This condition is most commonly found in the Collie and Shetland Sheepdog. Breeding trials conducted in collie dogs suggest a dominant mode of inheritance. Although immunologic mechanisms have been proposed for the pathogenesis of canine dermatomyositis, the etiology is unknown.
In young dogs with familial dermatomyositis, skin lesions typically develop first with variable myopathies occurring later, similar to what is observed with human dermatomyositis. Lesions are characterized by papules, vesicles, pustules, and focal alopecia of the face, ears, tail, and extremities.
Ulcerative dermatosis may be a variant of this condition. occurring in middle-aged to older dogs as blisters and crusting in the inguinal and axilla regions.
Diagnosis usually requires skin biopsy to confirm a suspicion. The most consistent cutaneous histologic features of dermatomyositis are an inflammatory alopecia characterized by follicular atrophy and perifollicular inflammation.
Biochemical levels of creatine kinase and aspartate aminotransferase are generally elevated in affected dogs and electromyographic abnormalities.
Other skin diseases which could be confused with this condition are erythema multiforme, bacterial pyoderma, pemphigus foliaceus, systemic lupus erythematosus, zinc-responsive dermatosis, vitamin A–responsive dermatosis, toxic epidermal necrolysis and drug eruptions.
Although steroids such as oral prednisolone may induce a measure of clinical improvement, treatment of familial dermatomyositis has been partially successful with oral pentoxifylline at 25 mg/kg twice daily for 3 months.
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