Gamma-Linolenic acid levels correlate with clinical efficacy of evening primrose oil in patients with atopic dermatitis

Introduction: In patients with atopic dermatitis (AD) there is an imbalance in fatty acid metabolism related to a deficiency in the delta-6-desaturase, an enzyme responsible for the conversion of linoleic acid (LA) to gamma-linolenic acid (GLA). Evening primrose oil (EPO, Oenothera biennis ) is extracted from seeds of this plant which contains high amounts of GLA (approximately 80 mg per 1 g of EPO). Aim: The aim of the study was to investigate whether EPO supplementation results in an increase in plasma GLA and its metabolite dihomo-gamma-linolenic acid (DGLA) correlating with clinical improvement of AD, assessed by the SCORing Atopic Dermatitis (SCORAD) index. Method: The open study included 21 patients with AD (intention to treat population; ITT). Thereof seven patients had to be excluded from the ITT population because of poor treatment compliance (< 75% of study medication intake) and so the per-protocol population comprised 14 patients. EPO (4 – 6 g) was administered daily for 12 weeks. Before treatment, and 4 and 12 weeks after initiation of EPO supplementation, objective SCORAD was assessed and plasma concentrations of GLA and DGLA were determined by gas chromatography. Results: A significant increase in plasma GLA and DGLA levels and a decrease in the objective SCORAD were observed 4 and 12 weeks after initiation of EPO treatment (Table 1). In the per-protocol population (n = 14), a significant inverse correlation between the changes in plasma GLA levels and SCORAD was found (p = 0.008) (Figure 1). Conclusion: The clinical disease activity under EPO treatment correlates with the individual increase in plasma GLA levels. Thus, the results of this pilot study indicate that an increase in plasma GLA might be used as predictive parameter for responsiveness of AD to EPO therapy [1]. Tab. 1: Elements of the objective and the total SCORAD (mean ± SD) in the intention-to treat population (n = 21) at baseline and at last visit (Wilcoxon Signed Rank Test). SCORAD items Baseline Last visit P value A: extent of AD (%) 13.7 (12.0) 4.0 (3.6) < 0.001 B: total intensity of AD 6.9 (1.9) 4.0 (2.4) < 0.001 B1 intensity of erythema 1.4 (0.5) 1.0 (0.7) 0.046 B2: intensity of edema 0.7 (0.7) 0.2 (0.4) 0.021 B3 intensity of weeping/crusting 0.4 (0.7) 0.2 (0.5) 0.470 B4: intensity excoriation 1.1 (0.8) 0.5 (0.6) 0.004 B5: intensity lichenification 1.5 (0.7) 1.0 (0.9) 0.046 B6: intensity dryness of skin 1.8 (0.8) 1.0 (0.6) 0.003 Objective SCORAD 26.7 (7.6) 14.6 (6.9) < 0.001 C: total subjective symptoms (itching + insomnia. VAS in mm) 51.0 (34.5) 43.5 (49.8) 0.145 Total SCORAD 31.8 (8.7) 19.0 (12.7) < 0 002 The objective SCORAD formula is A/5 + 7B/2 The Total SCORAD formula is: A/5 + 7B/2 + C. Where, A = extent (rule of nine in %) of AD, B = sum of intensity of 6 symptoms erythema, edema, weeping/crusting, excoriation, lichenification, dryness of skin of AD (B1 to B6), and C = subjective symptoms (0 – 20). AD, atopic dermatitis; SCORAD, SCORing Atopic Dermatitis; VAS, Visual Analogue Score. Fig. 1: Correlation analysis on the per-protocol population (n = 14) between the change in objective SCORAD (%) and change of plasma GLA (%) from baseline versus last visit. GLA gamma-linolenic acid. SCORAD SCORing Atopic Dermatitis. Disclosure statement: The clinical study was sponsored by Zeller Medical AG. Catherine Zahner and Cordula Moll are employees of Zeller Medical AG.