During the last decade, oral cyclosporin (CsA) has proven to be effective, in randomized controlled trials, for the treatment of atopic dermatitis (AD) in human patients. The purpose of this blinded randomized controlled trial was to test the hypothesis that CsA was successful in reducing the gravity of clinical signs of AD in dogs. Thirty dogs with nonseasonal AD were randomly allocated to receive an oral solution of either NEORAL CsA (5 mg kg-1) or prednisolone (0.5 mg kg-1) once daily for 6 weeks. Before, and 3 and 6 weeks after therapy, skin lesions were graded by clinicians using the Canine AD Extent and Severity Index (CADESI). Pruritus was assessed by the owners using a visual analog scale (PVAS). In both groups, CADESI and PVAS values were significantly lower at 6 weeks post treatment than before the initiation of therapy (Friedman test, P < 0.0004). The percentage reductions in CADESI and PVAS values from baseline were not statistically different between groups (Mann-Whitney test, P > 0.3). In this experiment, the tolerability and safety of oral CsA and prednisolone appeared similar. One-fifth of dogs given oral CsA occasionally developed diarrhoea or soft stools. One dog that was given CsA developed a generalized papillomatous skin eruption during the second half of the trial. Our study provides randomized controlled trial evidence that CsA reduces the severity of clinical signs in dogs with nonseasonal AD. Moreover, the anti-allergic efficacy of CsA appears comparable with that of prednisolone. We propose that oral CsA should be considered as a valuable alternative to glucocorticoid therapy in dogs with AD.

In this blinded randomized placebo-controlled trial, 20 dogs with atopic dermatitis (AD) were given placebo (8 dogs) or misoprostol (12 dogs) at 5 micro g kg-1, orally, three times daily for 3 weeks. Administration of the active drug, but not of placebo, led to a significant decrease in lesional and pruritus scores. The median reduction from baseline of both scores was approximately 30%. Misoprostol therapy did not lead to decreases of dermal cell counts or skin tumour necrosis factor (TNF)alpha mRNA copy numbers that were significantly different from those of placebo. Skin TNFalpha protein production, assessed using indirect immunofluorescence, decreased or remained unchanged in dogs receiving misoprostol. In contrast, post treatment TNFalpha fluorescence scores were higher in all but two dogs given placebo. The changes from baseline of TNFalpha fluorescence scores did not correlate significantly with those of lesional or pruritus indices. These observations confirm the modest efficacy of misoprostol for treatment of canine AD and suggest that its mild anti-allergic effects are not associated with either inhibition of inflammatory cell emigration or TNFalpha production.

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In humans with pemphigus foliaceus (PF), pathogenic autoantibodies are suspected to be of IgG4 subclass. The goals of this study were to determine the isotypes of circulating autoantibodies in dogs with PF, and to assess whether serum autoantibody titers decreased during successful treatment outcome. Using an indirect immunofluorescence assay performed on neonatal mouse skin sections, circulating IgG autoantibodies were detected in 36 out of 44 dogs with PF (82%). Serum autoantibodies belonged predominantly to IgG4 (35/44; 80%) and IgG1 (30/44; 68%) subclasses. Circulating IgA and IgE autoantibodies were not found. Serum IgG autoantibodies targeted autoantigens in both superficial and/or basal epidermal layers. Remarkably, antikeratinocyte IgG autoantibodies were detected in 16 out of 20 normal dogs (80%), and these autoantibodies were of IgG1 (16/20, 80%) but rarely of IgG4 (2/20; 10%) isotypes. Antikeratinocyte IgG, IgG1 and IgG4 autoantibody serum titers were followed in six dogs with PF while the severity of their clinical signs decreased with immunosuppression. IgG, IgG1 and IgG4 autoantibody serum titers decreased during remission in four (67%), one (17%) and four (67%) dogs, respectively. Conversely, serum IgG, IgG1 and IgG4 autoantibody titers increased during remission in one (17%), one (17%) and no dogs, respectively. These observations suggest that, in dogs with PF, antikeratinocyte IgG4 autoantibodies could be relevant to the pathogenesis of the disease and that monitoring of IgG4 autoantibody titers could be useful for assessment of clinical outcome. Remarkably, the detection of circulating IgG1 antikeratinocyte autoantibodies in normal dogs is similar to the situation observed in geographical areas where human PF is endemic.