Publish date: Posted on
Last updated: March 31, 2021
Keywords #
eczema
pruritus
atopic dermatitis
Diagnosis #
Atopic dermatitis (AD) is a chronic, relapsing, pruritic inflammatory skin disease that occurs most frequently in children.[1] It usually presents early in infancy, continuing through childhood and disappearing by adulthood in two-thirds of patients. Its etiology is not fully understood, but it is likely the result of an interplay among environmental, immunologic, and genetic factors. Loss of function mutations of the filaggrin gene have a strong association with AD.[2] Other genes, such as CARD11 and SPINK5/LEFT1, may also be involved.
Atopic dermatitis can cause significant morbidity, psychological distress, school and work absences, and sleep disturbance.
Key Concepts #
- Atopic dermatitis is not contagious.
- Although people can have dietary flares, AD is not directly caused by food allergies.
- Mild skin care and maintenance of the skin barrier with emollients is critical in management. Patients should avoid fragrances and other triggers.
- 1st-line therapy includes topical corticosteroids. Patients should have the appropriate strength for the location being treated and an adequate amount (correct tube size for length of therapy).
- Infections frequently cause flares. Watch for this and treat accordingly.
Epidemiology #
AD affects 10-20% of children and 1-3% of adults around the world.[2] It affects up to 20% of people during their lifetime, with 50% of patients manifesting initial symptoms before age 1 and 95% before age 5.[5]
Clinical Features #
- AD has been nicknamed “the itch that rashes.”
- It is characterized by xerosis (dry skin), an erythematous rash, and intense pruritus.
- Scratching of the skin perpetuates the “itch-scratch cycle” and further disrupts the skin barrier, eventually leading to an increased risk of infections, erosions, and lichenification.
- Acute flares may present with xerosis, edema, vesicles, oozing, and crusting over an erythematous rash.
- Chronically, AD presents with lichenification secondary to chronic scratching with excoriations, dyspigmentation, nodules, and papules[5].
The distribution and extent of AD varies by age:
Infancy | Childhood | Adolescence and Adulthood |
---|---|---|
|
|
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Differential Diagnoses #
- Allergic or irritant contact dermatitis
- Psoriasis
- Seborrheic dermatitis
- Dermatitis herpetiformis
- Nummular dermatitis
- Urticaria
- Scabies
- Cutaneous T-cell lymphoma
Diagnostic Workup #
The diagnosis of AD is made clinically based on history, signs, and symptoms. Elevated total/allergen-specific serum IgE levels support the diagnosis but may be normal in up to 20% of patients.[4]
If biopsied, an acute episode of AD shows intercellular edema, parakeratosis and perivascular lymphocytic infiltrates, while a chronic specimen is characterized by hyperkeratosis and acanthosis with sparse lymphocytic infiltrates.[5]
Treatment #
AD is a chronic condition and patients and families need to understand that it is not curable and waxes and wanes over time. Treatment is targeted at preventing flares and managing symptoms when they occur. Understanding triggers helps prevent flares, and daily mild skin care is critical. It is also important to discuss the specific medications prescribed, how to use them, potential side effects, and expected duration of treatment.
Application of emollients (moisturizing creams and ointments) several times a day—especially immediately after a tepid water bath—is important for the treatment of xerosis and to reduce flares. Ointments and creams (i.e., products that must be scooped out of jars rather than pumped out of a bottle) are more effective than lotions. These act as occlusive barriers, maintain skin hydration and help reduce pruritus, erythema, fissuring, and lichenification.[4] Avoiding irritating fabrics and prolonged baths in hot water further helps to reduce the frequency of flares.[5]
Medical treatment includes topical corticosteroids (TCS) which reduce inflammation both acutely and as maintenance therapy. Mid- to high- potency TCS are helpful during acute flares but should be used for short courses; for chronic maintenance, the least potent TCS that controls the disease should be used.[4] Alternative topical treatments used for maintenance include calcineurin inhibitors (tacrolimus, pimecrolimus).
Moderate to severe disease may require systemic treatment. Options include phototherapy, immunosuppressive medications (methotrexate, cyclosporine, mycophenolate mofetil, and others) and dupilumab, which is an injectable biologic medication. A number of other biologic therapies are in clinical trials and expected to provide new treatment options in the near future.
Skin infections should be treated accordingly with topical or systemic antibiotics and antivirals.
References #
- Eichenfield LF, Tom WL, Chamlin SL, et al. Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis. J Am Acad Dermatol. 2014;70(2):338-351.
- Nutten S. Atopic dermatitis: global epidemiology and risk factors. Ann Nutr Metab. 2015;66 Suppl 1:8-16.
- Bantz SK, Zhu Z, Zheng T. The Atopic March: Progression from Atopic Dermatitis to Allergic Rhinitis and Asthma. J Clin Cell Immunol. 2014;5(2).
- Eichenfield LF, Tom WL, Berger TG, et al. Guidelines of care for the management of atopic dermatitis: section 2. Management and treatment of atopic dermatitis with topical therapies. J Am Acad Dermatol. 2014;71(1):116-132.
- Thomsen SF. Atopic dermatitis: natural history, diagnosis, and treatment. ISRN Allergy. 2014;2014:354250.
- Chang A, Robison R, Cai M, Singh AM. Natural History of Food-Triggered Atopic Dermatitis and Development of Immediate Reactions in Children. J Allergy Clin Immunol Pract. 2016;4(2):229-236 e221.