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Allergy mimickers (Proceedings)

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Nov 01, 2010

When a clinician is presented with a pruritic patient, it is correct to initially consider, and rule out, the more common hypersensitivity disorders. Atopic dermatitis, adverse food reactions, and parasite hypersensitivities (especially flea allergy dermatitis) are seen on a daily basis. The challenge is to not overlook other dermatological conditions which might cause pruritus. An overview of some of the "allergy mimickers" will be presented with emphasis on specific clinical changes which should alert the clinician to consider these mimickers.

Four common conditions misdiagnosed as allergic skin disease are sebaceous adenitis, folliculitis (specifically demodicosis and dermatophytosis), cutaneous epitheliotropic T cell lymphoma and pemphigus foliaceus

Sebaceous adenitis (SA) is an inflammatory disease of the sebaceous glands which can lead to their destruction. An inheritance mode is suspected, especially in breeds such as the Standard Poodle. Breeds predisposed for development include the Akita, Standard poodle, Vizsla, Samoyed, German shepherd and Havanese. However SA is seen in many other breeds, as well as mixed breeds.

When sebaceous glands are damaged or destroyed by SA, resulting changes are predicable. Lesions include alopecia (patchy or generalized), scale and dry skin, follicular cast formation, variable amounts of erythema, and nodule or plaque formation in some patients. Occasionally the affected skin and hair will become discolored or hyperpigmented. Bacterial pyoderma is common in these patients as sebum from sebaceous glands is important for both barrier function of the epidermis and for the bactericidal properties.

Sebaceous adenitis is misdiagnosed as allergic skin because these patients can be pruritic, both because of the actual disease, and also because of the concurrent secondary infections. Keys to help distinguish SA from allergic disease is the amount of scale tends to be greater in SA, as well as the alopecia tends to be more dramatic compared to allergic skin. The skin is actually dry (hypohidrosis) where as in most allergic patients there is often increased amounts of sebum. Remember that scaly skin is not necessarily dry skin. Because the alopecia can be generalized and bilaterally symmetrical, SA can also be misdiagnosed an endocrine disorder. Finally, the presence of follicular casts are very suggestive of SA and warrants biopsy. Sebaceous adenitis is confirmed with histopathology.

Therapy basically attempts to replace sebum and its function, as well as potentially allow regeneration of sebaceous glands. Supportive care of the skin includes anti-seborrhea baths and rinses. If the shampoo also contains chlorhexidine, antibacterial benefits will be achieved which could reduce the need for systemic antibiotics. New products such as ceramides or phytosphingosine act as the mortar of a brick wall which improves barrier function and improves clinical signs. Concurrent therapy with Vitamin A (600-1,000 IU/kg daily) and omega 3/6 fatty acid supplementation are also encouraged. Baby oil (or other oils) applied to the skin as a "soak' for 30-60 minutes are labor intensive, but many owners are pleased with the results. The oil is washed off with a gentle shampoo after the soak. Topical humectants such as Propylene glycol, urea, lactic acid, glycerin (Humilacâ„¢) can be applied daily or as desired by the owner. Cyclosporin (5-10 mg/kg daily) has been shown to cause improvement of clinical signs and there is documentation that sebaceous glands can regenerate when patients are receiving cyclosporin therapy. In my experience complete control or "cures" are uncommon, and balancing the therapy with clinical signs, patient comfort, and cost is the goal and challenge for the owner and clinician.