Pathophysiology of pruritus in atopic dermatitis: an overview

Ständer, Sonja; Steinhoff, Martin

doi:10.1034/j.1600-0625.2002.110102.x

Cited by 218 publications

(185 citation statements)

References 177 publications

(184 reference statements)

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“…However, we now know that the sensation of itch and nociception cannot be equated with each other. In fact, the once-popular theories that itch is based on a specific pattern of action potentials running through pain pathways or that itch results from the combination of other primary sensory signals have now fallen out of favor (3,10). Likewise the confirmation of the long-denied existence of central itch-specific neuronal pathways in the human and feline systems supports the concept that the sensation of itch and nociception represent distinct sensory systems (9,11).…”

Section: The Sensation Of Itch and Nociception Are Distinct Entitiesmentioning

confidence: 52%

“…TRPV1 activation first excites (84), then desensitizes, the sensory afferents - an effect that establishes the basis for the therapeutic application of vanilloids to mitigate pain and itch (3, S16). Vanilloid administration results in a depletion of neuropeptides (such as SP) in the C-fibers, which suspends the interplay between skin sensory neurons and mast cells (Figure 1) (3,6,10). Indeed, topical capsaicin suppresses histamine-induced itch (86) and is increasingly used in the therapy of pruritus in numerous skin diseases (reviewed in refs.…”

Section: Endovanilloids and The Trpv1 Ion Channel Are Promising Targementioning

confidence: 99%

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Frontiers in pruritus research: scratching the brain for more effective itch therapy

Paus

Schmelz

Bı́ró

et al. 2006

Journal of Clinical Investigation

329

287

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This Review highlights selected frontiers in pruritus research and focuses on recently attained insights into the neurophysiological, neuroimmunological, and neuroendocrine mechanisms underlying skin-derived itch (pruritogenic pruritus), which may affect future antipruritic strategies. Special attention is paid to newly identified itch-specific neuronal pathways in the spinothalamic tract that are distinct from pain pathways and to CNS regions that process peripheral pruritogenic stimuli. In addition, the relation between itch and pain is discussed, with emphasis on how the intimate contacts between these closely related yet distinct sensory phenomena may be exploited therapeutically. Furthermore, newly identified or unduly neglected intracutaneous itch mediators (e.g., endovanilloids, proteases, cannabinoids, opioids, neurotrophins, and cytokines) and relevant receptors (e.g., vanilloid receptor channels and proteinase-activated, cannabinoid, opioid, cytokine, and new histamine receptors) are discussed. In summarizing promising new avenues for managing itch more effectively, we advocate therapeutic approaches that strive for the combination of peripherally active antiinflammatory agents with drugs that counteract chronic central itch sensitization. The study of pruritus in a nutshellItching (pruritus) is perhaps the most common symptom associated with numerous skin diseases and can be a lead symptom of extracutaneous disease (e.g., malignancy, infection, and metabolic disorders) (1, S1). However, despite approximately a century of pruritus research (2, S2, S3), there is no generally accepted therapy for the treatment of itch, and many mysteries, misconceptions, and controversies still haunt this rather neglected, yet clinically important and scientifically fascinating, niche in the life sciences (3, 4, 5). It is the brain that itches, not the skinPruritus causes the desire to scratch the skin and is experienced as a sensation arising in the skin. However, like all other skin sensations, itch, strictly speaking, is an extracutaneous event - a product of CNS activities. The intense itch we feel after an insect bite, in a patch of atopic eczema, during an episode of food-induced urticaria, or in association with diabetes, uremia, or scabies mite infection (S1) represents a neuronal projection of a centrally formed sensation into defined regions of the integument (localized pruritus) or into large territories of our body surface (generalized pruritus).Interestingly, our individual reception of and emotional response to itch strongly depends on its exact quality: while a tickling sensation usually is experienced as pleasurable, persistent itch is an annoying or even torturous sensation (S4). While one is tempted to interpret this as indicating a distinct molecular and/or structural basis of these different itch qualities, it has proven excruciatingly difficult to identify their molecular, structural, and neurophysiological differences (ref. 1; see below).As pruritus can arise from localized or systemic, peripheral o...

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Section: The Sensation Of Itch and Nociception Are Distinct Entitiesmentioning

confidence: 52%

Section: Endovanilloids and The Trpv1 Ion Channel Are Promising Targementioning

confidence: 99%

Frontiers in pruritus research: scratching the brain for more effective itch therapy

Paus

Schmelz

Bı́ró

et al. 2006

Journal of Clinical Investigation

329

287

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“…These results suggested that opioid receptor is involved in Gsp-induced USRs. Opioids have been reported to play an interesting role in itch induced not only by histamine release from dermal mast cells but also by a direct central and peripheral pruritogenic effect in addition to their major well-known role in pain (Stander and Steinhoff, 2002).…”

Section: Discussionmentioning

confidence: 99%

Glucosylsphingosine Induces Itch-Scratch Responses in Mice

Kim¹,

Kim²,

Noh³

et al. 2010

Biomolecules and Therapeutics

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-Pruritus is one of major symptoms in atopic dermatis. The pathophysiological mechanism of pruritus is unclear. The search for pruritogen is important in elucidating the pathophysiological mechanism of pruritus in atopic dermatitis. Glucosylsphingosine (Gsp) is upregulated in the strateum corneum of atopic dermatitis patients. We investigated to determine whether Gsp induces itch-scratch responses (ISRs) in mice. Intradermal administration of Gsp induces ISRs. Gsp dose-dependently induced scratching response at 50-500 nmol/site range. Pretreatment with naltrexone, an opioid μ receptor antagonist, and capsaicin, a TrpV1 receptor agonist, inhibited Gsp-induced ISRs. Additionally, Gsp-induced ISRs were also suppressed by cyproheptadine, an antagonist of serotonin receptor. These findings suggest that Gsp-induced scratching might be at least partly mediated by capsaicin-sensitive primary afferents, and the opioids receptor systems might be involved in transmission of itch signaling in the central nervous system. Furthermore, our findings suggest that Gsp-induced ISRs may be attributable to the serotonin-mediated pathways and Gsp is not any more one of byproducts of abnormal skin barrier but can lead to induce pruritus, one of typical symptoms of atopic dermatitis.

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“…Heat may play a harmful role in some AD patients by provoking perspiration, which is one of the most commonly reported aggravants in children with AD [139][140][141][142][143]. Perspiration may have an irritant effect on the skin mediated by the acidic pH of sweat, possibly promoting Th-2 inflammation [88], increased cutaneous blood flow due to vasodilation in hot environments [142], and possibly a neuroanatomic mechanism mediated by C nerve fibers [144]. The worsening of AD symptoms by increased temperature likely explains patient preference toward lighter clothing, thereby allowing for better skin ventilation and facilitating heat dissipation [86].…”

Section: Climatementioning

confidence: 99%

Environmental risk factors and their role in the management of atopic dermatitis

Kantor

Silverberg

2016

Expert Review of Clinical Immunology

268

225

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Introduction-The etiology of atopic dermatitis (AD) is multifactorial with interaction between genetics, immune and environmental factors.Areas covered-We review the role of prenatal exposures, irritants and pruritogens, pathogens, climate factors, including temperature, humidity, ultraviolet radiation, outdoor and indoor air pollutants, tobacco smoke exposure, water hardness, urban vs. rural living, diet, breastfeeding, probiotics and prebiotics on AD.Expert commentary-The increased global prevalence of AD cannot be attributed to genetics alone, suggesting that evolving environmental exposures may trigger and/or flare disease in predisposed individuals. There is a complex interplay between different environmental factors, including individual use of personal care products and exposure to climate, pollution, food and other exogenous factors. Understanding these complex risk factors is crucial to developing targeted interventions to prevent the disease in millions. Moreover, patients require counseling on optimal regimens for minimization of exposure to irritants and pruritogens and other harmful exposures.

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Pathophysiology of pruritus in atopic dermatitis: an overview

Cited by 218 publications

References 177 publications

Frontiers in pruritus research: scratching the brain for more effective itch therapy

Frontiers in pruritus research: scratching the brain for more effective itch therapy

Glucosylsphingosine Induces Itch-Scratch Responses in Mice

Environmental risk factors and their role in the management of atopic dermatitis

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