Barrier repair therapy in atopic dermatitis: an overview.

Atopic eczema or dermatitis (AD) is a chronically relapsing dermatitis associated with pruritus, sleep disturbance, psychosocial symptoms, and impaired quality of life. It affects 10-20 % of school-aged children, and there is evidence to suggest that this prevalence is increasing. Filaggrin (filament-aggregating protein) has an important function in epidermal differentiation and barrier function. Null mutations within the filaggrin gene cause ichthyosis vulgaris and appear to be a major risk factor for developing AD. The affected skin of atopic individuals is deficient in filaggrin degradation products or ceramides. Avoidance of triggering factors, optimal skin care, topical corticosteroids, and calcineurin inhibitors are the mainstays of therapy for AD. Proper moisturizer therapy can reduce the frequency and intensity of flares, as well as the need for topical corticosteroids or topical calcineurin inhibitors. Recent advances in the understanding of the pathophysiological process of AD involving filaggrin and ceramides has led to the concept of barrier therapy and the production of new moisturizers and topical skin products targeted to correct reduced amounts of ceramides and natural moisturizing factors in the skin with natural moisturizing factors, ceramides, and pseudoceramide products. Emollients, both creams and ointments, improve the barrier function of the stratum corneum by providing it with water and lipids. Studies on AD and barrier repair treatment show that adequate lipid replacement therapy reduces the inflammation and restores epidermal function. We reviewed 12 randomized trials and 11 cohort studies and found some evidence that certain products had therapeutic efficacy in improving clinical and/or biophysical parameters of patients with AD. Nevertheless, study methods were often flawed and sample sizes were small. Additional research is warranted to better understand the optimal formulary compositions. Also, long-term studies would be important to evaluate whether lipid barrier replacement therapy reduces bacterial colonization or prevents progression of the atopic march.