Eczema, or atopic dermatitis, is a common inflammatory disease of the skin. The condition often has its start in childhood and follows a variable and sometimes unremitting course. Historically, this disease has been considered a part of a triad of “atopy” that included asthma and allergic rhinitis, though this association has recently come into question. Although not a cause of significant mortality, the visible and chronic nature of eczema can be a source of emotional stress.

Pathophysiology
The precise mechanism for the development of eczema is unknown. Whether the clinical manifestations of atopic dermatitis (AD) are the result of violation of the epidermis and the subsequent contact between environmental irritants and immune cells, or the reverse sequence, is debatable. Nonetheless, the epidermis is the first line of defense between the body and the environment and, when intact, shields the body from a variety of irritants, allergens, and microbes. This barrier, which is maintained by differentiated keratinocytes and structural proteins, can be compromised by inheritance, trauma, decreased humidity, change in pH, and infection.

Frequency

Atopic dermatitis is the most common inflammatory skin disease in children, affecting up to 17% of the pediatric population in the United States, with increasing prevalence over the past several decades.

United States

Prevalence of atopic dermatitis ranges from approximately 7-17% in children.2 A small percentage of affected children will have the disease into adulthood.

International

Studies in Japan and Northern Europe have found similar prevalence, with industrialized and westernized nations noting increasing trends of patients with atopic dermatitis.

Physical

Atopic dermatitis is a spectrum of disease that varies in presentation, severity, and distribution. Eczema defies a simple definition as the disease has differing characteristics depending on the age of the patient and the stage of the disease course.

• Lesions may be acute, subacute, or chronic, each with a characteristic appearance. Lesions from one stage can convert into another stage at any time due to processes such as manipulation, irritation, allergy, or infection.
  • Acute lesions are intensely itchy and present as vesicles and blisters with intense redness.
  • Subacute disease is characterized by slight-to-moderate itching, pain, stinging, burning and redness, scaling, and fissuring of the skin with a parched and scalded appearance.
  • Chronic eczematous inflammation demonstrates thickened skin, accentuated skin lines, excoriations, and fissuring accompanying a moderate-to-intense itch.
• The pattern of skin manifestations also differs across the lifespan.
  • In infantile atopic dermatitis, pruritic, red, scaly, and crusted lesions are typically found on the extensor surfaces and cheeks or scalp, with severe cases possibly presenting with vesicles, serous exudates, or crusting. The diaper area is protected and usually spared.
  • The lesions in the childhood stage have less exudation; the skin often demonstrates lichenified plaques in a flexural distribution, commonly antecubital and popliteal fossae, volar aspect of the wrists, ankles, and neck.
  • Adult eczema has a similar distribution to that in childhood atopic dermatitis but is increasingly localized and lichenified with thickened skin, increased skin markings, and excoriated and fibrotic papules.

Causes

Atopic dermatitis is a complex genetic disease that results from an array of gene-gene and gene-environment interactions. Most experts believe that atopic dermatitis has a genetic basis. This is supported by twin studies and chromosome studies that suggest the trait might be inherited via a maternal gene located on chromosome 11. Clinical studies have also shown a higher risk of atopy in children with maternal atopy than in children with paternal atopy.5

Two theories have been proposed to explain the manifestations of atopic dermatitis. Atopic dermatitis was traditionally thought to be caused by an innate immunologic disturbance leading to IgE sensitization, which later results in disruption of the epithelial barrier, though this supposed mechanism is falling out of favor. Alternatively, it is thought that skin breakdown precedes the inflammatory process and an intrinsic epithelial cell defect leads to barrier disruption of the skin and that immunologic imbalance is an “epiphenomenon”.1 Genetic defects in filaggrin, a group of structural proteins, have been cited as a major cause of atopic dermatitis.6,7 The upregulation of a protease stratum corneum chymotryptic enzyme is also being investigated in the cause of atopic dermatitis.

Chronic eczema is a disease that is somewhat behaviorally mediated. Skin thickening and plaque formation is dependent on habitual scratching.