Several non-pharmacological treatment options are available for managing atopic dermatitis. Emollients, as discussed in the management section, are recommended to help restore and maintain the skin’s moisture. It has been shown that their use in combination with topical corticosteroids decreases the total dose of corticosteroids required to resolve flares.4
In the Understanding Atopic dermatitis section, it was revealed that impaired skin-barrier functions contribute significantly to the pathophysiology of atopic dermatitis. Lesional and non-lesional skin from atopic dermatitis patients exhibits altered lipid composition and keratinocyte function – when compared to non-atopic skin – resulting in increased rates of transepidermal water loss (TEWL) and a reduced capacity for water retention.5,6
The use of emollients as the basis of therapy for atopic dermatitis helps to limit fluid loss, restore the skin’s lipid content and improve its barrier function. As shown in Figure 2, there are three stages at which an emollient can theoretically help: skin occlusion, replacing lost lipids and incorporating lipids into lamellar bodies.
Figure 2. The three stages of emollient use in skin repair
It is recommended that emollients be applied immediately after bathing to maximise water retention in the skin, and bath-additive emollients and emollient lotions are also advocated as soap substitutes. The combination of emollient creams with pharmacological therapies has proven to be a highly successful treatment approach for both short-term relief and the long-term control of atopic dermatitis. LOCOBASE REPAIR®, an emollient cream that can be used without additional interventions, has been specifically formulated to contain high levels of lipids and lipid-components known to be important in the treatment of atopic dermatitis (ceramide 3, cholesterol, palmitic acid and oleic acid in a nanomolecular formulation). This special formulation can potentially act at three different stages in skin repair; the immediate prevention of TEWL by occlusion, short-term replacement of lost lipids in the stratum corneum, and long-term delivery of supplemental lipids to facilitate the formation of lamellar bodies.
Another non-pharmacological approach to reducing the impact of atopic dermatitis is patient education coupled with ‘trigger’ avoidance. Patient education is an extremely valuable therapy as, once identified, specific allergens that induce or exacerbate flares can be avoided. Lifestyle changes, such as alterations to diets, clothing, choice of detergents or bedding materials, can help to reduce the overall exposure to allergens and serves to reduce the frequency and severity of flares significantly.
References
5. Jensen JM, Folster-Holst R, Baranowsky A, et al. Impaired sphingomyelinase activity and epidermal differentiation in atopic dermatitis. J Invest Dermatol 2004; 122: 1423–31.
6. Proksch E, Folster-Holst R, Jensen JM. Skin barrier function, epidermal proliferation and differentiation in eczema. J Dermatol Sci 2006; 43: 159–69.
7. Roelofzen JH, Aben KK, Khawar AJ, et al. Treatment policy for psoriasis and eczema: a survey among dermatologists in the Netherlands and Belgian Flanders. Eur J Dermatol 2007; 17: 416–21.
© February 2010 Astellas Pharma Europe LTD.
Disclaimer:
The Atopic Dermatitis Knowledge centre contained within www.epgonline.org and available at www.atopicdermatitisinfo.org is intended to be for educational use only and not designed to provide medical advice or professional services.