Dysfunction of normal sweating, which is necessary to cool and hydrate the skin, may cause or exacerbate skin disorders. Skin barrier dysfunction is a primary mechanism in the production of the common symptoms of atopic dermatitis (AD), including skin dryness, irritation, and itching, and leaves the body vulnerable to allergens and pathogens. Studies have begun to identify a major role for sweat dysfunction in the development of all of these symptoms.1-3

The Normal Functions of Sweat

Sweating provides an exterior defense system that protects the body in 3 ways. Although it is well recognized as a main mediator in regulating body temperature, sweat also plays an important role in moisturizing the skin and the maintenance of the skin as the innate host defense system.1

Sweat is a clear hypotonic secretion produced by eccrine glands throughout the body in response to increases in core body temperature triggered by the environment, exercise, illness, or heightened emotions.2 Sweat is composed of sodium lactate and urea, both of which contribute to the skin’s moisture retention. Vaporization of sweat on the skin is the main autonomic mechanism through which the body cools itself, requiring about 100 cc of sweat for cooling of 1 degree in adults who weigh  approximately 70 kg.1  S:\Dermatology Advisor\Articles\2019 Website Content\05 May\Features\DA_Feature_Peckel_Sweat.Gland.Dysfunction.Dermatitis Inadequate quantities of sweat on the skin can interfere with these normal mechanisms, resulting in excessive drying of the skin and overheating of the body.1

Other components of sweat include antimicrobial peptides such as cathelicidin, β-defensins, and dermcidin, which are key to sustaining a natural barrier against pathogens, while chemical reactions to the components of sweat may also inhibit the activity of potential allergens.1

Altered Sweat Mechanisms in AD

In patients with AD, both the quantity and quality of sweat have been shown to be altered.2,3 In terms of quantity, study results are conflicting, reporting both hyperhidrosis and anhidrosis. Too much sweat can certainly increase skin irritation, but autonomic imbalances leading to reduced sweating have also been identified in patients with AD. In addition to observed abnormalities in sweat production, there is often leakage into tissues surrounding the sweat glands. The pores of the skin may become clogged with keratin, preventing sweat from permeating the skin’s surface.1

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Another contributing factor to the expression of AD is a proposed “sweat allergy,” in which the makeup of the sweat produces an allergenic response. The presence of specific immunoglobulin E (IgE) antibodies has been found to be significantly higher in patients with AD. A study by Hide and colleagues4 reported that IgE antibodies were present in the sweat of 84% of patients with AD compared with 11% in the non-AD control group, which correlated directly with complaints of itching. The study found that histamine release was induced by basophils in the sweat of both the AD and control groups, but that IgE in the sweat of patients with AD largely blocked histamine release, resulting in a type I sensitivity to their own sweat. This was defined as a sweat allergy, which correlated positively with the severity of AD.4