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Direct and indirect immunofluorescence can detect antikeratinocyte autoantibodies and circulating pemphigus autoantibodies respectively.
Treatment options:
Immunosuppressive therapy is used to treat Pemphigus foliaceus. In dogs, the treatment of choice is oral glucocorticoid with or without concurrent steroid sparing therapies such as azathioprine, chlorambucil, ciclosporin and mycophenolate mofetil.
In cats, glucocorticoid (most commonly prednisolone or triamcinolone) monotherapy usually produces a good response. Steroid sparing therapies include ciclosporin or chlorambucil.
Topical glucocorticoids (moderate to high potency e.g. 0.1% mometasone) are also very effective at treating focal lesions.
Veterinarians should also try to identify any potential triggers such as drugs, preventatives and ultraviolet light. If a dog/cat relapses, it is important to rule out development of bacterial pyoderma, dermatophytosis or demodicosis. These diseases can be managed without the need to increase the level of immunosuppression.
Regular blood and urine monitoring is recommended to identify potential side effects to immunosuppressive therapy.
The outcomes for both canine and feline pemphigus foliaceus are generally good. The main reasons for euthanasia are lack of response to treatments and unacceptable side effects to treatments. These can be managed by client education, and regular blood and urine monitoring.
2. Cutaneous lupus erythematosus (CLE) in dogs
Current recognised forms of cutaneous lupus erythematosus in dogs are discoid lupus erythematosus (localised and generalised), vesicular cutaneous
lupus erythematosus, exfoliative cutaneous
lupus erythematosus and mucocutaneous lupus erythematosus. Localised facial-predominant discoid lupus erythematosus is the most common form seen in dogs.
Localised (facial-predominant) discoid lupus erythematosus (FDLE)
· German Shepherds and their crosses make up about 31% of cases.
· Median age of onset is 7 years (range from 1 to 12 years)
· Female to male ratio is 0.7. Clinical signs:
The early signs include erythema, depigmentation and scaling most commonly affecting the nasal planum. These progress to erosions and ulcerations, atrophy and loss of the normal cobblestone appearance on the nasal planum. Less commonly, lesions may also affect the skin around the dorsal muzzle, lips, eyes and pinnae. Pruritus is variable and more likely with secondary bacterial infections. The main differential diagnoses include mucocutaneous pyoderma (MCP), uveodermatologic syndrome and localised epitheliotropic lymphoma.
Diagnostic approach:
Depigmentation of the nasal planum without loss of
the cobblestone surface architecture may be normal in certain breeds e.g. nasal hypopigmentation in Golden and Labrador retrievers. Conversely, a thorough and immediate examination of the eyes for uveitis should be performed in breeds predisposed to uveo-dermatologic syndrome e.g. Akitas and Alaskan Malamutes.
MCP and DLE can be difficult to differentiate clinically and on histopathology. Furthermore, most cases of DLE are secondarily infected. It is important to perform cytology and treat any secondary infections before proceeding to further diagnostics.
DLE is characterised by a lichenoid cell rich, lymphocytic interface dermatitis with basal keratinocyte vacuolar degeneration apoptosis, loss of basal cells and basement membrane thickening. The interface reaction may be mild in FDLE but is usually well developed in generalised DLE.
Treatment options
Systemic and/or topical immunosuppressive or immunomodulatory therapies can be used depending on the severity of disease.
For severe cases, oral prednisolone is recommended
to achieve remission. The prednisolone doses can then be reduced or potentially withdrawn as less potent immunomodulatory therapies are added. These include combination of tetracycline/doxycycline and niacinamide, fish oils, Vitamin E.
Topical therapies include topical cortisone (starting with higher potency e.g. 0.1% mometasone then changing to less potent e.g. 1% hydrocortisone) or 0.1% tacrolimus.
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