Dr. Marsella is a board-certified veterinary dermatologist and full professor at the University of Florida. She has authored more than 150 peer-reviewed articles and has written several books (Manual of Equine Dermatology and Clinical Approach to Feline Dermatologic Diseases) and contributed to many others as either author or author and editor (e.g., BSAVA Manual of Canine and Feline Dermatology). She has served as president of the American College of Veterinary Dermatology and co-editor of Veterinary Dermatology.Read Articles Written by Rosanna Marsella
Seborrhea (scaly skin) is a very common presentation in clinical practice and can be associated with many diseases. Some forms of seborrhea are due to a primary disease of keratinization (e.g., the maturation process of the skin is altered). However, most cases of seborrhea are secondary, such as the scaling and crusting seen with bacterial folliculitis. Correctly identifying the cause of seborrhea is necessary to ensure that the correct treatment is prescribed, which greatly increases the chances of therapeutic success.
One disease that presents with seborrhea is sebaceous adenitis. In this condition, sebaceous glands are the target of an inflammatory process and, with chronicity, are completely destroyed. This article presents clinically relevant information about sebaceous adenitis to increase familiarity with this condition and its various clinical presentations, diagnosis, and treatment options. This knowledge is important because, in most patients, the disease is progressive and, in some cases, it can lead to bacterial infections and ulcers severe enough to be the cause of euthanasia. Thus, sebaceous adenitis can significantly impact the quality of life of affected dogs and their owners.
Pathogenesis of Sebaceous Adenitis
The exact mechanism of disease in sebaceous adenitis is not completely understood and is most likely multifactorial. Genetic factors have been considered to play a role, as has stress. In 1 report, owners of most affected dogs mentioned a stressful event or illness that preceded the development of the disease.1 This is an interesting observation, as stress has been associated with autoimmunity in people.2 Specifically, cortisol is known to suppress the activity of natural killer cells,3 which may allow autoimmunity to go unchecked.4,5
Genetic predisposition is suggested by the fact that, although sebaceous adenitis can occur in any breed, some breeds are overrepresented, including the Akita, Vizsla, poodle, springer spaniel, and Havanese.1,6,7 An autosomal recessive inheritance has been postulated for Akitas.1 Previous attempts to identify specific genetic causes of sebaceous adenitis in poodles using genome-wide association studies have been nonproductive.8 More specifically, 1 study observed no difference in haplotype heterozygosity between affected and unaffected dogs from the same country and found no disease association for sebaceous adenitis within the dog leukocyte antigen region.9 Instead, it found that sebaceous adenitis was concentrated in most inbred poodles, but no specific genetic markers other than those reflecting the degree of inbreeding were consistently associated with the disease. These findings highlight the importance of avoiding inbreeding.
One theory proposes that sebaceous adenitis is a primary disease of keratinization that affects the opening region of the hair follicles, leading to obstruction of the sebaceous ducts. Indeed, follicular keratosis (dilation of the follicle due to accumulation of keratin) is a characteristic histologic feature of sebaceous adenitis, and the inflammation of the sebaceous glands is theorized to be secondary to the obstruction. The belief that sebaceous adenitis is a disease of keratinization is the reason retinoids and vitamin A (treatments aimed at normalizing keratinization) have been proposed as treatment options. Affected dogs are believed to have abnormal lipid production.
An alternative theory is that the inflammatory process that targets the sebaceous glands is an autoimmune process. This explanation has been used for the waxing and waning course observed in some patients and is one of the reasons cyclosporine is used as a treatment option.
Clinical Presentations of Sebaceous Adenitis
Clinical signs develop in young to middle-aged adult dogs. Males appear to be more affected than females. Follicular casts (FIGURE 1), scaling, and hypotrichosis affecting the head (FIGURE 2) are the most common clinical signs at initial presentation (92%), followed by development of pyoderma (42%).3,5,10 Follicular casts are keratinized material that envelops the hair like a cast on a limb. They are considered the hallmark of sebaceous adenitis in long-haired breeds. Changes in hair color and structure precede the development of scales and crusts in some dogs (FIGURE 3). Hair may look lighter, darker, or straighter. Affected dogs eventually develop patches of alopecia.
Since normal sebum production is important for its antimicrobial properties, these dogs are prone to secondary bacterial infections, which further contribute to hair loss. Short-haired dogs like Vizslas tend to develop superficial pyoderma with papules, pustules, collarettes, and circular areas of alopecia (FIGURE 4), while long-haired dogs like Akitas can develop severe, deep pyoderma with nodules and draining tracts.11,12 Nodular lesions can be painful, and the combination of follicular casts and draining purulent material from the deep bacterial infection can create hair mats and significantly impact the quality of life of the animal. In 1 report, the median survival time of dogs with sebaceous adenitis was 42 months, with 32% (14/44) euthanized due to sebaceous adenitis.7
An uncommon presentation is ulcerative lesions on the inside of the pinnae. These lesions have been described in 3 unrelated Vizslas and were seen either concurrently with or preceding generalized skin lesions.13 In 1 dog, these severe ulcerative lesions were the cause for euthanasia when they recurred and failed to respond to treatment.
Diagnosis of Sebaceous Adenitis
Scaling, crusting, and patches of alopecia are common signs of superficial folliculitis. Thus, it is important to address diagnostic differentials such as demodicosis, dermatophytosis, and staphylococcal folliculitis by obtaining deep skin scrapings and samples for cytology and fungal culture at the initial presentation. Clinically speaking, the distribution of the lesions is a useful hint, as staphylococcal folliculitis is typically on the trunk while sebaceous adenitis characteristically starts on the head. Malassezia dermatitis can present with scaling and crusting; thus, tape impression cytology is useful to find yeasts and determine the magnitude of any Malassezia infection.
Clearing secondary infections, ruling out demodicosis, and waiting on fungal culture results is a reasonable initial approach. Once infections are resolved, if scaling and follicular casts are still present, other diagnostic differentials are considered, including primary diseases of keratinization, follicular dysplasia, and sebaceous adenitis. These diseases require biopsy samples for diagnosis. Biopsying lesions without a secondary infection makes the diagnosis easier and less complicated. Endocrine diseases can also present with scaling and hypotrichosis, but these diseases typically spare the head and extremities and primarily affect the trunk.
On histopathology, characteristic findings in sebaceous adenitis include granulomatous inflammation that targets the sebaceous glands. The granulomatous inflammation is typically more pronounced in short-haired breeds. At times, the inflammation can be so severe that the glands are not visible and are replaced by granulomas. In late-stage cases, no sebaceous glands are visible. Follicular keratosis can be a prominent feature.
Management of Sebaceous Adenitis
When counseling owners, it is important to explain that sebaceous adenitis is a lifelong disease that requires treatments for extended periods of time and that can have periods of remission and exacerbation. Although it is not curable, it can be managed in most cases. Understanding what owners can do consistently and sustainably, as well as the temperament of the dog, is necessary so that recommendations can be tailored accordingly.
Secondary infections are a large component of the clinical signs and can dramatically worsen the quality of life of the animal. Therefore, it is important to diagnose and treat these infections in a way that owners can sustainably perform. Due to the increased frequency of resistant bacterial infections and the need for recurring therapy, topical antimicrobial therapy plays an important role in treatment. Since many medicated antimicrobial products (e.g., benzoyl peroxide and chlorhexidine-based shampoos) are also drying, they should be combined with other ingredients that are aimed at moisturizing the skin and hair coat.
Topical therapy that provides moisture to the skin and improves skin barrier function is an essential component of treatment. For owners who cannot afford systemic medications like cyclosporine, this therapy may be the only option. Humectants (e.g., propylene glycol) and emollients (e.g., oils) are both effective. Oil soaks, in which Alpha Keri, baby oil, or plain mineral oil is applied to the skin and allowed to sit for as little as 30 minutes to as long as several hours, have been reported to be beneficial in many cases. Multiple baths with a degreasing shampoo are then needed to remove the excess oil. If owners are willing to do them, these soaks can help to greatly decrease the dryness and improve the quality of the coat. Oil soaks may be needed weekly or less often depending on the severity of the disease.
For owners who object to oil soaks, leave-on spray products that are moisturizing without being too greasy can be proposed. In the author’s experience, these options are more likely to be used in the long run by owners. Topical products with phytosphingosine (a ceramide precursor) or spot-on fatty acid products can be useful. Mousse or spot-on sphingolipid emulsion products are also easy to use. These products are labeled for canine atopic dermatitis but have suitable ingredients to be helpful in sebaceous adenitis.
Resistant cases may initially benefit from topical treatment with 50% to 75% propylene glycol. Propylene glycol is a humectant that increases the moisture content of hair and skin without being oily and is well tolerated in most cases.
Systematic Treatments for Sebaceous Adenitis
Cyclosporine is the most commonly prescribed systemic treatment for sebaceous adenitis and has the highest level of evidence for usefulness. Several studies have reported on the efficacy of oral cyclosporine used at 5 mg/kg daily. A beneficial effect has been reported within the first 4 months of treatment.14 One prospective multicentric study compared the efficacy of oral cyclosporine alone and in combination with topical therapy.15 It found that oral cyclosporine helped with regeneration of the sebaceous glands and had a synergistic effect with topical therapy in improving scaling and alopecia. Lifelong therapy is needed in most cases.
Retinoids have previously been recommended for treatment of sebaceous adenitis.16 Isotretinoin is still available and was reported to help less than 50% of treated dogs.16 Etretinate was removed from the U.S. market in 1998 due to high risk of birth defects. Acitretin, a metabolite of etretinate, is still available; however, no studies have been done with this medication in dogs.
Vitamin A can help some patients when prescribed at 800 IU/kg PO q24h. In a retrospective study, half of dogs (12/24) treated with vitamin A showed improvement of clinical signs that was considered good by their owners.17 Some dogs (3/24) worsened while on vitamin A treatment. Six dogs showed no improvement.
Tetracycline and niacinamide have been reported to have some response, although there are no studies to assess the rate of response to this combination.8
Oral essential fatty acids can also be tried as an adjunctive treatment. Eicosapentaenoic acid can be used at 180 mg/4.5 kg of body weight.10 Currently, there are no reports of oclacitinib use for this disease.
Glucocorticoids have been shown to be ineffective for sebaceous adenitis.10 This lack of efficacy may be linked to the propensity of glucocorticoids to induce sebaceous gland atrophy,18 so that although these medications may have a useful effect on inflammation, the effect on sebaceous glands is nonproductive.
Sebaceous Adenitis in Other Species
Cats can develop sebaceous adenitis, although much less commonly than in dogs. One case of a cat with mural folliculitis and almost complete loss of sebaceous glands has been described.19 This cat did not improve with oral fatty acids but responded to topical fatty acids. Two other cats diagnosed with immune-mediated sebaceous adenitis were reported to respond to oral cyclosporine.20
Sebaceous adenitis can also affect rabbits and typically manifests with scaly skin and patchy alopecia in this species (FIGURE 5). A rabbit diagnosed with sebaceous adenitis was reported to have responded to oral cyclosporine dissolved in a medium-chain triglyceride solution (Miglyol 812) and oral essential fatty acids.21 In this patient, complete resolution was noted within 2 months of oral treatment combined with a propylene glycol spray. Relapse occurred when cyclosporine was used without the miglyol. Miglyols are synthetic triglycerides used to facilitate drug absorption. Some improvement in this case was also noted when miglyol was used alone, suggesting that triglycerides are important components of the sebum for rabbits and possibly facilitated the absorption of the fatty acids administered to this patient.
Sebaceous adenitis has been described in horses. In 1 case, it presented as patches of nonpruritic scaling, crusting, alopecia, and leukoderma of the periocular areas.22 In that case, lesions resolved spontaneously when a sarcoid also regressed. In another case, sebaceous adenitis was described in a 5-year-old gelding presented for nonpruritic crusting, scaling, and alopecia.23 This patient had developed hypersensitivity to its own sweat and would also develop hives when sweating.
Sebaceous adenitis is an important diagnostic differential to consider when presented with an animal with follicular casts, scaling, and alopecia. Diagnosis is obtained by biopsy once other differentials have been considered and infections have been diagnosed and treated appropriately. This disease may have a genetic component; therefore, breeding of affected dogs is not advisable. This condition can significantly affect a dog’s quality of life and requires long-term management by the owner. A combination of oral cyclosporine and topical therapy with humectants has the highest chance of being successful. As these dogs are prone to recurrent skin infections, care should be taken to control these infections, possibly using topical antimicrobials to avoid long courses of oral antibiotics that can promote antibiotic resistance.
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