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The pathogenetic rationale and effectiveness of including ω-3 polyunsaturated fatty acids in the complex therapy of atopic dermatitis in adults

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We examined 101 patients with moderate to severe AD aged 18 to 59 years (Me 31 [23; 41] years). Sixty-five subjects were administrated ω-3 PUFAs in addition to basic therapy and were randomized into subgroups receiving a high (3.6 g/ day, 200/240 mg EPA/DHA) or low (0.72 g/day, 40/48 mg EPA/DHA) dose of fish oil for 30 days. The control group consisted of 36 patients on standard therapy. Efficacy was assessed by the dynamics of the SCORAD index, the severity of subjective symptoms (itching, sleep disorders), and the proportion of patients with complete resolution of clinical manifestations. The most significant reduction in disease severity was observed in patients receiving a high dose of ω-3 PUFAs: the SCORAD index decreased by 81.8% (from 55 [41; 70] to 10 [8; 13] points, p<0.001), itching intensity by 87.5%, and sleep disorders by 66.7%. In the low-dose group, the reduction in SCORAD was 63.6% (to 16 [12; 20], p<0.001), and in the control group - 50% (to 20 [17; 22], p<0.001). The inclusion of ω-3 PUFA in the complex therapy showed a statistically significant advantage in the degree of AD manifestation reduction over the control group (p<0.05). Analysis of the proportions of patients with complete symptom resolution confirmed the dose-dependent effect: for key symptoms (rash, itching, dry skin), the responder rate was significantly higher in the high-dose group compared to both the control and the low-dose group (p<0.05). No adverse events have been reported. The study demonstrated the dose-dependent efficacy of ω-3 PUFAs in the complex therapy of AD in adults. The intake in a dose of 200/240 mg EPA/DHA provides a significantly greater reduction in disease severity according to SCORAD, a decrease in the severity of subjective symptoms, and an increase in the proportion of patients with complete regression of symptoms compared to both a low dose of ω-3 PUFAs and standard therapy. The obtained data confirm the pathogenetic rationale for including ω-3 PUFAs in the AD treatment.

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