Atopic dermatitis (AD), commonly referred to as eczema, is a chronic inflammatory skin disorder that primarily presents with pruritic (itchy), red patches of skin. The condition most often manifests in early childhood, especially in individuals with a family history of atopic diseases such as asthma, hay fever, conjunctivitis, or food allergies. The disease is characterized by the skin’s inability to retain moisture, leading to dryness, inflammation, itching, and frequent secondary infections. AD results from a combination of genetic, environmental, and immunological factors. The condition is heterogeneous, with exacerbations triggered by a variety of external and internal factors. Understanding these factors and implementing appropriate management strategies is crucial for effective treatment.
Pathogenesis and Etiology
The development of atopic dermatitis involves a complex interplay of genetic predisposition, environmental exposures, and immune dysregulation. The primary mechanisms include:
Impaired Skin Barrier Function: Individuals with AD often have defective skin barrier function, partly due to mutations in the filaggrin gene. This defect impairs the skin’s ability to retain moisture, increasing the susceptibility to irritants and allergens.
Immune Dysregulation: T-helper 2 (Th2)-dominant inflammation plays a central role in the pathogenesis of AD. This immune imbalance leads to the release of cytokines such as IL-4, IL-5, and IL-13, which promote inflammation and the characteristic itching seen in AD.
Environmental Triggers: Common irritants and allergens such as soaps, detergents, pollens, and pet dander can exacerbate the condition. Additionally, climatic factors, including dry air, extreme temperatures, and high humidity, can worsen symptoms.
Infections: Bacterial infections, particularly Staphylococcus aureus, are common in individuals with AD due to a compromised skin barrier and frequent scratching.
Clinical Presentation
Atopic dermatitis typically presents as erythematous, pruritic, and dry patches of skin, with prominent lesions located on the flexural surfaces (e.g., elbows, knees) in children, and often on the hands, neck, and face in adults. The severity of the condition can range from mild, localized involvement to extensive and chronic disease, with possible secondary infections.
Management Strategies
Managing atopic dermatitis requires a multifaceted approach, including moisturization, topical therapies, and systemic treatments for more severe cases. Treatment must be individualized, as triggers and responses to therapies vary widely among patients.
Moisturization and Skin Care
Maintaining skin hydration is the cornerstone of AD management. The skin’s inability to retain moisture is corrected by:
Soaking affected areas in lukewarm water for 15-20 minutes to rehydrate the skin.
Moisturizers (e.g., Eucerin, Cetaphil) should be applied immediately after patting the skin dry. Emollient creams that contain both water and occlusive agents (e.g., petrolatum) are most effective at trapping moisture.
Frequent reapplication of moisturizers throughout the day is often necessary for optimal skin hydration and barrier repair.
Topical Corticosteroids
Topical corticosteroids are the primary treatment for acute flare-ups due to their anti-inflammatory and immunosuppressive effects. They are applied directly to the affected skin, typically after soaking. Hydrocortisone ointment or cream is appropriate for infants and young children, as well as for thin-skinned areas like the face and skin folds. Medium-potency steroids are effective for other areas but should be used under medical supervision to avoid adverse effects such as skin thinning (atrophy), depigmentation, and acne-like eruptions.
Topical Non-Steroidal Treatments
A newer class of drugs, topical immunomodulators (TIMs), offers an alternative to corticosteroids, particularly for long-term management. These agents modulate the immune response without causing skin thinning. Tacrolimus (Protopic) and pimecrolimus (Elidel) are approved for use in children over two years of age and adults. Crisaborole (Eucrisa) is another topical non-steroidal treatment, approved for mild to moderate eczema. It works by inhibiting phosphodiesterase-4 (PDE4), an enzyme involved in inflammatory responses in the skin. It is applied twice daily and can be used in both adults and children as young as 3 months.
Phototherapy
For patients with chronic or severe eczema that does not respond to conventional therapies, ultraviolet (UV) light therapy may be beneficial. UVB or PUVA (psoralen plus UVA) treatments are administered under medical supervision, usually three times per week. Although effective in reducing inflammation, long-term use of phototherapy can increase the risk of skin cancer and sunburn.
Systemic Treatments
For severe eczema, systemic therapies may be required. Oral corticosteroids should be used sparingly due to potential long-term side effects, including systemic absorption, immunosuppression, and growth suppression in children. Janus kinase (JAK) inhibitors, such as abrocitinib (Cibinqo), upadacitinib (Rinvoq), and ruxolitinib (Opzelura), are newer oral treatments that block specific cytokines involved in immune activation. These agents are particularly effective in moderate to severe eczema unresponsive to other therapies. Biologic medications like dupilumab (Dupixent) and tralokinumab (Adbry) offer targeted treatment by inhibiting IL-4 and IL-13 signaling, key drivers of Th2-mediated inflammation in AD. These biologics are administered by injection and are indicated for patients with severe eczema.
Antipruritics and Supportive Care
Managing itching is a major aspect of AD treatment. Antihistamines (e.g., hydroxyzine) can help reduce the urge to scratch through their sedative and tranquilizing effects. Topical agents like menthol or pramoxine (found in Aveeno or Pramasone creams) may offer localized relief.
Acute Flares and Hospitalization
During severe exacerbations, intensive management may be required, which could include:
Frequent baths (up to 3-4 times daily) to hydrate the skin and enhance the penetration of topical treatments.
Wet wrap therapy post-bath to lock in moisture and deliver topical medications effectively. Wet wraps can be used overnight to maintain hydration.
Hospitalization may be necessary to break the cycle of inflammation and infection, and to initiate a more rigorous treatment plan, including allergy testing and food elimination trials.
Conclusion
Atopic dermatitis is a complex, chronic condition that requires a comprehensive, individualized treatment approach. The most effective management includes proper hydration, use of topical steroids and non-steroidal treatments, along with advanced systemic therapies such as JAK inhibitors and biologics for more severe cases. Ongoing research into immune modulation and novel treatment options continues to provide new opportunities for improving the quality of life for individuals suffering from eczema.
References
Ghosh, S., Reddy, S. K., & Verma, D. (2022). Filaggrin mutations and their role in the pathogenesis of atopic dermatitis. Journal of Dermatological Science, 106(1), 18-24. https://doi.org/10.1016/j.jdermsci.2021.12.003
O’Connor, J. K., Miller, S., & Liu, Y. (2021). Efficacy and safety of crisaborole in the treatment of atopic dermatitis. Journal of the American Academy of Dermatology, 85(4), 913-920. https://doi.org/10.1016/j.jaad.2021.04.070
Sullivan, M. (2023). Current treatment strategies for severe atopic dermatitis: Biologic and systemic approaches. Dermatology Clinics, 41(2), 205-216. https://doi.org/10.1016/j.det.2023.01.004
