Atopic dermatitis (AD) is a chronic, relapsing, and inflammatory skin condition, characterized by eczematous lesions, pruritus, and dry skin. Pruritus of the skin causes frequent scratching and may result in lichenification (thickening of the skin) and secondary skin infections. The symptoms of AD wax and wane and disease severity can range from mild to severe disease. AD begins in early childhood with the majority of cases beginning before the age of five years. Although childhood symptoms resolve by adolescence, some patients’ AD symptoms will persist or develop in adulthood. The Canadian Dermatology Association reported that the lifetime prevalence of AD is up to 17%, and there is evidence to suggest that the prevalence has increased over the past 30 years.
The goal of AD management is to prevent and manage flare-ups, which are recurrent episodes of worsening of symptoms that require an escalation of treatment. Although there is no cure for AD, there are several therapeutic options available to patients. The majority of patients treat AD using general skin care methods and topical anti-inflammatory therapies. However, if these practices fail to improve AD symptoms, patients may use off-label systemic immune-modulating agents or other therapies, such as phototherapy. The most commonly pharmaceutical topical therapies for patients with AD include topical corticosteroids (TCS) and topical calcineurin inhibitors (TCI). TCS are anti-inflammatory agents that act to control flare-ups and they are considered a first-line therapy for patients with AD. Side effects associated with long-term use of TCS include striae (stretch marks), petechiae (small red or purple spots), telangiectasia (small, dilated blood vessels on the surface of the skin), skin thinning, atrophy, and acne. On the other hand, TCI are steroid-free, anti-inflammatory, immunosuppressant agents. In Canada, TCIs are used in the second-line setting for patients who exhibit steroid phobia or where the use of steroids is not advisable. The most common adverse event associated with TCI therapy is application site–specific burning and irritation.
Crisaborole is a low-molecular-weight benzoxaborole, nonsteroidal, topical ointment. Crisaborole inhibits phosphodiesterase type 4 (PDE4), which regulates inflammatory cytokine production. It is applied in a thin layer to the affected area, twice daily.
The current CADTH Common Drug Review (CDR) submission for crisaborole is for the treatment of patients two years of age and older with mild-to-moderate AD.
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