Dermatitis, Atopic

Article Author:
Logan Kolb
Article Editor:
Sarah Ferrer-Bruker
Updated:
9/7/2018 9:24:37 AM
PubMed Link:
Dermatitis, Atopic

Introduction

Atopic dermatitis (AD), which is a specific form of eczema, is the most common chronic inflammatory skin disease.[1][2][3]

Etiology

Atopic dermatitis has a complex etiology including genetic and environmental factors which lead to abnormalities in the epidermis and the immune system. Atopic dermatitis is part of the atopic triad (atopic dermatitis, allergic rhinoconjunctivitis, and asthma) which may start simultaneously or in succession in what is known as the "atopic march." Patients with the atopic triad have a defective barrier of the skin, upper respiratory, and lower respiratory tract which leads to their symptomatology. If one parent is atopic, there is more than a 50% chance that their offspring will develop atopic symptoms. If both parents are affected, up to 80% of offspring will be affected. Genetic alterations include loss of function mutations of filaggrin (Filamen Aggregating Protein), an epidermal protein that is broken down into natural moisturization factor. Filaggrin mutations are present in up to 30% of atopic dermatitis patients and may also predispose patients to ichthyosis vulgaris, allergic rhinitis, and keratosis pilaris. Food hypersensitivity may also cause or exacerbate atopic dermatitis in 10% to 30% of patients. Ninety percent of such reactions or flares are caused by eggs, milk, peanuts, soy, and wheat.[4][5]

Epidemiology

Atopic dermatitis is seen in approximately 10% to 30% of children and 2% to 10% of adults in developed countries. This prevalence has increased two to three-fold in recent decades. Atopic dermatitis has a higher incidence at higher latitudes, which may be related to decreased sun exposure and lower humidity levels. Atopic dermatitis is divided into three subsets based on the age of onset:

  1. Early-onset atopic dermatitis (birth to 2 years old):  most common type of atopic dermatitis, with approximately 60% of cases starting by age 1. Sixty percent of cases resolve by 12 years old
  2. Late-onset atopic dermatitis:  symptoms begin after the onset of puberty
  3. Senile onset atopic dermatitis: an unusual subset with onset in patients older than 60 years old.

Pathophysiology

Atopic dermatitis patients have a defective skin barrier that is susceptible to xerosis and environmental irritants and allergens that lead to inflammation, pruritus, and the classic clinical findings of atopic dermatitis. The barrier defect may be caused in part by decreased levels of ceramides, which are sphingolipids in the stratum corneum which play a role in the skin's barrier function and prevent transepidermal water loss. The defective skin barrier allows irritants and allergens to penetrate the skin and cause inflammation via an overactive Th2 response (with increased IL-4, IL-5 cytokines) in acute lesions and Th1 response (with IFN-gamma and IL-12) in chronic lesions. Scratching of the skin also stimulates keratinocytes to release inflammatory cytokines such as TNF-alpha, IL-1, and IL-6. Decreased anti-microbial peptides (human beta-defensins, cathelicidins) in the epidermis of atopic patients also contribute to Staphylococcus aureus colonization seen in more than 90% of atopic dermatitis patients. S. aureus may worsen the inflammation of atopic dermatitis lesions and lead to secondary infection and impetiginization. [6][7]

History and Physical

A practitioner should take a patient's history and focus on the following:

  • Onset and distribution of lesions
  • The severity of pruritus (e.g., keeping patient awake at night)
  • Family and/or personal history of the atopic triad
  • Presence of contact allergens
  • The presence of triggers including allergens (e.g., dust mites, animal dander), hot showers/sweating, soaps, fragrances, food hypersensitivities, and synthetic fabrics such as polyester.

Classic physical exam findings depend on age group. Infants develop edematous papules and plaques that may have vesicles or crust on the scalp, face, and extensor extremities. Infants rarely have atopic dermatitis lesions affecting the diaper area but may be susceptible to other causes of diaper dermatitis such as candida or seborrheic dermatitis. Atopic dermatitis children classically have less exudative patches and plaques on antecubital and popliteal fossae; adults have chronic lichenified (enhanced skin markings) lesions that have a predilection for hands. Individual lesions may also be further classified into acute (edematous, erythematous papules and plaques and/or vesicles/crusting), subacute (erythema, scale, variable crusting), or chronic (thick plaques with lichenification and scale) stages. Atopic dermatitis lesions may leave hypopigmentation or hyperpigmentation. Associated findings of atopic dermatitis include Dennie-Morgan lines (horizontal folds on lower lid margin of atopic dermatitis children), allergic shiners,  keratosis pilaris ("chicken skin" on proximal lateral arms, thighs, and buttocks), pityriasis alba (hypopigmented macules/patches on face, neck, and arms), and palmoplantar hyperlinearity. Complications include eczema herpeticum (vesicles or crust over pre-existing lesions caused by herpes simplex virus (HSV)) and secondary molluscum contagiosum infections.

Evaluation

Atopic dermatitis is typically a clinical diagnosis given the classic distribution of lesions in each age group. The presence of associated findings (e.g., keratosis pilaris) may facilitate diagnosis. A biopsy will show an eczematous pattern. In childhood cases that are recalcitrant to treatment, fluorescent enzyme immunoassays or skin prick testing can be performed to detect immunoglobulin E (IgE) antibodies against specific allergens, which may or may not be a clinically relevant exacerbating factor.[8][9]

Treatment / Management

The four major components of treatment include trigger avoidance, daily skin care, anti-inflammatory therapy, and other complementary modalities. Daily skin care includes the application of emollients twice daily, with the application within three minutes of exiting lukewarm shower or bath to prevent skin drying. Ointments are the most occlusive but may be more greasy. Topical steroids, which should be applied before emollients to "lock-in" their effect, are first-line agents for acute flares. The potency should be strong enough to control a flare quickly, and consideration should be given for tapering every other day and for maintenance therapy twice weekly (e.g., weekends) in the usual areas of involvement. Reversible side effects of steroid use include skin atrophy and telangiectasia. Sensitive areas (including the intertriginous areas of the axilla and groin, in addition to the face) may require topical nonsteroidal agents including calcineurin inhibitors such as tacrolimus and pimecrolimus. Newer non-steroidal agents include crisaborole, which exerts its effect by blocking PDE-4. When atopic dermatitis is not controlled with topical agents, systemic agents include phototherapy (ultraviolet (UV) A, UVB, and narrow-band UVB), cyclosporine, azathioprine, mycophenolate mofetil, and methotrexate.  A newly FDA-approved biologic therapy is dupilumab, which is a monoclonal antibody that blocks the IL-4 receptor and thus the effect of IL-4 and IL-13.  Other complementary therapies include bleach baths (0.5 cup bleach in full 40 gallon tub) one to two times weekly to decrease S. aureus colonization, low allergen maternal diets during breastfeeding, and probiotic and prebiotic use in pregnant mothers and at-risk infants which has shown 50% decreased frequency of atopic dermatitis at ages 1 to 4 years old compared to placebo.[10][11][12]

Differential Diagnosis

Complications

  • Kaposi varicelliform eruption
  • Bacterial infection
  • Uriticaria

Pearls and Other Issues

Treatment and management of atopic dermatitis should start with education of the patient and/or parents of the chronic nature of the disease and importance of maintenance therapy, which improves the epidermal barrier and prevents sensitization to allergens and possible prevention of atopic dermatitis.

Enhancing Healthcare Team Outcomes

Atopic dermatitis is a chronic skin disorder that can adversely affect the quality of life. While the condition can be managed with medical therapy, there are also non-medical remedies that can make a big difference in the quality of life. Both the pharmacist and nurse can play a vital role in educating the patient on nonmedical remedies to manage atopic dermatitis. The patient should be educated on wearing soft clothing- preferably cotton and avoid wool. The home temperatures should be kept low because the heat can cause sweating and exacerbation of the irritation. A humidifier should be used to prevent dryness in the home. All garments should be washed with a mild detergent with no fabric softener or bleach. When going outdoors, ample sunscreen and moisturizer should be applied. The patient should keep a diary of all the foods and avoid foods that trigger the attacks. The patient should avoid activities that cause excess diaphoresis. Finally, patients who have asthma should be compliant with their medications and avoid allergens.[13][14] (level II)

Outcome

The majority of patients with atopic dermatitis do improve with age. About 30% of patients will develop allergic rhinitis, and 30% will develop asthma. A long-term study that evaluated patients with Atopic Dermatitis indicates that mild to moderate symptoms often persist for a decade or more. And about 80% of these patients will need topical medications to control the symptoms. Symptoms relief is usually seen after the 2nd decade of life, but this also means a drastic change in lifestyle that includes avoiding all triggers like tobacco, pet dander, wool, and certain soaps. Atopic dermatitis may not be life-threatening, but it can seriously affect the quality of life. The constant dryness and itching of skin not only leads to a high financial burden and often requires multiple hospital visits. [1][15](Level V)