**6. Diagnosis**

The diagnosis of atopic dermatitis is based on a constellation of clinical signs and symptoms, physical examination and history. Laboratory tests are unnecessary and skin biopsy has been found to be little value, but they can exclude other diagnosis in adults. Although the majority of AD patients have elevated total serum IgE, up to 30% of these patients have normal total serum IgE and show no allergic sensitization to food or aeroallergens (Schmid-Grendelmeier, et al. 2005). However, monitoring of IgE remains a nonspecific finding of AD.

Normally, diagnosis is confirmed by chronicity of symptoms, pruritis, and age-specific morphology and distribution of symptoms (Ong P, et al. 2008). However, well-defined criteria are important in the diagnosis of AD and diagnostic criteria developed by Hanifin and Rajka are widely accepted (see Table 1). The American Academy of Dermatology has also developed diagnostic criteria for AD (Leung & Hong, 2007). Please see Table 2.

There are many exacerbating factors that are triggers, which can expedite the progress of inflammation. These triggers are found in food allergens, bacteria, viruses, stress and opportunistic pathogens. One of the major triggers is the microorganism *Staphylococcus Aureus* due to the fact that is organism secretes a toxin which can stimulate action of T cells (Ghazvini, et al. 2010). Among viruses, herpes simplex virus has been identified as one of the possible triggers of AD (Ghazvini, et al. 2010). Diagnostic testing is mainly utilized to determine specific allergens that may be causing the condition. These tests include:


Clinical Management of Atopic Dermatitis 255

Pruritis

reactivity Xerosis

Eczema (with typical morphology for age)

Personal or family history of atopy or IgE

Nonspecific dermatitis of the hands or feet

Positive skin test for immediate-type allergy

Atypical vascular response (facial pallor,

Keratosis pillaris, hyperlinearity of palms

Ocular or periorbital changes, including anterior subcapsular cataracts, Dennie-Morgan infraorbital folds, orbital darkening

Perifollicular accentuation, lichenification or


Metabolic and nutritional deficiencies

polyendocrinopathy, enteropathy, X-

Perioral or periauricular lesions

Immunodeficiency syndromes - Wiskott-Aldrich syndrome

syndrome with Omen's - Immune dysregulation,

Chronic or relapsing history

Early age at onset

Cutaneous infections

Elevated serum IgE levels

white dermatographism)

Pityriasis alba Nipple eczema

prurigo lesions

linked



Table 2. Diagnostic Criteria for Atopic Dermatitis by the American Academy of

Table 3. Differential Diagnosis in Atopic Dermatitis (Deshazo, 2009)7. Treatment

**Essential Features**  (must be present)

**Important Features** 

**Associated Features** 

diagnosis)

(seen in most cases; add support to

(nonspecific; help suggest diagnosis)

Dermatology (Ong P, et al. 2008)

Other dermatosis - Contact dermatitis - Irritant dermatitis - Nummular dermatitis - Seborrheic dermatitis - Psoriasis ichthyosis

Infections


Malignancies




	- Immediate type reactions such as urticaria, erythema and angioedema may occur without worsening the AD symptoms and they may occur within a few minutes after food intake (Ong P, et al. 2008).
	- Pruritis may be noted after ingestion of food, which makes the patient scratch and may trigger AD.
	- Late reactions may occur as 6 to 8 hours after food ingestion (Ong P, et al. 2008).


\*\*At least 3 major and minor features must be present for a diagnosis of atopic dermatitis.

Table 1. Hanifin-Rajka Diagnostic Criteria for Atopic Dermatitis (Ghazvini, et al. 2010)


 Immediate type reactions such as urticaria, erythema and angioedema may occur without worsening the AD symptoms and they may occur within a few minutes

Pruritis may be noted after ingestion of food, which makes the patient scratch and

 Late reactions may occur as 6 to 8 hours after food ingestion (Ong P, et al. 2008). - Serum IgE measurement – Even though a larger number of AD patients have elevated serum IgE levels, approximately 30% have normal levels and do not present with


**Major Features Minor Features** 

Chronic or relapsing dermatitis Ichthyosis, palmar hyperlinearity and

and children Nonspecific dermatitis of the hands or feet

keratosis pilaris

Nipple eczema Pityriasis alba

response

darkening

\*\*At least 3 major and minor features must be present for a diagnosis of atopic dermatitis.

Table 1. Hanifin-Rajka Diagnostic Criteria for Atopic Dermatitis (Ghazvini, et al. 2010)

Raised serum immunoglobulin (Ig) E levels

White dermatographism and delayed blanch

Anterior subcapsular cataracts Perifollicular accentuation Course influenced by

environmental/emotional factors

Dennie-Morgan infraorbital folds, orbital

Facial erythema or pallor

skin reactions which can be observed with this test:

allergic sensitization to allergens (Ong P, et al. 2008).

Typical morphology and distribution Cutaneous infections

adults Early age of onset

excluding other differentials of AD (see Table 3).

Pruritis Xerosis

Flexural lichenification of linearity in

Facial or extensor involvement in infants

Personal or family history of atopy (asthma, atopic dermatitits, contact

urticaria)

after food intake (Ong P, et al. 2008).

may trigger AD.


Table 2. Diagnostic Criteria for Atopic Dermatitis by the American Academy of Dermatology (Ong P, et al. 2008)


Table 3. Differential Diagnosis in Atopic Dermatitis (Deshazo, 2009)7. Treatment

Clinical Management of Atopic Dermatitis 257

The use of natural sunlight for the treatment of atopic dermatitis has been shown to be beneficial, but sunburn should be avoided. If sunlight occurs in the presence of high humidity, or heat which triggers sweating, aggravation of symptoms can occur. Ultraviolet (UV) light (UVB, narrowband UVB, and high-intensity UVA) therapy can be useful in adjunct with other treatments options for patients. Topical glucocorticoid therapy, high-dose UVA1 phototherapy, and UVA-UVB phototherapy were compared in patients with atopic dermatitis. This was a randomized, multi-center trial that found significant differences in favor of high-dose UVA1 and fluocortolone therapy were observed (p < 0.0001), as compared with UVA-UVB therapy. At day 10, high-dose UVA1R was superior to fluocortolone (p < 0.002) therapy. (Krutmann, et al. 1998). There are also several small trials that look at specific wavelengths of and equipment for UV therapy. Chemophototherapy, psoralen with UVA (PUVA), has also been shown to be effective, but should be limited to those patients with widespread AD. Comparison studies with PUVA are limited. Short-term adverse events of UV phototherapy are mild and include: erythema, pruritis, and pigmentation. Potential long-term adverse effects include: premature skin aging, and cutaneous malignancies (Leung, et al. 2004). UV phototherapy is proven to be an effective method of therapy, because of this it is usually used as a

Patients with atopic dermatitis are shown to have significant issues with anxiety, anger, and emotional stress (Bender 2002). They usually respond to embarrassment, frustration, anxiety, or other upsetting events with increased pruritis and scratching (Kodama, et al. 1999). Although emotional factors do not cause atopic dermatitis, studies show that psychological techniques, such as stress reduction approaches, behavior modifications, and group counseling sessions may reduce the exacerbation of atopic dermatitis, particularly

Oral antihistamines are usually recommended for pruritis. However, a recent study of 16 trials showed no little evidence associated with the relief of pruritis with sedating or nonsedating antihistamines (Klein & Clark, 1999). These observations, however, do not exclude the possibility that individual patients may benefit from antihistamines. Because pruritis can be worse at night, oral histamines have been beneficial at bedtime for their sedative properties in patients experiencing symptoms, and can be used as a short-term adjuvant to topical therapy (Kristal & Klein, 2000). The first generation antihistamines, hydroxyzine, diphenhydramine, and cyproheptadine all have sedative effects, but it is shown hydroxyzine to be more effective than the latter (Denman, 1986; Leung, et al. 1998). Newer generation antihistamines ceterizine, loratadine, and fexofenadine may not be beneficial since they lack the sedating properties of the first generation antihistamines. Topical antihistamines should be avoided to the risk of irritating the skin further (Shelley, et al.

**7.1.4 Phototherapy** 

second or third line of treatment.

**7.1.5 Psychological approaches** 

**7.2 Pharmacological therapies 7.2.1 Nonprescription therapies** 

**7.2.1.1 Antihistamines** 

those prone to habitual scratching (Melin, et al. 1986).
