Sorry, you need to enable JavaScript to visit this website.

Halting atopic march

The information and resources included below can help you educate your patients about Atopic Dermatitis and how the disease is diagnosed and managed.

Partial shot of a forearm and leg bent at the knee with blemishes and a hand appearing to scratch the arm.

Can more effective AD treatment prevent later manifestations of atopic disease?

Atopic march – also called allergic march – is a term that refers to the classical progression of atopic diseases from eczema (Atopic Dermatitis) to food allergies, asthma and allergic rhinitis. These conditions have common genetic and environmental predisposing traits and may appear very early in life, persist over decades or years and often remit spontaneously with age.1

The progression of atopic diseases follows an established path from Atopic Dermatitis (AD) and food allergies in early childhood to allergic rhinitis (AR) and asthma in later childhood. By some estimates, half of all patients with AD go on to develop AR and asthma. However, not all individuals with Atopic Dermatitis will progress through the atopic march, and not all individuals with one allergic disease will develop others.2

That said, the presence of one atopic or allergic condition does increase the risk for developing others. Indeed, the presence of certain common characteristics among atopic diseases have led some researchers to suggest that they are all different manifestations of the same atopic disease.3

As the first manifestation of the atopic march, some recent studies support the possibility of a causal link between AD and later onset atopic disorders. It follows then that more effective management of AD may slow or stop the progression of atopic march.4

Ultimately, the etiology of AD is multifactorial with interaction between genetics, immune system and environmental factors.5 Thus, more effective management of AD is generally focused on improving or preserving skin barrier function, modulating the immune response and limiting or eliminating exposure to environmental allergens.6

Skin barrier damage and/or dysfunction is the initial step in AD development. Multiple factors, including immune dysregulation, filaggrin mutations, deficiency of antimicrobial peptides, and skin dysbiosis can contribute to skin barrier defects.7

Once compromised, barrier integrity enables penetration of allergens, pollutants, and microbes that can trigger the initiation of an inflammatory immune cascade that leads to transcutaneous sensitization. The immune dysfunction is thought to further exacerbate the impaired skin barrier to create a vicious cycle.8

Genetically, understanding the variations that contribute to an individual’s risk of Atopic Dermatitis has improved our understanding of mechanisms in the skin and our surrounding environment that can lead to a leaky barrier and inflammation.9

We know, for instance, that the barrier protein filiggrin, has important roles in skin structure and composition and that mutations in the filaggrin gene (FLG) can impair skin barrier function and induce allergic response. And several studies have shown that patients with AD who have impaired or reduced levels of filaggrin are more susceptible to severe AD, food allergies and asthma.10 Based on their theoretical role in disease pathogenesis, a large number of candidate gene studies have been performed to elucidate the genetic background of AD.

Although the genetics of Atopic Dermatitis are not completely understood, AD has a strong genetic link to other diseases of skin dysregulation as well as future stops on the atopic march.

Individuals with Atopic Dermatitis also have an increased risk of developing other conditions related to inflammation, such as inflammatory bowel disease, rheumatoid arthritis and hair loss caused by a malfunctioning immune reaction (alopecia areata). They also have an increased risk of having a behavioral or psychiatric disorder, such as ADHD or depression.11

Potential strategies for preventing the atopic march from AD to asthma include primary and secondary prevention of AD by systemic moisturizer use and management with a proactive regimen, which involves long-term, low-dose intermittent topical anti-inflammatory therapy for previously affected areas with subclinical inflammation.12 The goal is not only to prevent ongoing epidermal barrier dysfunction, residual inflammatory skin infiltrate and the immunological abnormalities which are all present but clinically invisible, but also to delay or prevent progression of the atopic march.13

The potential benefits of halting atopic march at AD are exciting to consider: reduced burden of AD, fewer food allergies, less allergic rhinitis, lower asthma incidence; asthma alone is responsible for more than one-third of childhood emergency room visits.14 These benefits go a long way towards explaining why there is so much interest in preventing or protecting the skin barrier from developing a proinflammatory atopic state. Evidence for the role of barrier defects and skin barrier dysfunction in atopic diseases is accumulating.15

About Atopic Dermatitis (AD)

AD (eczema) is a pruritic skin condition that usually starts in early infancy (though it can also occur in adults). In 85% of cases, AD occurs in the first year of life; in 95% of cases, it occurs before age 5 years. The disease may have periods of complete remission, particularly in adolescence, and may then recur in early adult life.16

AD causes the immune system to send inflammatory signals to the surface of the skin, which can lead to itching and rashes. AD is characterized by pruritus, eczematous lesions, xerosis (dry skin), and lichenification (thickening of the skin and an increase in skin markings). Even when skin looks clear, inflammation is still active under the skin.17

An estimated 16.5 million U.S. adults (7.3%) have AD. AD typically occurs in the early years of life. Some epidemiology studies have shown that 45% of affected children had the condition before 6 months of age, 60% before 1 year of age, and up to 85% before 5 years of age.18

AD has a significant physical and quality of life burden: 86% of patients report daily itching, 77% of patients moderate or extreme pain or discomfort and 61% report severe or unbearable itch. More than half report sleep disturbances at least five times per week. Anxiety and depression are also common; patients with severe AD report higher depression and anxiety scores.19