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The main problem does not appear to be an actual underproduction of sweat, but a number of obstructions to efficient distribution. According to the results of a study by Shiohara et al,5 “most AD patients exhibit a defective ability to deliver sweat to the skin surface in response to thermal stress.” This dysfunction may paradoxically result in less sweat on the skin, despite a significant increase in the underlying production of sweat, suggesting a mechanism of compensatory hyperhidrosis.
They also reported that, “Dermcidin, a new[ly discovered]antimicrobial peptide exclusively produced by sweat glands, was abundantly detected not only in the sweat glands and ducts, and the lumen, but also in the dermal tissues adjacent to the sweat glands.”5 This kind of sweat retention in the lumen and/or leakage into surrounding dermal tissues is a key mechanism leading to chronic inflammation, itching, and dry skin, which are all characteristic of AD.
Therapy for Sweating Dysfunction
Understandably, sweat management has emerged as a therapeutic strategy for AD. One of the main recommendations for patients with AD is to look for opportunities to sweat through moderate exercise and exposure to warmth and humidity.2 In a review article, Shiohara and colleagues6 proposed a water-immersion therapy targeting sweat leakage for the treatment of AD. They reported that a daily warm bath with immersion of the legs serves the multiple purposes of inducing more efficient sweat responses, allowing the body to cool, and reducing inflammation.
Although sweat on the skin is the main mechanism for cooling, moisturizing, and protecting the body from allergens, these activities dissipate with time and are most prominent with early sweat. Leaving sweat on the skin has also been associated with increased plugging of the pores by keratin, a common feature in AD. The most effective treatment is simply washing away excess sweat by showering after exercise; wiping away excess sweat on the face, neck and body with a damp towel; and frequently washing from the hands up to the elbows, and the feet, if possible.1,6
Investigation into sweat mechanisms in AD continues with the hope of gaining a better understanding of the disease pathogenesis, leading to more effective treatment strategies.
References
1. Murota H, Yamaga K, Ono E, Katayama I. Sweat in the pathogenesis of atopic dermatitis. Allergol Int. 2018;67:455-459.
2. Hendricks AJ, Vaughn AR, Clark AK, Yosipovitch G, Shi VY. Sweat mechanisms and dysfunctions in atopic dermatitis. J Dermatol Sci. 2018;89:105-111.
3. Wruhs M, Gleiß A, Steiner A, Sator P. Quantity and quality of sweating in atopic dermatitis. Arch Dermatol Res. 2017;309:787-793.
4. Hide M, Tanaka T, Yamamura Y, Koro O, Yamamoto S. IgE-mediated hypersensitivity against human sweat antigen in patients with atopic dermatitis. Acta Derm Venereol. 2002;82:335-340
5. Shiohara T, Doi T, Hayakawa J. Defective sweating responses in atopic dermatitis. Curr Probl Dermatol. 2011;41:68-79.
6. Shiohara T, Mizukawa Y, Shimoda-Komatsu Y, Aoyama Y. Sweat is a most efficient natural moisturizer providing protective immunity at points of allergen entry. Allergol Int. 2018;67:442-447.
