Glands sakes! Diagnosing and treating sebaceous adenitis in dogs
Sebaceous adenitis is a skin disease that causes the destruction of sebaceous glands. These glands produce a fatty secretion called sebum that lubricates the skin and has antimicrobial properties. Damaged sebaceous glands can cause a decrease or cessation of sebum flow and can ultimately lead to scaling, follicular plugging and progressive hair loss. In severe and chronic cases, the sebaceous glands can be completely destroyed.
The true pathogenesis of the disease is unknown at this time, though a number of theories exist. Hypotheses include a primary or secondary keratinization defect, an inflammatory disease of the sebaceous glands, a lipid metabolism abnormality, idiopathic disease or a destructive autoimmune response against sebaceous glands. A genetic or hereditary basis for the disease is likely in predisposed breeds, including the standard poodle, vizsla, Akita, Samoyed, Havanese, English springer spaniel and dachshund.
Idiopathic sebaceous adenitis has been diagnosed in more than 50 purebred dog breeds and mixes, and dogs typically present between 1 and 5 years of age. The pathogenesis likely differs within breeds and individual animals since there is variability in age of onset, clinical presentation and response to therapy.
In addition to dogs, sebaceous adenitis has been described in cats, rabbits, horses and humans. However, the condition is rare in cats and is therefore not well described. Typical clinical signs in cats include changes in hair coat quality, crusting, scaling and alopecia.
The clinical signs are variable and are often divided into two presentations:
Long-coated form. Clinical signs start with skin lesions and hair loss on the head, ear flaps, and muzzle and often progress along the dorsal part of the body. Lesion distribution is usually bilaterally symmetrical. Common early abnormalities include mild scaling, dull or brittle hair, hair thinning and changes in hair pigment. As lesions progress, scaling becomes more severe (thick silver or white) and hair becomes more matted with follicular casting. The patient’s skin can also become erythematous, with some papules and pustules as secondary infections develop. Rarely, fever and weight loss are reported. Breed examples include the standard poodle, Akita, German shepherd, Havanese and Samoyed.
Short-coated form. Clinical signs often present as multifocal to coalescing patches of hair loss with scaling (also referred to as a “moth-eaten” appearance). Some dogs will present with nodular lesions and plaques without the classical scaling and crusting. Breed examples include the vizsla and dachshund.
A variety of differential diagnoses should be ruled out, including superficial pyoderma, demodicosis, dermatophytosis, primary seborrhea, ichthyosis, follicular dysplasia and endocrinopathies like hypothyroidism and hyperadrenocorticism.
Here are the components you’ll need to dig down to a diagnosis:
> Detailed history and examination
> Skin cytology—secondary infection should always be treated
> Bacterial culture—if skin condition has not responded to first-line antibiotics and there is still evidence of secondary infection
> Skin scraping—to rule out demodicosis
> Trichogram—can also be used to rule out demodicosis; hairs with marked follicular casting often contribute to a greater suspicion of sebaceous adenitis
> Fungal culture—to rule out dermatophytosis
> Biopsy for dermatohistopathology—multiple samples should be taken to obtain adequate numbers of adnexal units
- Early lesions: discrete granulomas in areas of sebaceous glands; perifollicular inflammation targeting sebaceous glands; no involvement of other adnexa
- Chronic lesions: fibrosis replaces absent sebaceous glands; hyperkeratosis and follicular plugging may be seen
Sebaceous adenitis is primarily a cosmetic disease and isn’t particularly bothersome to the pet unless there is an associated secondary infection. All modes of therapy (topical and oral) are intended to slow the disease progression and manage the skin condition. Additionally, treatment with appropriate antibiotics and antifungals is necessary if a secondary bacterial or yeast infection is present.
> Oral omega-3 fatty acid supplementation daily—typically, 180 mg of combined eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) per 5 kg of body weight
> Topical therapy: keratolytic shampoos and emollient rinses; humectants every two to four days (Douxo Seborrhea shampoo and spray and Dechra DermAllay shampoo and spray are products that have been used with success)
> Oral omega-3 fatty acid supplementation daily—typically, 180 mg of combined EPA and DHA per 5 kg of body weight
> Propylene glycol (50%-70%) spray or water-based moisturizing spray daily (we typically recommend a 50-50 mixture of water and propylene glycol)
> Baby or mineral oil soaks (two to three hours) followed by bathing to remove excess oil; repeat weekly until condition has improved and then every two to four weeks for maintenance
Additional oral therapies:
> Vitamin A: 1,000 IU/kg orally every 24 hours with a maximum daily dose of 20,000 IU/kg to minimize adverse effects
- Schirmer tear testing should be performed on a regular basis since retinoids can alter the lipid content of the tear film, causing increased tear evaporation and qualitative tear film abnormalities.
> Tetracycline and niacinamide
- Dogs weighing less than 10 kg: 250 mg of each orally every eight hours
- Dogs weighing more than 10 kg: 500 mg of each orally every eight hours
- Doxycycline (5-10 mg/kg every 12 hours) can be used instead of tetracycline
> Prednisone: 2 mg/kg orally every 24 hours until lesions are controlled, then tapered slowly to reach the lowest dose (typically every other day) that controls clinical signs
> Isotretinoin (first-generation synthetic retinoid): 1-1.5 mg/kg orally every 12 to 24 hours until lesions are improved, then tapered to every 24 to 48 hours or 0.5 mg/kg every 24 hours
- Has potent sebostatic effects—effectively decreases scaling and alopecia in around 50% of cases
- Can be expensive and teratogenic, so there are tight regulations in the United States
- Liver enzyme activities should be monitored every two weeks during induction
> Cyclosporine (Atopica—Elanco): 5 mg/kg orally every 24 hours
- The only treatment that may lead to sebaceous gland regeneration
- Improvement in clinical signs is typically used to determine response to therapy
- The frequency of administration is decreased to the lowest effective dose once remission is reached
Sebaceous adenitis is a disease that needs to be monitored on a regular basis, especially in the early treatment phases. Bloodwork should be checked at recommended intervals when patients are on long-term steroids, cyclosporine and retinoids. In addition to formulating and adjusting medication protocols, ongoing client communication is extremely beneficial to the success of treatment.
The prognosis for sebaceous adenitis is variable, as it depends on when the disease is diagnosed, control of secondary infections, response to therapy and client compliance. The majority of dogs show some improvement within three to four months of starting treatment, but it’s important to inform clients that treatment is lifelong.
The intensity and cost of the treatment plan will vary from case to case, and since there are many forms of therapy available, owners have a variety of options to choose from if the first treatment protocol isn’t effective. Some cases of sebaceous adenitis have been refractory to treatment, which could be related to chronicity of disease or concurrent disease.
This is a disease that will need to be managed for the duration of a dog’s life. Owners should be made aware that sebaceous adenitis is not curable but there are a variety of therapies that have been successful in managing the disease.