Atopic Dermatitis 

Atopic dermatitis (AD) is a pruritic disease of unknown origin that usually starts in early infancy (an adult-onset variant is recognized); it is characterized by pruritus, eczematous lesions, xerosis (dry skin), and lichenification (thickening of the skin and an increase in skin markings). Atopic dermatitis may be associated with other atopic (immunoglobulin E [IgE]) diseases (eg, asthma, allergic rhinitis, urticaria, acute allergic reactions to foods).^[1] Atopic dermatitis has enormous morbidity, and the incidence and prevalence appear to be increasing. Other conditions with different etiologies and prognoses are often grouped under the umbrella of a diagnosis of atopic dermatitis.

Good evidence indicates that genetic factors are important in the development of atopic dermatitis, but the pathophysiology is still poorly understood. Two main hypotheses have been proposed regarding the development of the inflammatory lesions. The first suggests an immune dysfunction resulting in IgE sensitization and a secondary epithelial-barrier disturbance. The second proposes a defect in epithelial cells leading to the defective barrier problem, with the immunological aspects being epiphenomena.

In healthy individuals, balance exists between 2 important subdivisions of T cells (ie, T_H 1, T_H 2). The immune hypothesis invokes an imbalance in the T lymphocytes, with T_H 2 cells predominating; this results in cytokine production of interleukins 4, 5, 12, and 13 and granulocyte macrophage colony-stimulating factor, causing an increase in IgE and lowered interferon gamma levels. Later, in persons with chronic atopic dermatitis, the T_H 1-type cells predominate. Other cell types are also involved in the process, including eosinophils, Langerhans cells, keratinocytes, and B cells.^[2]

The second hypothesis involves defective barrier function in the stratum corneum of Atopic dermatitis patients, leading to the entry of antigens that result in the production of inflammatory cytokines. Some authors question whether the antigens can also be absorbed from the gut (eg, from food) and the lungs (eg, from house dust mites). Xerosis is known to be an associated sign in many atopic dermatitis patients. Evidence has shown multiple loss-of-function mutations in the filaggrin gene (FLG) on band 1q21.3 in patients with atopic dermatitis in Europe and other filaggrin mutations in Japanese patients. This gene is mutated in persons with ichthyosis vulgaris; it is associated with early-onset atopic dermatitis and with airway disease in the setting of atopic dermatitis. These changes are only found in 30% of European patients, begging the question of whether other genetic variants may also be responsiblefor some of the findings in the pathogenesis of atopic dermatitis.

In atopic dermatitis, transepidermal water loss is increased. Defective lamellar bodies may be caused by abnormalities of ceramide production. Whether the inflammation causes primary or secondary epidermal barrier breakdown is not known, but with the knowledge that filaggrin is involved in epithelial disruption, it is now thought that this finding leads to increased transepidermal penetration of environmental allergens, increasing inflammation and sensitivity.^{[3, 4]}

Frequency

United States

The prevalence rate for atopic dermatitis is 10-12% in children and 0.9% in adults. More recent information examining physician visits for atopic dermatitis in the United States from 1997-2004 estimates a large increase in office visits for atopic dermatitis occurred. In addition, blacks and Asians visit more frequently for atopic dermatitis than whites. Note that this increase involves all disease under the umbrella of atopic dermatitis and it has not been possible to allocate which type has increased so rapidly.^[5]

International

The prevalence rate of atopic dermatitis is rising, and atopic dermatitis affects 15-30% of children and 2-10% of adults. This figure estimates the prevalence in developed countries. In China and Iran, the prevalence rate is approximately 2-3%. The frequency is increased in patients who immigrate to developed countries from underdeveloped countries.^[6]

Mortality/Morbidity

Incessant itch and work loss in adult life is a great financial burden. A number of studies have reported that the financial burden to families and government is similar to that of asthma, arthritis, and diabetes mellitus. In children, the disease causes enormous psychological burden to families and loss of school days. Mortality due to atopic dermatitis is unusual.

• Kaposi varicelliform eruption (eczema herpeticum) is a well-recognized complication of atopic dermatitis.

  • It usually occurs with a primary herpes simplex infection, but it may also be seen with recurrent infection. Vesicular lesions usually begin in areas of eczema and spread rapidly to involve all eczematous areas and healthy skin. Lesions may become secondarily infected. Timely treatment with acyclovir ensures a relative lack of severe morbidity or mortality.
  • Another cause of Kaposi varicelliform eruption is vaccination with vaccinia for the prevention of small pox, but because this is no longer mandatory, patients with atopic dermatitis do not develop the sequelae of eczema vaccinatum that has been seen in the past. It was usually contracted by the patient from the vaccination of themselves or their close relatives. This condition had a high mortality rate (up to 25%). In the current climate of threats of bioterrorism, vaccination may once again become necessary, and physicians should be aware of eczema vaccinatum in this setting.
  • Note that chickenpox vaccine does not carry the same risk as herpes simplex and vaccinia.
• Bacterial infection with Staphylococcus aureus or Streptococcus pyogenesis is not infrequent in the setting of atopic dermatitis . The skin of patients with atopic dermatitis is colonized by S aureus. Colonization does not imply clinical infection, and physicians should only treat patients with clinical infection. The emergence of methicillin-resistant S aureus (MRSA) may prove to be a problem in the future in these patients. Eczematous and bullous lesions on the palms and soles are often infected with beta-hemolytic group A Streptococcus.
• Urticaria and acute anaphylactic reactions to food occur with increased frequency in patients with atopic dermatitis. The food groups most commonly implicated include peanuts, eggs, milk, soya, fish, and seafood. In studies in peanut-allergic children, the vast majority were atopic.
• Latex allergy is more common in patients with atopic dermatitis than in the general population.
• Of atopic dermatitis patients, 30% develop asthma and 35% have nasal allergies.

Race

• Atopic dermatitis affects persons of all races. Immigrants from developing countries living in developed countries have a higher incidence of atopic dermatitis than the indigenous population, and the incidence is rapidly rising in developed countries

Sex

• The male-to-female ratio for atopic dermatitis is 1:1.4.

Age

• In 85% of cases, atopic dermatitis occurs in the first year of life; in 95% of cases, it occurs before age 5 years. The incidence of atopic dermatitis is highest in early infancy and childhood. The disease may have periods of complete remission, particularly in adolescence, and may then recur in early adult life.
• In the adult population, the rate of atopic dermatitis frequency is 0.9%, but onset may be delayed until adulthood.