About 30% to 40% of AD children with moderate to severe AD have immediate IgE-mediated food reactions. Patients or families also describe delayed cutaneous reactions after ingesting certain foods. These reactions are more difficult to reproduce or characterize as to mechanism of action.

In children older than 1 year, negative allergy skin tests for foods have high negative predictive value (O95%), essentially ruling out IgE-mediated food allergy. On the other hand, a positive skin test to a food allergen has a positive predictive value of only approximately 50%.

More recently, food-specific IgE levels measured by serum ImmunoCAP assay have been shown to have predictive values up to 95% for selected foods at specific levels. These foods include cow’s milk, eggs, peanuts, and fish. However, it is crucial to recognize the limitations of this assay.

It is especially important to note that the lower end of sensitivity for the assay is not zero, but less than 0.35kU/L. Rarely do patients still react at very low levels of food-specific IgE. In addition, specific IgE levels do not define severity of the clinical reaction.

The clinical history of the patient remains important in conjunction with the use of in vivo or in vitro allergy tests. This is important because unnecessary limitation of diet based on testing can severely compromise the patient’s nutrition status. Ultimately, food challenges may be needed for diagnosing clinically relevant food allergies.

These should be done with the involvement of an allergist familiar with the procedure. Foods that are confirmed to cause allergic reactions should be eliminated from the patient’s diet as repeat ingestion may cause a spectrum of allergic reactions.

The ImmunoCAP assay may also be useful in following the natural history of a patient’s food allergy with repeat measurements obtained approximately 12 months apart because most children become tolerant to cow’s milk and egg protein, as opposed to peanuts, tree nuts, fish, or shellfish.

Although there is limited data on the role of domestic animals or pollens as triggers for AD, case reports and atopy patch testing suggest a role for these allergens in sensitized AD patients. The best-studied aeroallergen in AD is house dust mite (HDM).

However, blinded placebo-controlled studies have shown conflicting results on the role of HDM-control measures in AD. Nevertheless, HDM control measures should be considered in sensitized patients, as these patients often have concurrent respiratory allergies or are at risk for developing these allergies.

The control measures include the use of HDM-proof encasings, frequent vacuuming (eg, once a week) and washing linens in hot water. At this time, specific allergen immunotherapy (‘‘allergy shots’’) is not indicated for AD, although limited studies suggest benefit in HDM-sensitized adult AD patients.

S aureus can be cultured from the skin lesions of most AD patients. AD patients are predisposed to colonization and infections by S aureus through deficiency in endogenous antimicrobial peptides as well as through a defective skin barrier.

S aureus from patients with AD typically secrete toxins that can cause T cell activation by acting as superantigens, which can exacerbate and perpetuate cutaneous inflammation. AD patients also make specific IgE directed against these toxins, thus further triggering activation of mast cells and other IgE receptor–bearing cells in AD lesions.

Although AD patients are at risk for infections by S aureus, use of antibiotics in the absence of clinical signs of infection is not recommended because of the risk of bacterial resistance. A first-generation cephalosporin, such as cephalexin, for 7 to 10 days for overt infections is effective unless the patient is infected by a resistant strain of S aureus.

Baths and cleansers as part of routine care can reduce S aureus colonization. Most AD patients do not tolerate harsh antiseptic cleansers, such as chlorhexidine or bleach baths, although some dermatologists recommend dilute bleach baths for AD patients with recurrent methicillin-resistant S aureus superinfections.

Antibacterial cleansers, such as Lever 2000, can be considered, although some patients may still find these to be irritating to their skin. The nose is a major reservoir of S aureus and intranasal mupirocin (Bactroban) applied twice daily for 5 to 7 days may eradicate S aureus and improve AD.

Herpes simplex virus can cause life-threatening eczema herpeticum in AD patients. Therefore, physicians who treat AD must be vigilant for this infection. The infected area may not present with vesicular lesions or the area may appear as punched-out lesions with an erythematous base.

Ideally, viral polymerase chain reaction (PCR), Tczank smear, and/or culture should be obtained by unroofing an intact vesicle because the yield from excoriated lesions is low. The mainstay of treatment is systemic acyclovir.

Patients with disseminated lesions who appear toxic should be admitted to the hospital for intravenous acyclovir and antistaphylococcal antibiotic pending PCR and culture results.

Patients with periocular or suspected ocular involvement should be evaluated by an ophthalmologist emergently. AD patients are also more susceptible to molluscum contagiosum (MC) virus infection. The lesions typically present as single or multiple flesh-colored papules, which may be distributed on the trunk, extremities, or face.

The treatment of MC depends on the location and number of the lesions, and the ability of the patient to tolerate painful procedures. If lesions are not periocular, they can be observed, as spontaneous resolution does occur. However, they are contagious and can spread through autoinoculation.

In addition, they can occasionally scar with resolution. Treatment options include curettage under topical anesthetic cream, cryotherapy, cantharidin (a blistering agent), or topical imiquimod and tretinoin, although none of the treatments are currently approved by Food and Drug Administration for MC.

Sensitization to the yeast Malassezia species has also been demonstrated in a subgroup of AD patients. Specific IgE levels to Malassezia furfur (previously known as Pityrosporum orbiculare) have been correlated with severity of AD.

Antifungal therapy has been shown to be effective in a subgroup of AD patients in several studies, with most studies showing a correlation between response to antifungals and the levels of specific IgE.

However, the mechanism of antifungal therapy in AD remains to be clarified. It is likely that antifungal therapy may exert anti-inflammatory effects in addition to the fungicidal activity. Further studies are needed to confirm the use of antifungal agents in AD patients who are colonized by these organisms.