**Food Allergy in Atopic Dermatitis**

### Geunwoong Noh1 and Jae Ho Lee1,2

*1Subdivision of Allergy and Clinical Immunology Department of Paediatrics, Chungnam National University Hospital, Daejoen <sup>2</sup>Department of Paediatrics, Chungnam National University College of Medicine, Daejeon Korea* 

#### **1. Introduction**

228 Atopic Dermatitis – Disease Etiology and Clinical Management

Goodwin H (2008). *Eczema and allergy: how useful is allergy testing?* Paediatr Nurs; 20(10): 25-30 Jacob S et al.(2008) *Patch testing: Another steroid-sparing agent to consider in children.* Paed

Kedzierska A et al. (2008). *Susceptibility testing and resistance phenotype detection in* 

Kim JS (2008). *Paediatric atopic dermatitis: The importance of food allergens.* Semin Cutan Med

Lipozencić J, Wolf R (2010). *The diagnostic value of atopy patch testing and skin prick testing in* 

McFadden JP, White JM (2008). *Reduced frequency of atopic dermatitis quinoline-allergic patients:* 

Most tables in the text have been taken from Reitamo S, Luger TA, Steinhoff M (2008).

Reese I et al (2009). *Diagnostic approach for suspected peudoallergic reaction to food ingredients*. J

Reitamo S, Luger TA, Steinhoff M (2008). *Textbook of Atopic Dermatitis*, (Chapters 3-5 and 7-9)

Schlievert PM et al. (2008). *Superantigen Profile of Staphylococcus aureus Isolates from Patients with Steroid-Resistant AtopicDermatitis*. Clin Infect Dis;15;46(10):1562-7 Van den Oord RA, Sheikh A (2009). *Filaggrin gene defects and risk of developing allergic* 

*sensitisation and allergic disorders: systematic review and meta-analysis*. Brit Med

Robinson M, Smart J (2008). *Allergy testing in children*, Aust Fam Physician.;37(4):210-3 Ronchetti R et al. (2008). *Reproducibility of atopy patch tests with food and inhalant allergens*. J

Textbook of Atopic Dermatitis, (Chapters 3-5 and 7-9) Informa healthcare, ISBN

*and recurrent skin colonization*. Br J Dermatol;159(6):1290-9

*atopic dermatitis:facts and controversies*. Clin Dermatol;28(1):38-44 Macias ES et al (2011) *Superantigens in dermatology,* J Am Acad Dermatol;64(3):455-72

*the "hapten-atopy hypothesis"*. Contact Dermatitis.;58(5):291-5

*Staphylococcus aureus strains isolated from patients with atopic dermatitis, with apparent* 

Dermatol;25 (1):81-87

Surg;27(2):156-60

978-1-84184-246-2

J;339:b2433

Dtsch Dermatol Ges;7(1):70-7

Informa healthcare, ISBN 978-1-84184-246-2

Biol Regul Homeost Agents;22(1):27-33

Atopic dermatitis (AD) is a form of allergic skin inflammation characterized by late eczematous skin lesions [1]. These skin lesions occur through non-Immunoglobulin E (non-IgE)-mediated immune responses, and therefore, AD can be regarded as a non-IgE-mediated allergic inflammatory skin disease [2]. Many causes, including inhalant allergens, food allergens, and other factors, have been implicated in AD [1]. In addition to information about the causes, knowledge of the immunologic nature of AD is extremely important in order to understand AD. Without an understanding of the immunologic nature of AD, the cause of food allergy in patients with AD may be wrongly identified. Because of this confusion in establishing the cause of a food allergy in AD, the role of food allergy in AD remains poorly understood [2]. However, with the recent advance in the diagnosis and treatment of food allergy, it is necessary inevitably to distinguish between IgE- and non-IgE-mediated food allergies that co-exist with AD in order to better understand and control AD [2].

It is well-known that food allergy is an important cause of atopic dermatitis [3]. Although food allergies can be either IgE- or non-IgE-mediated, due to a lack of diagnostic modalities such as laboratory tests to diagnose non-IgE-mediated food allergy [4], it is difficult to clarify the nature of the food allergy, leading to confusion about role of food allergy in AD. Tests that determine IgE levels cannot predict the likelihood of an eczematous reaction because eczematous reactions are the result of non-IgE-mediated food allergies [2].

Until recently, discrimination of IgE-mediated and non-IgE-mediated food allergies was not considered necessary for diagnosis or treatment. Therapeutic modalities, including tolerance induction for food allergy (TIFA), have been developed for patients with food allergy [5,6]. However, the principles for diagnosing and treating IgE-mediated or non-IgE-mediated food allergies are quite different [7]. Presently, a differential diagnosis is absolutely necessary for relevant, proper, and successful treatment of IgE-mediated and non-IgEmediated food allergies, independently. Clinical approaches to treat food allergy in AD patients, including laboratory tests and diagnosis, should consider the conceptual differences between IgE-mediated and non-IgE-mediated food allergies.

In the past, avoidance has been suggested as the main principle for treating food allergies [8]. More recently, however, the clinical and laboratory characteristics of IgE-mediated and non-IgE-mediated food allergy in atopic dermatitis have been well-characterized, and the

Food Allergy in Atopic Dermatitis 231

Humans are continually challenged by foreign particles, including pathogens and foods. Protection from these foreign substances is mediated by effective immune responses (effectors). Protection from immune responses directed against food occurs by an immune tolerance response (tolerance). Allergy is one type of effector immune response that is the consequence of allergic sensitization. Allergic sensitization occurs from a Th1/Th2 imbalance [9]. There are 2 classes of allergic effector mechanisms: IgE-mediated and non-IgE-mediated allergic reactions. An IgE-mediated allergic response occurs if allergenspecific IgE is activated after exposure to the specific allergen. IgE-mediated immune

IgE has been positioned at the center of focus in allergy and allergic disease research.

The clinical phenotype of AD varies with age and course of the disease [10]. The eczematous lesions may present as acute (oozing, crusted, or eroded vesicles or papules on erythematous plaques), subacute (thick and excoriated plaques), or chronic (lichenified, slightly pigmented, or excoriated plaques) forms. Furthermore, xerosis and a lowered threshold for itching are usual hallmarks of AD. Pruritus attacks can occur throughout the day and worsen at the night, causing insomnia, exhaustion, and a substantial impairment in quality of life. To date, the symptoms and signs of AD have been listed horizontally. However, the primary clinical manifestations of AD include eczematous skin lesions and itching caused by allergen-specific Th2 immune responses. Some clinical manifestations of AD, including papule, plaque, and xerosis, are descriptions of skin manifestations; some manifestations, including excoriation, are related to the primary AD symptoms and signs; and some manifestations, including viral infection and impetigo, insomnia, and exhaustion,

The clinical manifestations of IgE-mediated food allergy (IFA) are uniform in AD and in the absence of AD; they include dermatologic manifestations, such as immediate urticaria and

The clinical manifestations of non-IgE-mediated food allergy (NFA) are not uniform. Although IFA has been described as a central immunopathogenesis of atopic dermatitis, the symptoms and signs of IFA do not correspond to those of atopic dermatitis. Rather, the

Food allergies have clinical manifestations on the skin as well as gastrointestinal and respiratory systems. Cutaneous reactions have been categorised as non-eczematous versus eczematous and early versus late [11]. Non-eczematous reactions tend to occur immediately after exposure to the food, usually immediately or within less than 1 hour. The typical reactions include pruritus, urticaria, angioedema, and diffuse morbilliform erythema. These reactions do not cause immediate exacerbations of AD, and they are commonly associated with gastrointestinal or respiratory symptoms. Acute urticaria and angioedema are among the most common symptoms, and acute contact urticaria or allergy can also occur. One-half of the reactions after the ingestion of milk are not mediated by specific IgE antibodies to

rashes, as well as other cardiovascular and respiratory symptoms and signs [2].

symptoms and signs of NFA are those of atopic dermatitis itself.

However, a major characteristic of AD is its non-IgE-mediated response.

reactions include urticaria, asthma, and rhinitis.

**3.1 Clinical features of AD** 

**3. Clinical characteristics of food allergy in AD** 

are secondary to the primary symptoms and signs.

**3.2 Clinical features of food allergy in AD** 

relevant treatment techniques, including tolerance induction for food allergy (TIFA), have been markedly advanced and well-established [7]. In this chapter, updates on the diagnosis and relevant treatments for food allergy in AD are described
