Sweat mechanisms and dysfunctions in atopic dermatitis

Hendricks, Aleksi J.; Vaughn, Alexandra R.; Clark, Ashley K.; Yosipovitch, Gil; Shi, Vivian Y.

doi:10.1016/j.jdermsci.2017.11.005

Cited by 38 publications

(36 citation statements)

References 51 publications

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“…When healthy athletes underwent endurance cardio exercise, stratum corneum hydration and surface pH significantly increased after exercise, while sebum content declined significantly . In a separate study, stratum corneum hydration and surface pH significantly increased after exercise, while sebum content declined significantly.…”

Section: Mental and Physical Stressmentioning

confidence: 80%

The impact of stress on epidermal barrier function: an evidence‐based review

Maarouf

Yosipovitch

et al. 2019

Br J Dermatol

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Summary Background The epidermal barrier functions to limit skin infection and inflammation by inhibiting irritant and immunogen invasion. Abundant evidence suggests that psychological stress stemming from crowding, isolation, nicotine smoking, insomnia, mental arithmetic tasks, physical pain, real‐life stressors (examinations and marital strain) and lack of positive personality traits may impart both acute and chronic epidermal dysfunction. Objectives To review the relationship between stress and epidermal barrier dysfunction. Methods A review of the PubMed and Embase databases was conducted to identify all English‐language case–control, cross‐sectional and randomized control trials that have reported the effect of stress on epidermal barrier function. The authors’ conclusions are based on the available evidence from 21 studies that met the inclusion and exclusion criteria. Results Psychological stressors upregulate the hypothalamic–pituitary–adrenal axis to stimulate local and systemic stress hormone production. This ultimately leads to aberrant barrier dysfunction, characterized by decreased epidermal lipid and structural protein production, decreased stratum corneum hydration and increased transepidermal water loss. Conclusions This evidence‐based review explores the adverse effects of psychological stressors on epidermal barrier function. Future investigations using more real‐life stressors are needed to elucidate further their impact on skin physiology and identify practical stress‐relieving therapies that minimize and restore epidermal barrier dysfunction, particularly in at‐risk populations. What's already known about this topic? The literature reports the negative effect of stress on prolonged wound healing. Less is known about the relationship between stress and epidermal barrier dysfunction, a chronic, superficial wound involving the upper epidermal layers. What does this study add? Psychological stressors impact epidermal barrier function by activating the hypothalamic–pituitary–adrenal axis to stimulate local and systemic stress hormone production. Stress hormones negatively affect the epidermal barrier by decreasing epidermal lipids and structural proteins, decreasing stratum corneum hydration and increasing transepidermal water loss. Identification of such stressors can promote stress‐avoidance and stress‐reduction behaviours that protect epidermal barrier function and prevent certain dermatological conditions.

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Section: Mental and Physical Stressmentioning

confidence: 80%

The impact of stress on epidermal barrier function: an evidence‐based review

Maarouf

Yosipovitch

et al. 2019

Br J Dermatol

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“…In fact, AD is commonly referred as "the itch that rashes," which reflects itch often precedes skin lesions in AD. 18 The pruritus in AD is very difficult to treat and does not respond well to traditional antipruritic treatments such as oral antihistamines. 15 Furthermore, transepidermal water loss (TEWL) is associated with itch intensity in AD, 16 and TEWL increases at night in patients with AD, which may explain why AD patients have nocturnal bouts of itch.…”

Section: Itch Characteristics In Admentioning

confidence: 99%

“…17 Moreover, patients with AD often develop lesions on flexor surfaces, which has led others to suggest that sweating may play a role in the pathogenesis of AD. 18 The pruritus in AD is very difficult to treat and does not respond well to traditional antipruritic treatments such as oral antihistamines. 1 There is an "itch-scratch cycle" that exacerbates skin lesions and pruritus.…”

Section: Itch Characteristics In Admentioning

confidence: 99%

Immune mediators and therapies for pruritus in atopic dermatitis and psoriasis

Zhou

et al. 2019

J Cutaneous Imm & Allergy

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractAtopic dermatitis (AD) and psoriasis (Pso) are two common inflammatory skin diseases which are symptomatically characterized by pruritus to variable degrees.Whereas AD is nearly always associated with pruritus, only 50%-70% of patients with Pso suffer from itching. Within the last decade, the development of biologic agents targeting specific cytokines or cytokine receptors has led to tremendous progress in suppressing inflammation (and thus improving quality of life) in these two diseases.While suppressing inflammation would generally reduce pruritus in these inflammatory diseases, pruritus is still recalcitrant for treatment in some patients due to relative lack of therapeutics that specifically inhibit pruritus signaling. There is abundant evidence that certain cytokines and neuropeptides-ion channels signaling mediate pruritus that is independent of inflammation in AD and psoriasis. Of note, Janus kinase (JAK) and nerve growth factor (NGF)-tropomyosin receptor kinase A (TrkA)transient receptor potential vanilloid 1 (TRPV1) signaling partially regulates pruritus in AD and psoriasis. JAK kinases inhibitors decrease the extent of itch in patients with AD and psoriasis. In clinical trials, topical inhibitors of TrkA and TRPV1 have been reported to reduce pruritus in patients with Pso and AD, respectively. In this article, we review recent literature knowledge regarding the mechanisms underlying pruritus in AD and Pso, providing hypotheses for why pruritus may be more common in AD than in Pso. In light of the different mechanisms underlying these two diseases, the current and developing therapeutics, either in human clinical trials or animal studies, for targeting pruritus are also discussed. K E Y W O R D SIL-31, neuropeptide, PAR2, SP, thymic stromal lymphopoietin, TRPA1, TRPV1

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“…Sweat can contribute to the development or exacerbation of itching . Indeed, in daily clinical practice, “itchy when sweating” is a complaint frequently heard from patients with dermatoses, especially atopic dermatitis (AD).…”

Section: Introductionmentioning

confidence: 99%

“…Sweat‐related itch can be divided into two categories: direct and indirect involvement of sweat. As an example of the former, it is conceivable that sweat permeates into the tissues through the epidermis or sweat gland organs and causes itching . Examples of the latter include itch associated with skin diseases (eg miliaria, xerosis due to anhidrosis, dyshidrotic eczema and vulvar syringoma) .…”

Section: Introductionmentioning

confidence: 99%

Why does sweat lead to the development of itch in atopic dermatitis?

Murota

Yamaga

Ono

et al. 2019

Experimental Dermatology

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Sweating plays an important role in maintaining temperature homeostasis in humans. However, under certain circumstances, sweat can cause itching. For example, when excessive sweat accumulates on the skin surface for a long period, miliaria can develop and cause itching. Subjects with dermatoses, such as atopic dermatitis (AD), suffer from itch when exposed to heat or psychological stresses, which are also known perspiration stimuli. Recently, some mechanisms of sweat‐induced itch have been revealed. For instance, attenuated sweating ability is observed in subjects with AD, causing heat retention, skin dryness, and high susceptibility to itch. Furthermore, the decreased tight junction of the sweat gland in AD leads to sweat leakage in the dermis, which could be designated as a “sweat endocrine response” and may be the cause of tingling itch during sweating. Additionally, metabolomic analysis of sweat from patients with AD revealed that glucose concentration in sweat increases according to disease severity. Sweat with elevated glucose concentration retards the recovery of the damaged skin barrier and may promote itching. This viewpoint essay outlines the relationship between sweat and itch based on recent evidence.

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Sweat mechanisms and dysfunctions in atopic dermatitis

Cited by 38 publications

References 51 publications

The impact of stress on epidermal barrier function: an evidence‐based review

The impact of stress on epidermal barrier function: an evidence‐based review

Immune mediators and therapies for pruritus in atopic dermatitis and psoriasis

Why does sweat lead to the development of itch in atopic dermatitis?

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