Atopic dermatitis is defined by the Japanese Dermatological Association’s guidelines as “a disease characterized by eczema as the primary lesion, accompanied by itching, and following a course of exacerbation and remission, where most patients exhibit atopic predisposition.”

Atopic predisposition refers to: (1) a family or personal history of bronchial asthma, allergic rhinitis, allergic conjunctivitis, or atopic dermatitis, or (2) a tendency to produce IgE antibodies.

In atopic dermatitis with atopic predisposition, skin barrier dysfunction is present. It often starts in infancy or childhood and frequently involves a clinical history of other allergic diseases such as asthma or allergic rhinitis, and a family history of allergies. Most cases of extrinsic atopic dermatitis fall under this category.

On the other hand, as the population ages, there is an increasing trend in atopic dermatitis without atopic predisposition. These cases typically involve adult-onset dermatitis with severe itching, cycles of exacerbation and remission, but without a history of skin barrier dysfunction or family history. This is referred to as intrinsic atopic dermatitis.

Both extrinsic and intrinsic atopic dermatitis share common features of itching and chronic inflammation.

Diagnosis is based on characteristic skin symptoms and their distribution, clinical course, and family history. However, in cases of late-onset atopic dermatitis, differential diagnoses such as cutaneous T-cell lymphoma must be carefully considered. In such situations, diagnostic accuracy is enhanced with skin biopsies or blood tests.

Blood tests measure eosinophils, nonspecific IgE, and TARC to assess disease activity. Nonspecific IgE levels are important for understanding atopic predisposition. For moderate to severe cases requiring systemic therapy, these values influence treatment choices.

Environmental factors such as food, dust mites, house dust, medications, and personal care products may aggravate symptoms. Specific IgE tests, prick tests, drug lymphocyte stimulation tests, or patch tests may be conducted as necessary.

Treatment has rapidly evolved, with increased options available. In addition to traditional treatments like steroids and moisturizers, tacrolimus, JAK inhibitors, and PDE4 inhibitors have become available. Systemic therapies now include UV therapy, oral cyclosporine, and advanced targeted biologics.

While these treatments manage symptoms effectively, they are not curative. Proper symptom management helps maintain healthy skin and alleviates stress caused by itching or eczema.

Although many patients seek fundamental solutions to improve their atopic predisposition, therapies such as sublingual immunotherapy used for allergic rhinitis are not effective for atopic dermatitis and are not covered by insurance. Therefore, our department does not offer such treatments.

Atopic dermatitis results from interactions between environmental and genetic factors, such as skin barrier dysfunction and inflammation-related genes. Comprehensive treatment is essential, as targeting a single factor is often insufficient. For instance, while anti-IL-13 antibodies are commonly used in moderate to severe cases, combining them with steroids, immunosuppressants, and moisturizers achieves better outcomes.

Itching is the most distressing symptom for atopic dermatitis patients, and controlling it is a critical treatment goal. Recent advancements in itch-relieving medications have allowed patients who previously required extended hospitalization for UV therapy to manage their condition through outpatient care. For patients struggling with proper topical medication use or requiring lifestyle adjustments, educational hospitalization is still provided.

Our ultimate goal is to tailor treatments to individual needs based on age, severity, and lifestyle, enabling collaborative care between physician and patient to achieve better skin health.