Atopic Dermatitis Clinical Presentation

Incessant pruritus is the only symptom of atopic dermatitis, children often scratch themselves uncontrollably. Although pruritus may be present in the first few weeks of life, parents become more aware of the itch as the itch-scratch cycle matures when the patient is aged approximately 3 months. The disease typically has an intermittent course with flares and remissions occurring, often for unexplained reasons.

Primary findings of atopic dermatitis include xerosis, lichenification, and eczematous lesions. Excoriations and crusting are common. The eczematous changes and its morphology are seen in different locations depending on the age of the patient.

• Infancy

  • Atopic dermatitis is usually noticed soon after birth. Xerosis occurs early and often involves the whole body; the diaper area is usually spared.
  • The earliest lesions affect the creases (antecubital and popliteal fossae), with erythema and exudation. Over the following few weeks, lesions usually localize to the cheeks, the forehead and scalp, and the extensors of the lower legs; however, they may occur in any location on the body, usually sparing the diaper area and the nose. Lesions are ill-defined, erythematous, scaly, and crusted (eczematous) patches and plaques.
  • Lichenification is seldom seen in infancy. A typical presentation is shown in the image below.Typical atopic dermatitis on the face of an infant.
• Childhood

  • Xerosis is often generalized. The skin is flaky and rough.
  • Lichenification is characteristic of childhood atopic dermatitis. It signifies repeated rubbing of the skin and is seen mostly over the folds, bony protuberances, and forehead.
  • Lesions are eczematous and exudative. Pallor of the face is common; erythema and scaling occur around the eyes. Dennie-Morgan folds (ie, increased folds below the eye) are often seen. Flexural creases, particularly the antecubital and popliteal fossae, and buttock-thigh creases are often affected. See the image below. Flexural involvement in childhood atopic dermatitis.
  • Excoriations and crusting are common. The crusting with atopic dermatitis should not be confused with infection because both may manifest oozing and crusting.
• Adulthood

  • Lesions become more diffuse with an underlying background of erythema. The face is commonly involved and is dry and scaly.
  • Xerosis is prominent.
  • Lichenification may be present.
  • A brown macular ring around the neck is typical but not always present. It represents localized deposition of amyloid. See the image below. Dirty neck sign in chronic atopic dermatitis.

Until Hanifin and Rajka^[16] developed diagnostic criteria for the diagnosis of atopic dermatitis in 1980, no standardized methods were available to make the diagnosis. Since then, numerous other experts have developed different criteria suitable for their own environment, and varying with age. The original criteria of Hanifin and Rajka have been modified many times. Efforts to develop practical clinical criteria have not been successful, and those available are not suitable for all geographic areas and age groups. The lack of a good chemical marker for diagnosing the disease is an enormous obstacle to the study of atopic dermatitis.

The following is a constellation of criteria commonly used for the diagnosis of atopic dermatitis:

• Pruritus
• Eczematous changes that vary with age
• Chronic and relapsing course
• Early age of onset
• Atopy (IgE reactivity)
• Xerosis
• Personal history of asthma or hay fever or a history of atopic diseases in a first-degree relative in patients younger than 4 years
• Onset younger than age 2 years (not used if child is aged < 4 y)

A firm diagnosis of atopic dermatitis depends on excluding conditions such as scabies, allergic contact dermatitis, seborrheic dermatitis (SD), cutaneous lymphoma, ichthyosis, psoriasis, immunodeficiency, and other primary disease entities.

• Genetics^{[17, 18]} : A family history of atopic dermatitis is common. The strongest known genetic risk factor for developing atopic dermatitis is the presence of a loss-of-function mutation in filaggrin. More recently, genome-wide association studies (GWAS) have identified susceptibility loci at 11q13.5 in European populations, at 5q22.1 and 1q21.3 in a Chinese Han population, and at 20q13.33 in both Chinese Han and German populations. A recent meta-analysis of GWAS studies in European populations identified SNPs rs479844 near OVOL1, rs2164983 near ACTL9, and rs2897442 in intron 8 of KIF3A. Many of these loci contain genes that encode proteins involved in epidermal proliferation and differentiation or inflammatory cytokines.
• Infection: The skin of patients with atopic dermatitis is colonized by S aureus. Clinical infection with S aureus often causes a flare of atopic dermatitis, and S aureus has been proposed as a cause of atopic dermatitis by acting as a superantigen.
• Hygiene: The hygiene hypothesis is touted as a cause for the increase in atopic dermatitis. This attributes the rise in atopic dermatitis to reduced exposure to various childhood infections and bacterial endotoxins.^{[19, 20]}
• Climate: Atopic dermatitis flares occur in extremes of climate. Heat is poorly tolerated, as is extreme cold. A dry atmosphere increases xerosis. Sun exposure improves lesions, but sweating increases pruritus. These external factors act as irritants or allergens, ultimately setting up an inflammatory cascade.
• Food antigens: The role of food antigens in the pathogenesis of atopic dermatitis is controversial, both in the prevention of atopic dermatitis and by the withdrawal of foods in persons with established atopic dermatitis. Most reported studies have methodologic flaws. Because of the controversy regarding the role of food in atopic dermatitis, most physicians do not withdraw food from the diet. Nevertheless, acute food reactions (urticaria and anaphylaxis) are commonly encountered in children with atopic dermatitis.
• Probiotics:^[21] The role of probiotics in the diet of patients with atopic dermatitis remains controversial
• Aeroallergens: A role for aeroallergens and house dust mites has been proposed, but this awaits further corroboration.
• Tobacco: A study by Lee et al. suggested a correlation between early and/or current exposure to cigarette smoking and adult onset of atopic dermatitis.^[22] The study also determined that exposure to tobacco smoke in childhood is linked to adult onset of atopic dermatitis.