Factors known to trigger atopic eczema (AE) consist of skin irritants (detergents), contact allergens ( perfume and preservatives), aeroallergens, food/dietary factors, microbial colonisation or infection, climate (dry, extreme cold or hot weather), environment (hard water) and psychological stress.
Food allergy is responsible for triggering/exacerbating atopic eczema in >35% of patients, of which largely are infants and young children. Recent studies also reveal flare-up of AE as a result of dietary factors in a significant percentage of older children and adult. Role of food allergy as the triggers of AE is of particular importance in children with uncontrolled and/or moderate-to-severe AE, especially those with gut dismotilit. Common food allergens triggering AE in children are cow’s milk, egg, fish, peanut, soy, tree nuts and wheat. Reaction to food in these patients can be immediate, delayed or a combination of both, therefore different methods of food allergy testing including skin prick test(SPT) and/or serum sIgE test and patch test might be necessary to identify food allergens. As positive SPT and sIgE test only indicate sensitisation not allergy, elimination diet and food challenge may be needed in identifying true food triggers. Children, especially those with multiple food allergy require additional attention, referral to dietician and reassessment of their food allergy every 6-18 months.
Aeroallergens such as animal danders, dust mite and pollens are common allergens capable of flaring-up AE in allergic patients. Role of aeroallergens as trigger is more critical in patients with asthma, rhinitis, older children and adults. Flare-up of symptoms in patients with rhinitis and/or asthma upon contact with animals, during pollen season or on the face and eyelids is suggestive of possible role of animal dander, pollen or dust mite as triggers, respectively. In patients with positive SPT or sIgE test to aeroallergens, atopy patch test may be used to confirm triggering effect of aeroallergens. Avoiding contact with animals and taking appropriate measures to reduce exposure to dust mite and pollens can decrease flare-up and exacerbation of AE in sensitive patients.
A variety of microorganisms such as bacteria, viruses and yeasts can play an important role in the pathogenesis, maintenance and provocation of AE. Epidermal barrier dysfunction in AE causes increased skin permeability and reduces skin antimicrobial properties, which make the skin susceptible to infection and/or colonisation by opportunistic microorganisms such as staphylococcal and streptococcal bacteria. Staphylococcus aureus produces potent endotoxins which act as superantigen causing stimulation of proinflammatory immune response leading to exacerbation of AE. Staphylococcus aureus colonization is present on skin of >80% of patients with AE compared with 5% presentation in healthy individuals. Severity of AE has a positive correlation with degree of bacterial colonization. Oral antibiotics are the medication of choice for active infection or heavy colonization. Research shows that topical corticosteroids without antibiotics are also capable of reducing S. aureus colonization in limited skin lesions, however effective bacterial eradication is achieved once topical antibiotics used. Use of antibacterial detergents are not widely recommended due to potential irritating effect. Eczema Herpeticum, eczema vaccinatum and molluscum contagiosum, though uncommon, are examples of cutaneous viral infection seen in AE patients. Due to epidermal barrier damage in AE, these viruses are capable of dissemination and causing life-threatening complications. Oral antiviral medications are common approach for treatment of viral infection in AE patients. Role of yeasts such as Candida and Malassezia furfur as triggering factors in AE and improvement of symptoms following treatment with topical or oral antifungal agents have been demonstrated in many studies.