Atopic dermatitis (AD) is one of the most common inflammatory and pruritic conditions in dogs. The pathogenesis of canine AD is complex and multifactorial.

The susceptibility to develop clinical disease is, however, associated with multiple genetic and environmental factors. Sensitisation to environmental and/or food allergens – microbial or from insects – leads to skin inflammation, with activation of resident cells and local production of inflammatory mediators¹.

Several factors are known to contribute to the development of sensitivities. These include epidermal barrier dysfunction, bacterial and yeast skin infections, psychogenic factors and concomitant skin diseases¹. These factors are inter-related, and it is not clear if they represent the cause of sensitisation by themselves or if they are a consequence of the allergic disease¹.

Diagnosis

The diagnosis of AD in dogs is based on the presence of characteristic clinical signs and exclusion of all diseases that result in a similar clinical presentation.

The diagnosis, therefore, is clinical and no need exists to carry out complementary tests – such as intradermal or serological ones – although these may contribute to making clinical and therapeutic decisions¹.

Management

AD is a chronic, lifelong disease. Clinical management is dependent on many variables that characterise the clinical signs in one specific patient, ranging from severity of the clinical signs to the extent in which they are affected.

For this reason, treatment has to be tailored to each individual and is invariably multimodal¹.

Traditionally, management of canine AD focused on reactive treatments, where therapeutic approach was aimed at the active inflammatory process after it had already become well established in the skin. It discontinued once clinical signs abated². However, in the past decade, this approach was complemented by a proactive therapy approach^1-4.

This approach will promote the remission of the skin lesions to reduce the residual subclinical cutaneous inflammation that is maintained after reactive therapy to prevent or delay their relapse⁴.

In the proactive therapy approach, the amplitude of anti-inflammatory action of a specific drug is favoured instead of the effectiveness time⁴.

Their long-term goal is to avoid the development of chronic inflammatory changes in the skin that can become much more difficult to reverse⁵.

Treatment

The therapeutic approach of the allergic dog is divided in to two different treatment phases².

Reactive phase

Phase I is where a reactive approach is adopted with the goal of inducing rapid remission of the clinical signs. This is the acute or flare phase, where the dog exhibits an increase in pruritus, whether as a first manifestation of the condition or in the context of a relapse.

In this phase, acute and/or chronic skin lesions will be present, and often with a significant degree of inflammation².

During the reactive approach, fast-acting and broad-range anti-inflammatory drugs would be preferred. Including, therefore, almost always a glucocorticoid (Panel 1).

In this phase, the use of a short-acting oral glucocorticoid is more logical than that of a topical one. Topical glucocorticoids are, however, very useful in conjunction with systemic formulations to treat highly inflamed or markedly lichenified local skin lesions².

However, if the initial inflammatory condition of the patient is mild, oclacitinib could be used instead, in monotherapy or with a topical glucocorticoid to amplify its anti-inflammatory effect (Panel 2)².

In the case of glucocorticoid use, authors recommend to use it in such a dose and for a length of time that will ensure complete resolution of the clinical signs to guarantee only minimal inflammation remains in the skin. Reducing treatment when inflammation is still present can result in a rapid aggravation of the clinical signs².

Proactive phase

Once the patient has been free of clinical signs for several weeks, then the proactive phase treatment approach can be instituted².

The drugs will also be chosen depending on the severity of its clinical disease. If mild, then topical glucocorticoids and injectable biologics, such as lokivetmab, can be considered (Panel 3)².

Proactive therapy with topical glucocorticoids is defined as the treatment of areas more susceptible to inflammation for two consecutive days per week, with or without visible inflammation³. A recent trial confirmed the benefit of proactive use of a topical spray of hydrocortisone aceponate in atopic dogs, with a nearly fourfold increase in median time to flare compared to placebo with no adverse events⁶.

However, if the patient’s degree of inflammation is historically moderate to severe and rather generalised, then it is recommended to intensify the anti-inflammatory treatment, with long-term drugs that have a broader anti-inflammatory action, such as oclacitinib or ciclosporin (Panel 4)⁷.

In the proactive approach phase, other interventions can help prevent acute flares⁸. These include:

• Modification of the immunologic response through allergen-specific immunotherapy (Panel 5).
• Where possible, decreasing allergen load by targeting environmental, parasitic, dietary and microbial allergens.
• Repairing the epidermal barrier to limit percutaneous penetration of allergens.

Conclusion

The management of atopic dermatitis must always be multimodal, adapted to each specific patient and re-evaluated frequently.

Although no cure exists for atopic dermatitis, many advances have been made in recent years regarding not only therapeutic options, but also in the approach to the use of the available drugs.

A proactive treatment approach will aim to control patients with AD long-term, preventing chronic inflammatory skin changes, less need of flare management interventions and, overall, providing better outcomes.