The aetiology of AD is multifactorial, involving genetic, environmental, immune, and microbiome factors. A key driver of AD is type 2 inflammation, which leads to epithelial barrier dysfunction. This dysfunction allows water loss and the penetration of irritants and allergens, triggering inflammation via the Th2 pathway.
Dendritic cell activation and the release of interleukins 4 and 13 further drive type 2 inflammation, resulting in lesion formation, pruritus, and bacterial colonization. This can lead to infections and hospitalisation.
AD affects ~4%-5% of the global population, with a prevalence of 4.4% in the European Union and 8.3% among children aged 13- to 14-years in Cape Town. The lifetime prevalence is 15%-30% in children and 2%-10% in adults, with incidence rates increasing two to three times since the 1970s. AD typically begins before the age of five, with risk factors for persistence into adulthood including later onset, greater severity, and a family history of atopy.
AD lesions vary in appearance and distribution based on patient age. In infants, lesions commonly affect the face and extensor surfaces. In children, flexural areas are more commonly involved, while adolescents often experience lesions on the wrists, ankles, eyelids, and scalp.
The disease's activity varies, and flares are not always seasonal. Pruritus is a major criterion for diagnosis, along with a history of flexural dermatitis, visible flexural dermatitis, history of dry skin, personal or family history of atopic disease, and onset under two years of age.
AD significantly impacts patients' quality of life, particularly in children, causing symptoms like itch, sleep disturbance, and increased asthma. Adults with AD often experience mental health disorders such as anxiety, depression, and suicidal ideations.
The disease also leads to impaired daily activities, reduced productivity, loss of work or school days, and sleep disturbances. Financially, AD is burdensome, with high annual costs and increased infections.
Treatment aims to balance efficacy, side effects, and cost. Initial steps include avoiding irritants and using emollients. For active disease, topical corticosteroids and calcineurin inhibitors are recommended. If these fail, phototherapy and systemic immunosuppressants like methotrexate and cyclosporine are used.
Biologics and Janus kinase inhibitors are options if traditional treatments fail. Early treatment is crucial to avoid comorbidities such as cardiovascular, respiratory, and autoimmune diseases.
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