Atopic Dermatitis Clinical Presentation
- Author: Brian S Kim, MD; Chief Editor: William D James, MD more...
Incessant pruritus is the central and most debilitating symptom of atopic dermatitis (AD); 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.
Data from a study by Garmhausen et al indicate that the natural course of the disease can be divided into subgroups with different clinical features. The most frequent course type (31.1% of the sample) was characterized by an early disease onset (before age 2 years) and a chronic persisting course through adulthood.
Of the 607 patients in the study, 85.7% were categorized into 5 main different course types. The greatest differences in the number of sensitizations, total immunoglobulin E serum levels, and predilection of skin lesions were seen between subjects with early-onset disease and a chronic persisting course until adulthood and those with late-onset AD developing after age 20 years.
AD patients often present with a personal or family history of type I hypersensitivity, allergic rhinitis, and asthma.
Essential historical features (must be present) are as follows:
Chronic or relapsing history of disease
Important historical features (supports the diagnosis) are as follows:
Early age of onset
Atopy: Personal and/or family history
Perform a routine skin examination to look for features associated with atopic dermatitis (AD). In younger patients, examine for dermatographism as many patient may have acute urticaria in the setting of AD.
Primary findings of AD include xerosis, lichenification, and eczematous lesions. Excoriations and crusting are common and some patients exhibit prurigo nodularis‒like lesions. The eczematous changes and its morphology are seen in different locations depending on the age of the patient.
Essential features (must be present) are as follows:
Eczema (acute, subacute, chronic): (1) Typical morphology and age-specific patterns (facial/neck/extensor involvement in children, flexural involvement in any age group, sparing the groin and axillary regions); (2) chronic or relapsing history
Important features (supports the diagnosis) are as follows:
Early age of onset
Atopy: (1) Personal and/or family history; (2) IgE reactivity
Associated features(nonspecific but suggest the diagnosis of AD) are as follows:
Atypical vascular responses (eg, facial pallor, delayed blanch response)
Keratosis pilaris/pityriasis alba/hyperlinear palms/ichthyosis
Other regional findings (eg, perioral changes/periauricular lesions)
AD 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.
Xerosis is often generalized. The skin is flaky and rough.
Lichenification is characteristic of childhood AD. 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.
Excoriations and crusting are common. The crusting with AD should not be confused with infection because both may manifest oozing and crusting.
Children with AD are likely to experience symptoms into their teens and beyond.[30, 31, 32]
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.
Until Hanifin and Rajka developed diagnostic criteria for the diagnosis of AD 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 biomarker for diagnosing the disease is an enormous obstacle to the study of AD.
Exclusionary conditions (conditions that should be excluded) are as follows:
Cutaneous T-cell lymphoma
Immune deficiency diseases
Erythroderma of other causes
Genetics [36, 37]
A family history of atopic dermatitis (AD) is common. The strongest known genetic risk factor for developing AD 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.
The skin of patients with AD is colonized by S. aureus. Clinical infection with S aureus often causes a flare of AD, and S aureus has been proposed as a cause of AD by acting as a superantigen. Similarly, superinfection with herpes simplex virus can also lead to a flare of disease and a condition referred to as eczema herpeticum.
The hygiene hypothesis is touted as a cause for the increase in AD. This attributes the rise in AD to reduced exposure to various childhood infections and bacterial endotoxins.[38, 39]
AD 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.
The role of food antigens in the pathogenesis of AD is controversial, both in the prevention of AD and by the withdrawal of foods in persons with established disease. Because of the controversy regarding the role of food in AD, most physicians do not withdraw food from the diet. Nevertheless, acute food reactions (urticaria and anaphylaxis) are commonly encountered in children with AD.
The role of probiotics in the diet of patients with AD remains controversial.
A role for aeroallergens and house dust mites has been proposed, but this awaits further corroboration.
A study by Lee et al suggested a correlation between early and/or current exposure to cigarette smoking and adult onset of AD. The study also determined that exposure to tobacco smoke in childhood is linked to adult onset of AD.
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