In atopic eczema, immune dysfunction occurs both in the skin and systemically, although whether treatment with topical steroids rectifies this dysfunction at both sites is unknown.
Atopic eczema is a chronic, inflammatory skin condition that affects up to 20% of children. The condition usually begins within the first year of life and treatment involves the regular use of emollients and disease flares are managed with topical steroids to dampen down the localised inflammatory response. Previous work has revealed how immune dysfunction in the skin is characterised by the production of pro-inflammatory cytokines but that there are also changes in the level of systemic markers during a disease flare.
In an attempt to gain a better understanding of how these markers change during therapy with topical steroids, researchers from the Department of Paediatric Dermatology, Children’s Health at Crumlin, Dublin, Ireland, examined the changes in cytokine markers in an observational study of children with atopic eczema experiencing a disease flare treated with the topical steroid, hydrocortisone 1%, in line with normal clinical practice guidance. All children were less than a year old with moderate to severe eczema based on a SCORAD (disease severity) score of 25 or greater. Team also included a control group of healthy children to compare any changes in cytokine levels. Samples of the skin and plasma were taken and both analysed for a large number of different biomarkers including inflammatory cytokines such interleukin-18 (IL-18), IL-5, IL-13, CXCL8, il-1 alpha and CCL17 and CCL22.
A total of 47 children with atopic eczema and 20 controls were included in the analysis and changes in biomarkers were compared between baseline and after 6 weeks of topical steroid therapy. The most pronounced differences in cytokine levels in the skin between eczema and healthy controls were for those associated with innate immune activation, e.g, IL-18, CXCL8, IL-1alpha, CCL17 and CCL22 although levels in eczema patients did not reduce to the levels observed in healthy controls. In contrast, the largest changes in the blood were with CCL17, IL-13, CCL22, IL-5 and CCL26. Interestingly, these latter changes, which represent key cytokines in the pathophysiology of atopic eczema, only occurred in the blood and not in the skin.
Commenting on their results, the authors suggested that their data indicates that topical steroids had both a local and systemic effect to minimise the inflammation response induced by an eczema flare.
McAleer MA et al. Topical corticosteroids normalise both skin and systemic inflammatory markers in infant atopic dermatitis. Br J Dermatol 2020 doi: 10.1111/bjd.19703