Pruritus in psoriasis: An update

Szepietowski, Jacek C.; Reich, Adam

doi:10.1002/ejp.768

Cited by 116 publications

(114 citation statements)

References 26 publications

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“…Psoriasis is a chronic inflammatory and scaly skin disease that is aggravated by psychosocial stress in 40‐80% of patients . Another common feature affecting 60‐90% of psoriatic patients is pruritus that can have different forms, such as stinging, pinching, tickling, crawling, burning, or even pain sensations …”

Section: Mast Cell‐neural Interactions and Itch In Psoriasismentioning

confidence: 99%

“…This plethora of systems activated during stress means that it is difficult to pinpoint a specific mechanism that is responsible for pruriception in psoriasis. However, one major focus in this context has been the concept of neurogenic inflammation where cutaneous nerve fibers and mast cells interact …”

Section: Mast Cell‐neural Interactions and Itch In Psoriasismentioning

confidence: 99%

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Mast cell‐neural interactions contribute to pain and itch

Gupta

Harvima

2018

Immunological Reviews

216

189

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Mast cells are best recognized for their role in allergy and anaphylaxis, but increasing evidence supports their role in neurogenic inflammation leading to pain and itch. Mast cells act as a "power house" by releasing algogenic and pruritogenic mediators, which initiate a reciprocal communication with specific nociceptors on sensory nerve fibers. Consequently, nerve fibers release inflammatory and vasoactive neuropeptides, which in turn activate mast cells in a feedback mechanism, thus promoting a vicious cycle of mast cell and nociceptor activation leading to neurogenic inflammation and pain/pruritus. Mechanisms underlying mast cell differentiation, activation, and intercellular interactions with inflammatory, vascular, and neural systems are deeply influenced by their microenvironment, imparting enormous heterogeneity and complexity in understanding their contribution to pain and pruritus. Neurogenic inflammation is central to both pain and pruritus, but specific mediators released by mast cells to promote this process may vary depending upon their location, stimuli, underlying pathology, gender, and species. Therefore, in this review, we present the contribution of mast cells in pathological conditions, including distressing pruritus exacerbated by psychologic stress and experienced by the majority of patients with psoriasis and atopic dermatitis and in different pain syndromes due to mastocytosis, sickle cell disease, and cancer.

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Section: Mast Cell‐neural Interactions and Itch In Psoriasismentioning

confidence: 99%

Section: Mast Cell‐neural Interactions and Itch In Psoriasismentioning

confidence: 99%

Mast cell‐neural interactions contribute to pain and itch

Gupta

Harvima

2018

Immunological Reviews

216

189

View full text Add to dashboard Cite

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“…Indeed, itch is a diagnostic criterion for AD and is an important clinical end point in AD studies. Similarly, itch is increasingly being recognized as one of the most burdensome symptoms of psoriasis . Nearly, all psoriasis patients are affected by itch .…”

Section: Introductionmentioning

confidence: 99%

Itch: an under‐recognized problem in psoriasis

Elewski

Alexis

Lebwohl

et al. 2019

Acad Dermatol Venereol

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Psoriasis has historically been considered a nonpruritic dermatosis, in contrast with atopic dermatitis. Thus, itch has often been underappreciated and overlooked in psoriasis. However, increasing evidence over the past decade has shown that itch can be one of the most prevalent and burdensome symptoms associated with psoriasis, affecting almost every patient to some degree. Itch can involve the entire body, although it predominantly affects the legs, hands, back, body and especially the scalp. Uncontrolled itch can significantly impact all aspects of the well‐being and quality of life of the patient. While there has been some progress in trying to better understand the pathophysiology of itch in psoriasis, more research effort and interest are needed. This under‐recognition of itch in psoriasis is clearly reflected in the dearth of treatment options targeting itch despite significant advancement in treating the lesions themselves. Recently, however, clinical studies have begun to include itch as a study outcome. The resulting data have demonstrated concomitant antipruritic benefits and improved Psoriasis Area and Severity Index (PASI) scores with mainstay treatments for psoriasis, such as topical corticosteroids and vitamin D analogs, phototherapies, and various systemics and biologics. This article takes a closer look at this debilitating symptom, reviewing the available epidemiology data for psoriatic itch, presenting the current understanding of psoriatic itch pathophysiology and highlighting important clinical data for various treatment options for itch. Practical considerations for increasing the recognition of itch as well as improving its management in psoriasis are also provided.

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“…88 Downstream events include the eventual activation and recruitment of the Th22 T-cell subsets into psoriatic lesions, which may further contribute to epidermal hyperplasia. 80 In con- heterodimerizes with the GRPR and is internalized to evoke itch. 80 In con- heterodimerizes with the GRPR and is internalized to evoke itch.…”

Section: Immune Mediators and Neuropeptides In The Pathogenesis Of mentioning

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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Pruritus in psoriasis: An update

Abstract: Neurogenic inflammation seems to be important for itchiness in psoriasis. Treatment of pruritus in patients with psoriasis should be directed towards the resolution of skin lesions, as disease remission usually is linked with pruritus relief.

Cited by 116 publications

References 26 publications

Mast cell‐neural interactions contribute to pain and itch

Mast cell‐neural interactions contribute to pain and itch

Itch: an under‐recognized problem in psoriasis

Immune mediators and therapies for pruritus in atopic dermatitis and psoriasis

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