
In Poodles, it is believed to be an autosomal recessive mode of inheritance due to the fact that 25 percent of affected dogs may be sub-clinical. Several theories have been formulated to explain this condition: According to one theory the disease is auto-immune in nature and the sebaceous glands are targeted by the immune system and destroyed. Another theory is that the destruction of the sebaceous glands is secondary to a disease of keratinization, which leads to obstruction of the duct and ultimately disappearance of the glands. It is also hypothesized that both the adenitis and the keratinization defects are secondary to an imbalance in lipid metabolism.
Related Symptoms or Ailments to Canine SA Bacterial folliculitis (superficial pyoderma) Demodex Dermatophytosis (ringworm) Disease of keratinization Mycosis fungoides Endocrinopathies (diseases of the endocrine system) Pemphigus foliaceous Follicular dysplasia
Deep skin scrapings should be done in any dog with these clinical signs to rule out demodicosis.
Diagnosis In-depth of Sebaceous Adenitis in Dogs
The early lesions include alopecia (hair loss) with excess scaling and brittle hairs. The top of the head, the dorsal planum of the nose, dorsal neck and dorsal midline are commonly affected areas.
Sebaceous adenitits has a cyclic pattern in some dogs with periods of improvement and worsening. Symptoms are slightly different according to the type of hair coat: In short coated breeds (Vizlas), circular areas of alopecia with fine, white, non-adhering scaling are commonly the first manifestation of the disease. Infections are not common in these dogs and itchiness is usually not present. In poodles, the scales are tightly adherent and follicular casts – accumulations of keratinous debris around the hair shaft seen protruding from the follicle – are visible. In Akitas, seborrhea oleosa is usually the first sign. Greasy, yellow follicular casts are common. These animals tend to get systemically ill. Concurrent epilepsy has been reported in some dogs. Secondary bacterial infection is common, causing itchiness. In Samoyeds the most severe sign is alopecia on the trunk with follicular casts.
Diagnosis of sebaceous adenitis is made by histopathology, and several biopsies may be needed to make a final diagnosis. Biopsies should be taken from affected and non-affected skin. Subtle early lesions are most useful to document active inflammation.
Secondary bacterial infection and Malassezia dermatitis are commonly present at the time of initial evaluation. Cytology is important to determine the type and severity of the infection. Infections should be cleared before skin biopsies are taken to minimize secondary non-specific changes.
Pathological changes of the tissue vary according to the stage of the disease. At the beginning, a nodular inflammation targeting the sebaceous glands is evident. Discrete nodules of histiocytes, neutrophils and lymphocytes are seen at the site of sebaceous glands. One disease that can appear similar to the inflammatory stage of sebaceous adenitis is the sterile pyogranuloma syndrome. However, in the latter, the inflammation is less focused on the sebaceous glands and clinically it has raised firm nodules rather than with scaling and alopecia. As the disease progresses, the inflammation decreases until sebaceous glands are no longer evident. When biopsy samples are submitted, pathologists should be made aware of the suspicion of sebaceous adenitis so that multiple biopsy sections are prepared and special attention is paid to the number and shape of the sebaceous glands.
Treatment In-depth of Sebaceous Adenitis in Dogs
Treatments include anti-seborrheic shampoos, emollients, essential fatty acids, antibiotics for the secondary bacterial folliculitis, and retinoids.
Topical therapy: Keratolytic shampoos are helpful in mild cases. The most commonly used include a combination of sulfur and salycilic acid. Alternately, antibacterial products like benzoyl peroxide in combination with sulfur (OxyDex) may be beneficial. Topical propylene glycol (50 to 75 percent) diluted with water is also effective to decrease the scaling. It is used as a spray once or twice daily. Soaks with baby oil have also been reported to help in severely affected dogs. Dogs need to be shampooed several times to remove the oil from the skin.
Systemic Therapy: Essential fatty acids at high doses. Evening primrose oil at 500 mg twice daily orally. Eicosapentaenoic acid at 180 mg per 10 pounds of body weight daily orally. Vitamin A administration at 10,000 IU orally once daily has also been helpful to some dogs. Retinoids (isotretinoin [Accutane®] or acitretin [Soriatane®]) is often used in refractory cases, due to their ability of modulating epidermal growth and differentiation. Retinoids should be given for a minimum of two months. Outcome cannot be predicted on the basis of clinical signs or histologic findings and a prognosis cannot be determined on the basis of whether sebaceous glands are evident histologically.
Toxicity in animals seems to be less severe than in humans. Adverse effects include: vomiting, diarrhea, erythema, keratoconjunctivitis and stiffness. Isotretinoin (Accutane®) has been reported to be very successful in Vizlas with sebaceous adenitis. Isotretinoin has marked sebostatic activity. It decreases the proliferation of basal sebocytes and it suppresses sebum (oil) production. Other retinoids have been reported to be only moderately successful. Cyclosporines (Sandimmune/Atopica) have been used in a few cases with good success. In some dogs, good clinical response is observed in spite of absence of sebaceous glands histologically. Although cyclosporine has immunosuppressive properties (strong inhibitory effect on lymphocyte proliferation), this drug also has inhibitory effects of keratinocyte proliferation, which may be beneficial in some cases. Adverse effects include: vomiting, diarrhea, gingival hyperplasia, kidney toxicity, liver toxicity and increased incidence of bacterial infections. Systemic antibiotics may be necessary for four to six weeks.