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Universitą degli Studi di Napoli Federico II |
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Facoltą di Medicina e Chirurgia Dipartimento di Patologia Sistematica Sezione di Dermatologia |
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Facoltą di Medicina Veterinaria Dipartimento di Scienze Cliniche Veterinarie Sezione di Clinica Medica |
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AMBIENTE ANIMALI E CUTE CORSO TEORICO PRATICO 6-7 dicembre 2002
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LA SEBORREA NEGLI ANIMALI DA COMPAGNIA R. Marsella DVM, DipACVD, Po Box 100126, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610-0126
Seborrhea or scaly skin is a common clinical presentation. The word seborrhea means - flow of sebum - but most of the cases of seborrhea in veterinary medicine are not diseases of sebaceous glands or sebum but diseases of keratinization. Sebum is composed of sterol, diester waxes, free cholesterol, triglycerides and fatty acids. Functions of sebum include barrier, antimicrobial, waterproofing the hairs, territorial marking and sexual attractant. Regulation of sebum production is hormonal (androgens, thyroid hormones and progesterone stimulate; estrogens and glucocorticoids decrease) and dietary (fat deficiency initially increases sebum production but later on it will decrease it). Keratinization is the process by which keratin is produced and the stratum corneum is formed. It takes usually 21 days for the cells of the stratum basale to migrate upward to the stratum corneum and be filled with high molecular weight keratin. A decreased (faster) transit time leads to hyperkeratosis (increased thickness of the stratum corneum). It is important to determine if the scaling is due to a primary disease of keratinization (primary seborrhea) or it is secondary to another disease (secondary seborrhea). To differentiate between primary and secondary seborrhea it is important to follow a well-organized plan to rule out other diseases. An accurate diagnosis is important for appropriate therapy and prognosis. Secondary seborrhea Secondary seborrhea is by far more common than primary seborrhea and the list of differentials is very extensive since almost any disease in veterinary dermatology may have scaling and flaking as a clinical sign. Scaling secondary to another disease may be divided into two big groups: pruritic and non-pruritic. Pruritic causes for secondary seborrhea include scabies, flea allergy, food allergy, atopy, Cheyletiellosis, pyoderma and Malassezia. Non pruritic causes for secondary seborrhea include demodicosis, dermatophytosis, endocrine diseases (hypothyroidism, Cushings, sex hormone imbalance), pemphigus foliaceous, mycosis fungoides (this disease can be very pruritic), chronic steroid administration, dietary (e.g. fatty acid deficiency) environmental factors (e.g. low humidity). Primary seborrhea Differentials for generalized primary keratinization disorders include primary idiopathic seborrhea, Vitamin A responsive dermatosis, epidermal dysplasia, sebaceous adenitis, follicular dystrophy, Schnauzer comedo syndrome, and ichthyosis. Differentials for localized primary keratinization disorders include lichenoid psoriasiform dermatosis (pinnae are usually affected), Zinc responsive dermatosis, nasodigital hyperkeratosis, canine ear margin dermatosis, canine acne. Primary diseases of keratinization are usually manifested by excess of scale formation. They are usually genetic diseases and affected patients have a familial history. Since these are hereditary conditions, the disease is usually evident at a young age (less than 2 years). Middle age dogs are less likely to have a primary seborrhea and for older animals mycosis fungoides should be considered very high in the list of differentials. Diseases of keratinization are characterized by mild to severe, dry to waxy scales. A rancid odor is often present. This is most of the time due to the secondary bacterial or yeast infections and the fatty acids that are produced by these microorganisms. Comedones (blackheads) are caused by a dilation of the hair follicle that is plugged with keratin. Follicular casts are tightly adherent scales around the hair shaft. Common secondary findings are alopecia, pruritus, erythema, pyoderma. In cases of primary seborrhea the scales and comedones are usually evident before any other sign develops (pruritus, inflammation and alopecia). However most of the times these cases are complicated by a concurrent pyoderma or Malassezia dermatitis and it is difficult to establish the sequence of events. Most cases are pruritic at the time of presentation. Diagnosis of primary seborrhea In establishing a diagnosis a few factors are important such as the breed, the age of onset, the response to previous antibiotic therapy and the exclusion of other more common diseases. A diagnosis of a primary disease of keratinization should not be made without a complete diagnostic plan to rule out secondary causes of scaling. It is common to have cases in which several diseases are present at the same time thus it is important to have a logical and systematic approach. It is important to discontinue any steroid, consider the possibility of flea infestation, demodicosis (deep skin scraping), cheyletiellosis (flea combing), scabies (superficial scraping and response to treatment), dermatophytosis, endoparasitism (fecal examination), Malassezia dermatitis (cytology) and pyoderma (examination and response to antibiotic therapy). If scaling resolves completely with antibiotic therapy, it is unlikely that a primary defect of keratinization is present. If scaling persists together with pruritus it is more likely that a parasitic or allergic disease is present. If scaling and follicular casts are present without pruritus after an appropriate antibiotic therapy, it is possible that a disorder of keratinization, or an endocrine disease is present. The possibility of pemphigus foliaceous or mycosis fungoides can be further evaluated with a skin biopsy. Environmental factors are also important (e.g. low humidity). Moisturizing agents are very effective in those cases. To confirm the diagnosis of primary seborrhea a biopsy is usually taken. The best time to take a biopsy is after the pyoderma has been treated. Although the disease is best diagnosed from an early lesion than is not complicated by chronic changes, it is also useful to biopsy several lesions at different stages of development. 1. Primary idiopathic seborrhea There is a strong breed predisposition. Cocker Spaniels, English Springer Spaniels, West Highland White Terriers, Basset Hounds, Irish Setters, Dachshunds, Doberman Pinshers are all predisposed. Irish Setters, Dachshunds, Doberman Pinshers are prone to get seborrhea secca (dry seborrhea), while the other breeds usually develop seborrhea oleosa (greasy seborrhea). Cocker Spaniels, English Springer Spaniels, West Highland White Terriers, Basset Hounds develop greasy, brownish, yellow clumps of lipid material that adhere to the skin and the base of the hairs. A ceruminous otitis is very common. Seborrheic dermatitis is a more severe form of seborrhea with significant inflammation and thick plaques of hyperkeratotic material. The most commonly involved areas are the ventral neck, the external era canals, pinnae, chest, axillae, inguinal and perineal area. Affected dogs start at very young age. Initially no pruritus is present, however, as secondary skin infections develop pruritus becomes a clinical sign. Scaling is also aggravated by the presence of secondary infection. Diagnosis is made by history, by clinical signs and exclusion of other diseases. Biopsy reveals hyperkeratosis, follicular keratosis and dilation. Treatment of primary idiopathic seborrhea includes treatment of secondary skin infections and of the underlying disease of keratinization. Shampoos like benzoyl peroxide, selenium disulfide together with a 3 or 4 week course of systemic antibiotic are commonly used. Glucocorticoids should not be used during the time in which the diagnostic evaluation is done as they may affect the ability to control the pyoderma and they interfere with the evaluation of pruritus. The use of topical therapy has become an important part of the everyday practice. However several facts have to be kept in mind about the rationale and expectations of topical therapy. Topical therapy rarely works when used alone. However, it is a very effective adjunct therapy to get faster resolution of a dermatosis. In general bathing should be continued over at least 10-15 minute period for proper hydration of the skin and to allow the active ingredients to work. Best results are obtained shampooing frequently to control the dermatosis initially and then decreasing the frequency for maintenance of remission. Topical therapy is not a substitute for managing the dermatosis by establishing a definitive diagnosis as soon as possible. The owner must be compliant with the recommended treatment program. Client communication is crucial for the success of therapy. Ingredients that are commonly used include humectants, emollients, keratolytic and keratoplastic agents. Humectancts are agents that work by being incorporated in the stratum corneum and by attracting the water that is in the lower layers of the epidermis. These agents include urea, sodium lactate, lactic acid, propylene glycol and work even if applied in between baths. Lactic acid has hygroscopic activity al low concentration and keratolytic activity at higher concentrations. It has been incorportated into liposomes to ensure a slow release over time and thus a longer residual activity (Microperl Humectant Spray®). Propylene glycol is a very effective humectant because it is hygroscopic. Urea is a humectant at low concentration and a keratolytic agent at higher concentrations. Emollients are agents that soften the skin because they decrease transepidermal water loss. They are usually oils and work if applied after a bath. They fill the spaces between dry flakes with droplets of oil. Used alone they provide only temporary relief.Keratolytic agents cause cellular damage of the cells in the stratum corneum with the result of cell shedding. Keratoplastic agents cause a normalization of the epidermal cell kinetics by a cytostatic effect on the basal layer and therefore slow down epidermal proliferation. Most agents used in veterinary dermatology for the treatment of seborrhea have both properties. Tar is keratolytic, keratoplastic, antipruritic, degreasing, drying. It may be irritating and cause photosensitivity. It may stain a white hair coat. It is contraindicated in cats. It is indicated for cases of greasy seborrhea (e.g. Cocker spaniel seborrhea). Sulfur is keratolytic, keratoplastic (0.5-2%), antipruritic, antibacterial, antiparasitic and antifungal (2-5%). Synergism with salicylic acid is proposed. It is not a good degreaser. It can be used on cats. Salicylic acid is keratolytic, keratoplastic, antipruritic, bacteriostatic. In the veterinary formulations it is usually in the same percentage of sulfur (0.5-2%). Selenium sulfide (Selsun Blue®) is keratolytic, keratoplastic, degreasing and effective against yeasts (e.g. Malassezia). It can be irritating and drying. It should not be used in cats. Benzoyl peroxide (2.5-3%) is keratolytic, antimicrobial, degreasing, very useful in severe cases of greasy seborrhea. It reduces sebaceous glands secretions and has a flushing activity on the bacteria in the hair follicles. Human products should not be used because irritating (10%). If the seborrhea is dry then humectants and emollients are indicated. Water by itself has a tremendous hydrating effect if used properly. Contact time of 10-15 minutes should be allowed to properly hydrate the stratum corneum. If contact time is too short or if baths are given too frequently the effect will be opposite. The application of bath oil when the skin is still wet will help to hold externally applied water to prolong hydration. If the seborrhea is greasy then degreasers and keratolytic agents are more appropriate. Tar, sulfur and benzoyl peroxide are effective topical to remove excessive scaling. Tar and sulfur are also keratoplastic and therefore inhibit the excessive production of scales. These products have to be used quite often in order to be effective. a cocker spaniel with a primary seborrhea will need a bath 3-4 times a week at the beginning of therapy and then maybe 2x/week. Owners are usually able to tell how often the dog needs to be bathed. Clipping is also an important part of topical therapy. A thick hair coat like the one of a cocker spaniel will prevent the shampoo from reaching the skin, therefore it is crucial to the success of therapy that the hair is always kept very short. This will reduce the amount of shampoo, will allow better contact with the skin surface and thus enhanced efficacy. Systemic therapy includes the use of retinoids and Vitamin A derivatives. Retinoids have been tried for the management of this disorder (retinol, isotretinoin, etretinate). The term retinoids refers to all the compounds, natural and synthetic, with vitamin A activity. These compounds have ability to regulate the proliferation and differentiation of epithelial tissues. Isotretinoin seems to work better in cases where the disease is the hair follicle and sebaceous glands (Schnauzer comedo syndrome and sebaceous adenitis) while etretinate works better in hyper proliferative epidermal disorders (e.g. idiopathic seborrhea of cocker spaniels, English, Springer Spaniels, Irish Setters). Response to therapy should be seen within the first 2 months of therapy. Synthetic compounds have a long half-life and are stored for long time in the body fat. Toxicity in animals seems to be less of a problem than in humans, however, keratoconjunctivitis secca, increase of triglycerides, cholesterol, liver enzymes, pruritus, vomiting, diarrhea and stiffness have been reported. All these compounds are teratogenic. 2. Vitamin A responsive dermatosis It is rare and primarily seen in Cocker Spaniels. This is not a true deficiency of Vitamin A but probably a local deficiency. Disease is characterized by dry hair coat with easy epilation. Prominent comedones and hyperkeratotic plaques with large fronds of keratinous material protruding from the follicular ostia are seen. Pruritus is common. It is differentiated from primary idiopathic seborrhea based on histologic findings and response to therapy. Vitamin A is administered at 625-800 IU/kg q24hr PO. Improvement is usually seen in 4-6 weeks. Topical therapy is very beneficial and it includes the same agents used for primary idiopathic seborrhea. 3. Sebaceous adenitis. It is an inflammatory disease of the sebaceous glands leading to the destruction of the glands. Vizlas, Akitas, Poodles and Samoyeds are predisposed to develop the disease. The exact pathogenesis has not been established but it is currently believed that this disease is autoimmune in nature and that it is a genetically inherited defect. Young dogs are usually affected. The early lesions include alopecia with excess scaling and brittle hairs. Head, the dorsal planum of the nose and dorsal neck are common affected areas. As the disease progresses tightly adherent silver scales and follicular casts around the base of the hairs are visible. Secondary bacterial infection is common. Vizlas often present with moth-eaten, circular areas of alopecia and scaling. Diagnosis is made by histopathology. Treatments include anti-seborrheic shampoos, emollients, essential fatty acids, antibiotic for the secondary bacterial folliculitis and retinoids. Isotretinoin (1 mg/kg q24hr PO) may be effective. 4. Zinc responsive dermatosis. Two syndromes have been reported. The first syndrome usually affects Siberian Huskies and Alaskan Malamutes. The second syndrome is seen in puppies of rapidly growing dogs that are fed with Zinc-deficient diets or regimens with a high level of Calcium that antagonize zinc absorption). Lesions usually develop at young age and include erythema, crusting and scaling around the mouth, chin, eyes, scrotum and legs. Hyperkeratosis of the footpads may be seen. Diagnosis is made from skin biopsies. Therapy of the first syndrome consists of zinc supplements (Zn sulfate at 10 mg/kg q24hr or Zn methionine at 2 mg/kg q24hr). The second syndrome simply requires correction of the diet without an additional Zinc supplement. Diarrhea may be observed with high doses of zinc. 5. Epidermal dysplasia of West Highland White Terriers. It is a disorder of keratinization usually evident in the first year of life. Erythema and pruritus are severe and with chronicity alopecia, hyperpigmentation and lichenification are evident. Secondary bacterial and yeast infections are very common in these dogs. It is important to evaluate these dogs for possible allergies due to the breed and the young age of onset before a diagnosis of epidermal dysplasia is made. All the secondary infections should be treated appropriately to evaluate the residual pruritus and to make these dogs more comfortable. All therapies usually fail in these dogs. Owners often request euthanasia due to the poor quality of life. In some cases ketoconazole is very beneficial even if yeasts are not present on cytology and the improvement with therapy might be due to the antiinflammatory (inhibition of 5-lipoxygenase enzyme responsible for the production of leukotrienes) and antiproliferative properties of ketoconazole. Keratinocytes proliferation is significantly reduced after administration of this drug and that may account for the beneficial effect in this disease. Sometimes immunosuppressive doses of steroids may be beneficial. It is very important however to have the right diagnosis before recommending this type of therapy and also to explain to the owner the possible side effects of therapy. |
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