**4.1 Allergy history**

A detailed clinical history is the key first step in the diagnosis of potential food allergy, followed by skin testing and immunoassay testing when indicated by the history [14]. Ultimately, however, in cases of non-anaphylactic reactions and especially non-IgEmediated food allergies, OFCs may be required for an accurate diagnosis.

Parents often consider their child's AD as an "allergic" manifestation of a presumed food allergy [11]. Although the influence of the media and popular culture may play a role, parents also receive differing opinions from primary care providers and dermatologists [11]. Greater than 90% of parents and 60% of primary care providers may suspect food allergy as the cause of AD, resulting in referrals to allergists and extensive testing.

Food allergies should be suspected from the patient's history of experiences of allergy provocation, especially in case of IgE-mediated food allergy [7]. However, apart from major immediate anaphylactic reactions, patient history has proven to be an unreliable way to diagnose food allergies [3]. A poor correlation between food allergy and medical history, with only 25%-48% sensitivity overall and a 72%-97% specificity for IFA, has been reported. Moreover, in NFA it is more difficult for patients and parents to recognise the relationship between the ingested food and allergy provocation because of the difficult clinical characteristics as well as delayed reactions of this condition, and a history of NFA is inconsistent with the final diagnosis of NFA [18]. The additional possibility of exerciseinduced food allergy should be considered and excluded by history.

#### **4.2 Laboratory approaches to food allergy in AD**

#### **Blood eosinophil numbers**

Increases in blood eosinophil counts due to NFA provocation by OFC have been demonstrated and blood eosinophilia is useful simply as a clue in the diagnosis of allergy [20]. The level of blood eosinophils has clinical significance as a predictor of the efficacy of IFN- therapy in atopic dermatitis [21].

#### **Total IgE**

Although not all patients with AD have elevated IgE, as many as 40% to 80% [11] have been found to have high food-specific IgE levels. Total IgE does not seem to be associated with current allergic disease activity.

#### **ECP**

Eosinophil cationic protein (ECP) is produced by activated eosinophils [22]. Food additives were shown to elevate blood ECP in atopic dermatitis [23]. Interestingly, ECP is

quantitation, along with the measurement of clinical severity changes on the basis of discrimination of IgE- and non-IgE-mediated food allergy, has clearly become the most important point in successful immunotherapy [7]. Because both the diagnostic and the therapeutic protocols for IgE- and non-IgE-mediated food allergies differ greatly, the

The two most important points regarding diagnosis of food allergy in atopic dermatitis are as follows: 1) distinction should be made between IFA and NFA and 2) the treatment dosage must be calibrated and the clinical severity assessed for the purposes of therapy

A detailed clinical history is the key first step in the diagnosis of potential food allergy, followed by skin testing and immunoassay testing when indicated by the history [14]. Ultimately, however, in cases of non-anaphylactic reactions and especially non-IgE-

Parents often consider their child's AD as an "allergic" manifestation of a presumed food allergy [11]. Although the influence of the media and popular culture may play a role, parents also receive differing opinions from primary care providers and dermatologists [11]. Greater than 90% of parents and 60% of primary care providers may suspect food allergy as

Food allergies should be suspected from the patient's history of experiences of allergy provocation, especially in case of IgE-mediated food allergy [7]. However, apart from major immediate anaphylactic reactions, patient history has proven to be an unreliable way to diagnose food allergies [3]. A poor correlation between food allergy and medical history, with only 25%-48% sensitivity overall and a 72%-97% specificity for IFA, has been reported. Moreover, in NFA it is more difficult for patients and parents to recognise the relationship between the ingested food and allergy provocation because of the difficult clinical characteristics as well as delayed reactions of this condition, and a history of NFA is inconsistent with the final diagnosis of NFA [18]. The additional possibility of exercise-

Increases in blood eosinophil counts due to NFA provocation by OFC have been demonstrated and blood eosinophilia is useful simply as a clue in the diagnosis of allergy [20]. The level of blood eosinophils has clinical significance as a predictor of the efficacy of

Although not all patients with AD have elevated IgE, as many as 40% to 80% [11] have been found to have high food-specific IgE levels. Total IgE does not seem to be associated with

Eosinophil cationic protein (ECP) is produced by activated eosinophils [22]. Food additives were shown to elevate blood ECP in atopic dermatitis [23]. Interestingly, ECP is

mediated food allergies, OFCs may be required for an accurate diagnosis.

the cause of AD, resulting in referrals to allergists and extensive testing.

induced food allergy should be considered and excluded by history.

**4.2 Laboratory approaches to food allergy in AD** 

**Blood eosinophil numbers** 

**Total IgE** 

**ECP** 

IFN- therapy in atopic dermatitis [21].

current allergic disease activity.

major points in these protocols should be revised.

and follow-up [7].

**4.1 Allergy history** 

elevated without the elevation of blood eosinophil numbers in AD patients and even in normal subjects in recent studies conducted [24]. In this report, food additives were shown to provoke xerosis (dry skin) and resultant pruritus consistent with AD. Among patients suspected to have AD, over 30% showed pseudoallergies to food additives [25]. The signs and symptoms caused by food additives can interfere with the interpretation of OFC and with the therapeutic process. ECP is specifically elevated in patients who ingest artificial chemical food additives [24] and elevated ECP has been used as a marker of pseudoallergic reactions due to food additives, particularly when blood eosinophil numbers are normal.
