Treatment satisfaction in atopic dermatitis relates to patient‐reported severity: A cross‐sectional study

Nakahara, Takeshi; Fujita, Hiroyuki; Arima, Kazuhiko; Taguchi, Yurie; Motoyama, Sadako; Furue, Masutaka

doi:10.1111/all.13712

Cited by 19 publications

(17 citation statements)

References 9 publications

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“…Scratching appears to exacerbate preexistent dermatitis in humans and mice [9,26], but it relieves the itching sensation [27]. Among cutaneous inflammatory skin diseases, the vicious itch–scratch cycle is particularly important in AD because it profoundly impairs the quality of life, treatment satisfaction and adherence, and socioeconomic stability of patients [28,29,30]. However, the subcellular biological effects caused by scratching keratinocytes remain elusive.…”

Section: Discussionmentioning

confidence: 99%

Scratching Counteracts IL-13 Signaling by Upregulating the Decoy Receptor IL-13Rα2 in Keratinocytes

Ulzii

Kido‐Nakahara

Nakahara

et al. 2019

IJMS

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The vicious itch–scratch cycle is a cardinal feature of atopic dermatitis (AD), in which IL-13 signaling plays a dominant role. Keratinocytes express two receptors: The heterodimeric IL-4Rα/IL-13Rα1 and IL-13Rα2. The former one transduces a functional IL-13 signal, whereas the latter IL-13Rα2 works as a nonfunctional decoy receptor. To examine whether scratch injury affects the expression of IL-4Rα, IL-13Rα1, and IL-13Rα2, we scratched confluent keratinocyte sheets and examined the expression of three IL-13 receptors using quantitative real-time PCR (qRT-PCR) and immunofluorescence techniques. Scratch injuries significantly upregulated the expression of IL13RA2 in a scratch line number-dependent manner. Scratch-induced IL13RA2 upregulation was synergistically enhanced in the simultaneous presence of IL-13. In contrast, scratch injuries did not alter the expression of IL4R and IL13RA1, even in the presence of IL-13. Scratch-induced IL13RA2 expression was dependent on ERK1/2 and p38 MAPK signals. The expression of IL-13Rα2 protein was indeed augmented in the scratch edge area and was also overexpressed in lichenified lesional AD skin. IL-13 inhibited the expression of involucrin, an important epidermal terminal differentiation molecule. IL-13-mediated downregulation of involucrin was attenuated in IL-13Rα2-overexpressed keratinocytes, confirming the decoy function of IL-13Rα2. Our findings indicate that scratching upregulates the expression of the IL-13 decoy receptor IL-13Rα2 and counteracts IL-13 signaling.

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Section: Discussionmentioning

confidence: 99%

Scratching Counteracts IL-13 Signaling by Upregulating the Decoy Receptor IL-13Rα2 in Keratinocytes

Ulzii

Kido‐Nakahara

Nakahara

et al. 2019

IJMS

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“…One of the major causes of poor medical adherence is insufficient therapeutic effect, resulting in decreased treatment satisfaction. The higher the severity of AD, the lower the treatment satisfaction level 9 . It is important to evaluate the effectiveness of current treatments and to introduce more effective therapeutic agents as needed.…”

Section: Introductionmentioning

confidence: 99%

“…The higher the severity of AD, the lower the treatment satisfaction level. 9 It is important to evaluate the effectiveness of current treatments and to introduce more effective therapeutic agents as needed. In addition, it may be effective to provide a treatment that not only has high efficacy but also allows the therapeutic effect to be realized at earlier stages.…”

Section: Introductionmentioning

confidence: 99%

Current treatments for atopic dermatitis in Japan

Miyano

Tsunemi

2020

The Journal of Dermatology

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The goal of a treatment regimen for atopic dermatitis is to reach and maintain a state where the patient exhibits mild symptoms or an absence of symptoms, and the patient should not experience disturbance during daily activities. The basis of a treatment regimen for atopic dermatitis is topical therapy, and currently there exist topical corticosteroids, tacrolimus and delgocitinib. Using these, proactive therapy is performed as maintenance therapy after remission induction therapy. However, in cases of moderate to severe atopic dermatitis, topical drugs alone cannot induce remission and systemic therapies such as cyclosporin, ultraviolet therapy, and dupilumab should be used in combination. In particular, dupilumab has many advantages such as high efficacy, relatively few adverse reactions, and ease of use in elderly patients with severe atopic dermatitis. In this review, we present a treatment algorithm for atopic dermatitis that emphasizes the importance of maintaining remission after induction of remission, and summarizes the characteristics of current medication therapy for atopic dermatitis in Japan.

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“…Standard therapeutics for AD include topical emollients for barrier dysfunction and topical steroids and calcineurin inhibitors for skin inflammation . These conventional treatments are more or less effective in reducing atopic inflammation and itch; however, patient satisfaction and adherence to conventional treatments are generally low, as reported in daily clinics …”

Section: Anti‐il‐13 Biologics For the Treatment Of Admentioning

confidence: 99%

“…11,66 These conventional treatments are more or less effective in reducing atopic inflammation and itch; however, patient satisfaction and adherence to conventional treatments are generally low, as reported in daily clinics. [67][68][69][70] The anti-IL-4Ra antibody dupilumab inhibits the binding of IL-4 and IL-13 to IL-4Ra and blocks IL-4Ra signaling. 22 Dupilumab significantly improved skin lesions and pruritus in patients with moderate to severe AD in two randomized, placebo-controlled phase 3 clinical trials.…”

Section: Il-13 and Periostin-il-24 Axismentioning

confidence: 99%

The IL‐13–OVOL1–FLG axis in atopic dermatitis

et al. 2019

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Summary Despite sharing interleukin‐4 receptor α (IL‐4Rα) in their signaling cascades, IL‐4 and IL‐13 have different functions in atopic inflammation. IL‐13 preferentially participates in the peripheral tissues because tissue‐resident group 2 innate lymphoid cells produce IL‐13 but not IL‐4. In contrast, lymph node T follicular helper cells express IL‐4 but not IL‐13 to regulate B‐cell immunity. The dominant microenvironment of IL‐13 is evident in the lesional skin of atopic dermatitis (AD). The IL‐13‐rich local milieu causes barrier dysfunction by down‐regulating the OVOL1–filaggrin (FLG) axis and up‐regulating the periostin–IL‐24 axis. Genome‐wide association studies also point to the crucial involvement of the IL‐13, OVOL1 and FLG genes in the pathogenesis of AD. Biologics targeting IL‐13, such as the anti‐IL‐4Rα antibody dupilumab and the anti‐IL‐13 antibody tralokinumab, successfully improve AD lesions and further highlight the importance of IL‐13 in the pathogenesis of AD.

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Treatment satisfaction in atopic dermatitis relates to patient‐reported severity: A cross‐sectional study

Cited by 19 publications

References 9 publications

Scratching Counteracts IL-13 Signaling by Upregulating the Decoy Receptor IL-13Rα2 in Keratinocytes

Scratching Counteracts IL-13 Signaling by Upregulating the Decoy Receptor IL-13Rα2 in Keratinocytes

Current treatments for atopic dermatitis in Japan

The IL‐13–OVOL1–FLG axis in atopic dermatitis

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