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Meningoencephalomyelitis of unknown aetiology (MUA) is a common inflammatory condition of the central nervous system and its adnexae in dogs. A presumptive clinical diagnosis of MUA is made based on signalment, history, neurological examination, cerebrospinal fluid assessment and magnetic resonance imaging findings following exclusion of infectious aetiologies. Definitive diagnosis requires histopathological examination of brain tissue, most commonly at postmortem examination, since antemortem brain biopsies are rarely performed (Granger and others 2010, Talarico and Schatzberg 2010). The disease is progressive and fatal unless treated with immunomodulatory therapy (Talarico and Schatzberg 2010), such as glucocorticoid monotherapy (prednisolone at 1–2 mg/kg twice daily, Granger and others 2010), or glucocorticoids in combination with other immunomodulatory agents, such as cytosine arabinoside (cytarabine). Cytarabine is an antineoplastic and immunosuppressive agent that causes premature chain termination during DNA synthesis in mitotically active cells. It is an attractive adjunctive agent with glucocorticoids in MUA due to its ability to cross the blood-brain barrier and to reduce long-term glucocorticoid requirement. Doses of 50 mg/m2 are administered as subcutaneous injections every 12 hours over a 48-hour time period, repeated every three to six weeks (Zarfoss and others 2006). In dogs, side effects of cytarabine include myelosuppression, vomiting, diarrhoea and alopecia (Scott-Moncrieff and others 1991). In humans, cutaneous side effects of cytarabine are acral erythema, papular or bullous eruptions and vasculitis (Cetkovska and others 2002).
Here, we report the development of severe focal calcinosis cutis and deep pyoderma at the interscapular injection site of cytarabine during combination therapy with prednisolone in three dogs with MUA. To the …