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Pe How treat Sebaceous Adenitis

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					                                  81st Western Veterinary Conference



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How I Treat Sebaceous Adenitis
John C. Angus, DVM, DACVD
Animal Dermatology Clinic, Pasadena, CA, USA

WHAT IS SEBACEOUS ADENITIS?
Sebaceous adenitis is an idiopathic, immune-mediated disease caused by inflammation targeting
sebaceous glands. Sebaceous glands produce an emulsion of triglycerides, fatty acids, cholesterols,
sphingolipids, ceramides, and esters that are essential for normal structure and function of hair, hair
follicles, and the nearby epidermis. In addition sebaceous glands contribute antimicrobial peptides and
immunoglobulins that contribute to local passive immunity. Destruction of sebaceous glands and loss of
this emulsion results in significant disruption of normal appearance and function of the skin and hair.

RECOGNITION AND DIAGNOSIS
Sebaceous adenitis has been described in more than 50 breeds and mixed breeds, but is most common in
the Standard Poodle, Akita, Samoyed, Chow Chow, and Vizsla. In long coated breeds, there is gradual
progression from mild, dry haircoat in patches typically with a dorsal distribution on the convex aspect of
the pinna, back of head, neck, and shoulders region. This progresses to waxy follicular casts, matting of
the hair, alopecia, and extensive scale formation. With time the disease may affect the face, trunk, tail, and
limbs. Some patients, particularly Akitas, have more severe and extensive granulomatous inflammation
and may experience systemic signs of chronic inflammation, including fever, malaise, and weight loss.
Pruritus is variable, but when present may be intractable. Malodorous secondary bacterial folliculitis or
pyoderma is common. Distribution, progression, and severity of both cutaneous and systemic disease are
highly variable between individuals. In short-coated dogs, sebaceous adenitis causes a patchy alopecia in
“moth-eaten,” annular, serpiginous, or geographic patterns. Typically inflammation is mild with minimal
pruritus or systemic signs.
      Differential diagnoses are bacterial folliculitis and demodicosis, dermatophytosis, endocrinopathy,
pemphigus foliaceus, Zinc responsive dermatosis, vitamin A-responsive dermatosis, ichthyosis, and
nutritional deficiencies. Diagnosis is based on ruling out other causes with cytology, skin scraping, and
dermatophyte culture and confirmation by biopsy. Collect 3–6 sections with 4–8mm punch, which
represent different stages and appearances. Use a dermatopathologist, inform them of your suspicion of
sebaceous adenitis and request specific comment on condition of the sebaceous glands.

TREATMENT
There are two goals of therapy: 1) restore normal function by neutralizing the consequences of sebaceous
gland destruction and loss of function, and 2) arrest ongoing inflammation and destruction of remaining
sebaceous glands. Engaging one goal and not the other will consistently result in poor response and
treatment failure. Curiously the more aggressively veterinarians employ topical therapy aimed at goal # 1
is employed, the less aggressively veterinarians need to apply immune suppressive therapy for goal #2.
This may be due to a cyclical feedback in pathogenesis and progression of disease, where secondary
infection, dysfunction of epidermal barrier, and plugging of follicle and sebaceous ducts contributes to
ongoing sebaceous gland inflammation.
      Topical therapy is critical for goal #1. The first task is to remove adherent waxy casts, scale, and
open plugged follicles with antiseborrheic shampoo therapy applied as often as 3–4 times per week.
Phytosphingosine, sulfur, salicylic acid, and benzoyl peroxide are potentially useful ingredients. If one
ingredient or shampoo is not sufficient try various combinations to improve outcome in each individual
patient. Clipping facilitates treatment and is recommended for all long-coated dogs. A soft brush may
assist removal of dead hair and scale. Inclusion of a systemic antibiotic and/or antiseptic topical shampoo
(chlorhexidine or benzoyl peroxide) assists in management of secondary bacterial infection.
      The second task for goal #1 is replacement of epidermal lipids and restoration of normal
desquamation and epidermal barrier function through aggressive use of topical emollients and
humectants. After bathing with an antiseborrheic shampoo, apply a 50:50 mix of bath oil (Alpha Keri or
generic) and warm water (1 cup each) directly the skin by pour on or spray bottle. This will result in a
very slippery and oil-soaked dog. Place dog in crate or otherwise confine with the oil on the skin for 2
hours. Then remove the oil with 3–7 baths with shampoo or Palmolive or Ivory dishwashing soap. Apply
a final humectant rinse. Warn owners that initially there will be increased hair loss as dead hairs are freed
from wax-encased follicles as well as increased scale as tightly adherent scales comes off the skin but are
caught in the coat. Repeat every 7 days for 4–6 weeks, until new hair growth is observed then decrease to
every 2–4 weeks. This protocol is labor intensive, but produces excellent results.
       In between baths, spray-on therapy with emollients such as 50:50 mix of propylene glycol and
water, or 0.2% phytosphingosine spray (Douxo Seborrhea Microemulsion Spray, Sogeval) can be very
effective in restoring and maintaining healthy skin and hair in dogs with sebaceous adenitis. A novel,
antiseborrheic product is a 1% phytosphingosine pipette (Douxo Seborrhea Spot-on, Sogeval). Apply in 2
or 3 spots to shoulders and lumbar area once weekly for 3–4 weeks: 1 pipette (<20 kg), 2 pipettes (21–45
kg), or 3 pipettes (>45 kg).
       Anti-inflammatory or immune-suppressive therapy is often necessary to stop ongoing destruction
of sebaceous glands and progression of disease (goal #2). Most dogs receive an initial course of therapy
until inflammation stops and progression is arrested, then therapy is gradually tapered to the lowest dose
and frequency that maintains remission. Like other immune-mediated diseases, if therapy is tapered
abruptly, or discontinued, inflammation and destruction recurs. In most cases, dogs continue to receive
some form of anti-inflammatory or immune-suppressive therapy for the rest of their lives.
       Oral cyclosporine (Atopica, Novartis) is currently the systemic treatment of choice for sebaceous
adenitis; initial protocol is 5mg/kg twice daily then gradual taper to the lowest frequency that maintains
remission. Taper by reducing the number of days given by one day per week every 2–4 weeks (i.e., give
5mg/kg BID 7 days per week, then 6 days per week, then 5 days per week, etc). One study showed
reduction of inflammation and regrowth of sebaceous glands from 2% to 40% of hair follicles in 12
months (Linek M, 2005). Other protocols include Tetracycline and Niacinamide (<10kg dogs receive
250mg Tetracycline and 250mg Niacinamide three times daily; >10kg dogs receive 500mg Tetracycline
and 500mg Niacinamide TID). Be sure owner is administering Niacinamide and does not ever substitute
Niacin. Avoid in dogs with previous seizure disorder. Sebaceous Adenitis is poorly responsive to
immune suppression with corticosteroids. However, consider corticosteroids if pruritus is a major clinical
feature (prednisone 2 mg/kg/day for 2–4 weeks then taper and withdrawal); even this may not resolve
pruritus. More aggressive protocols such as azathioprine, chlorambucil, gold salts, Cytoxan are not
recommended except in the most refractory cases, after all other therapies, including synthetic retinoids
and topical protocols, have failed. In most cases there is no need for this level of immune-suppression,
nor is there an indication that such therapy would be more effective.

OTHER THERAPY
Oral essential fatty acid supplementation is commonly included in therapy protocols and is unlikely to
harm the patient. Omega VI fatty acids (sunflower seed oil, safflower seed oil) are more important for
normal epidermal structure and function than Omega III fatty acids (fish oil, flax seed oil, evening
primrose); however, the anti-inflammatory action of Omega III fatty acids may be beneficial as well.
      Vitamin A and synthetic retinoids bridge the gap between the two goals of arresting ongoing
disease and restoring functionality. Retinol and retinoic acid play a vital and complex role in normal
epidermal, hair follicle, and sebaceous gland function. Vitamin A at 8,000 to 10,000 IU BID is a good
adjunctive therapy that may facilitate clinical improvement; if no improvement is seen in 3 months,
increase to 20,000 to 30,000 IU BID, not to exceed 1000 IU/kg/day. Dry, inflamed lips are an early sign of
toxicity. Synthetic retinoids isotretinoin (Accutane, Roche) and acitretin (Soriatane, Connetics) can be very
effective in management of refractory sebaceous adenitis. The isotretinoin protocol is 1mg/kg PO q 12 or
24 hours for 6 weeks, then decrease to 0.5–1.0mg/kg q 48 hours for maintenance. If one does not induce
substantial improvement in 6 weeks try the other. Because of high costs, handling concerns, and potential
side-effects, the author rarely starts with synthetic retinoids, and uses them only in the rare case that does
not respond satisfactorily to other therapy.
REFERENCES
1.   Blair GL. Home therapy of sebaceous adenitis. internet http://www.vipoodle.org/docs/hmrxsa.htm
2.   Linek M, et al. Effects of cyclosporine A on clinical and histologic abnormalities in dogs with sebaceous adenitis,
     J Am Vet Med Assoc 226:59, 2005.
3.   Rosser EJ. Sebaceous adenitis. In Bonagura JD, Twedt DC, ed Kirk’s Current Veterinary Therapy XIV. St Louis:
     Saunders Elsevier, 2009: 451–453.
4.   Sousa CA. Sebaceous adenitis. Vet Clin Small Anim, 36:243–249, 2005
                                                             

				
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