Eczema, also known as atopic dermatitis (AD), is a chronic, inflammatory skin condition characterized by itchy, red, and dry skin. It commonly begins in childhood and can persist into adulthood, with periods of exacerbation and remission. Eczema is a multifactorial disease influenced by genetic, environmental, and immunological factors.
Etiopathogenesis of Eczema
The etiopathogenesis of eczema involves a complex interplay between genetic predisposition, skin barrier dysfunction, immune dysregulation, and environmental triggers.
1. Genetic Factors: Mutations in the filaggrin (FLG) gene, which is essential for the formation and maintenance of the skin barrier, are strongly associated with eczema. Other genetic factors include polymorphisms in genes related to immune function, such as those encoding for cytokines and their receptors (e.g., IL-4, IL-13).
2. Skin Barrier Dysfunction: Eczema patients have a defective skin barrier that leads to increased transepidermal water loss (TEWL) and reduced lipid content in the stratum corneum. This dysfunction allows allergens, irritants, and microbes to penetrate the skin more easily, triggering inflammatory responses.
3. Immune Dysregulation: Eczema is characterized by a predominance of Th2 (T-helper 2) immune responses in the acute phase, leading to the production of cytokines such as IL-4, IL-5, and IL-13. In chronic eczema, there is also an involvement of Th1 and Th22 responses, contributing to the persistence of inflammation. There is often an elevated level of serum IgE, indicating an allergic component.
4. Environmental Factors: Allergens (e.g., pollen, dust mites), irritants (e.g., soaps, detergents), microbial agents (e.g., Staphylococcus aureus), and climatic factors (e.g., low humidity) can trigger or exacerbate eczema. Psychological stress and dietary factors may also play a role.
Clinical Manifestations
Eczema presents with various clinical features depending on the age of the patient and the chronicity of the disease.
1. Infantile Phase (up to 2 years): Erythematous, weeping, and crusted lesions predominantly on the face, scalp, and extensor surfaces. Intense pruritus leading to scratching and secondary infection.
2. Childhood Phase (2 to 12 years): Lesions are more localized to flexural areas (e.g., antecubital and popliteal fossae), wrists, and ankles. Skin becomes lichenified (thickened) due to chronic scratching. Persistent pruritus.
3. Adult Phase:
– Lichenified plaques on flexural surfaces, hands, feet, and the nape of the neck.
– Chronic relapsing course with periods of exacerbation and remission.
– Post-inflammatory hyperpigmentation or hypopigmentation.
4. General Symptoms:
– Dry, scaly skin.
– Pruritus, which can be severe and disruptive to sleep and quality of life.
– Secondary bacterial infections due to scratching (e.g., impetigo).
Non-Pharmacological Management of Eczema
Non-pharmacological strategies are essential in managing eczema and focus on maintaining skin barrier function and avoiding triggers.
1. Skin Care:
Emollients: Regular and liberal use of moisturizers to restore the skin barrier and prevent dryness.
Bathing Practices: Short, lukewarm baths or showers followed by immediate application of emollients.
Avoiding Irritants: Use of gentle, fragrance-free cleansers and avoidance of harsh soaps, detergents, and woolen clothing.
2. Environmental Modifications:
Allergen Avoidance: Reducing exposure to common allergens like dust mites, pet dander, and pollen.
Humidity Control: Using humidifiers in dry environments to prevent skin drying.
Temperature Regulation: Avoiding extreme temperatures and sudden changes.
3. Lifestyle Changes:
Stress Management: Techniques such as mindfulness, yoga, and cognitive-behavioral therapy to reduce stress, which can exacerbate eczema.
Diet: Identifying and avoiding food triggers if specific food allergies are present.
4. Patient Education and Support:
Educating patients and caregivers about the chronic nature of eczema, the importance of adherence to treatment, and strategies to manage flare-ups. Support groups and counseling to address the psychosocial impact of eczema.
Pharmacological Management of Eczema
Pharmacological treatments aim to control inflammation, reduce pruritus, and manage infections.
1. Topical Therapies:
Topical Corticosteroids: First-line treatment for reducing inflammation and pruritus. Potency should be tailored to the severity and location of eczema.
Topical Calcineurin Inhibitors: Tacrolimus and pimecrolimus are alternatives for sensitive areas (e.g., face, neck) or for long-term use to reduce steroid side effects.
Topical Phosphodiesterase-4 (PDE4) Inhibitors: Crisaborole for mild to moderate eczema.
2. Systemic Therapies:
Oral Antihistamines: For symptomatic relief of pruritus, especially sedating antihistamines for nighttime use.
Systemic Corticosteroids: Short courses for severe flare-ups; long-term use is avoided due to significant side effects.
Immunosuppressants: Cyclosporine, methotrexate, azathioprine, and mycophenolate mofetil for severe, refractory cases.
3. Biologic Therapies:
Dupilumab: A monoclonal antibody targeting IL-4 and IL-13 pathways, approved for moderate to severe atopic dermatitis not controlled with topical therapies.
4. Antibiotics and Antiseptics:
Topical and Oral Antibiotics: For secondary bacterial infections, typically caused by Staphylococcus aureus.
Bleach Baths: Diluted bleach baths to reduce skin bacterial load and prevent infections.
5. Phototherapy:
UVB (Ultraviolet B) Therapy: For moderate to severe eczema not responding to topical treatments. Narrowband UVB is preferred due to a better safety profile.
Conclusion
Effective management of eczema involves a comprehensive approach that integrates non-pharmacological and pharmacological strategies. Early intervention, regular skin care, avoidance of triggers, and appropriate use of medications are crucial to control symptoms, prevent complications, and improve the quality of life for individuals with eczema. Regular follow-up and patient education are essential components of long-term management.
