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Linoleic Acid Metabolites and Transepidermal Water Loss in Children With Atopic Dermatitis

Yang YH, Wang LC, Lee JH, Chiang BL. Ann Allergy Asthma Immunol. 2008;100(1):66–73 PURPOSE OF THE STUDY. To investigate whether n-6 essential fatty acid (EFA) deficits account for atopic dermatitis (AD) by affecting transepidermal water loss (TEWL). STUDY POPULATION. Children between the ages of 2 and 17 years with AD (n = 35), asthma or allergic rhinitis (AS/AR group, n = 35), or no atopic disease (n = 31) were studied. The AD group did not have allergic airway disease. METHODS. Synthesis of the n-6 EFA from linoleic acid (LA) involves alternating steps of desaturation and elongation with serial conversion to γ-linoleic acid (GLA), dihommo-γ-linoleic acid (DGLA), and arachidonic acid (AA). Fasting blood samples were obtained with immediate serum separation and freezing to prevent changes in fatty acid composition of serum lipids. Analysis of lipid content was performed by gas chromatography/mass spectrometry. Measurement of TEWL on the right volar forearm was reported as loss of grams of water per square meter of skin per hour. Nonparametric tests were used to evaluate differences between the groups. RESULTS. Although not statistically significant, patients in the AD and AS/AR groups had higher LA and lower AA levels than controls. Patients with AD but not AS/AR had statistically lower GLA (P = .04) and DGLA (P = .03) levels than control subjects. There were no differences between the 2 groups of atopic patients. Ratios of GLA/LA, DGLA/LA, and AA/LA were lower in the AD group than controls (P < .01 for each). However, in the AS/AR group, only the GLA/LA and DGLA/LA ratios were statistically lower than in controls. TEWL had a significant negative correlation with GLA and DGLA (P = .001) and near-significant negative correlation with AA (P = .06). In subjects with AD, TEWL and the Scoring Atopic Dermatitis (SCORAD) index were correlated (P < .001). The SCORAD index had a significant correlation with GLA and DGLA (P < .001) but not AA (P = .06). CONCLUSIONS. AD is associated with a defect in n-6 EFA metabolism. LA metabolites are involved in the maintenance of the epidermal water barrier. REVIEWER COMMENTS. Antimicrobial protein defects, filaggrin defects, and fatty acid defects are among the newer areas of research on the underlying pathogenesis of AD. Because human epidermis lacks the capacity to convert LA to GLA or DGLA to AA, it is likely that those LA metabolites are synthesized elsewhere and transported to the epidermis. Serum levels of n-6 EFAs, as reported here, presumably reflect epidermal concentrations. It follows, therefore, that dietary supplementation of GLA or topical application of LA metabolites may have therapeutic benefit.