Publications by authors named "Takafumi Kadono"

167 Publications

Elevated Myeloperoxidase-DNA Complex Levels in Sera of Patients with IgA Vasculitis.

Pathobiology 2021 Nov 23:1-6. Epub 2021 Nov 23.

Department of Dermatology, St. Marianna University School of Medicine, Kawasaki, Japan.

Introduction: IgA vasculitis is a systemic disease that results from the entrapment of circulating IgA-containing immune complexes in small-vessel walls in the skin, kidneys, and gastrointestinal tract. An excessive formation of neutrophil extracellular traps (NETs) is involved in the pathogenesis of vasculitis, especially in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. This study aimed to clarify whether NETs are implicated in IgA vasculitis.

Methods: Twenty-two patients with IgA vasculitis and 4 healthy volunteers were enrolled in this study. Serum levels of myeloperoxidase (MPO)-DNA complex, a fragment derived from NETs, were determined by enzyme-linked immunosorbent assay (ELISA), and the association between MPO-DNA complex levels and clinical parameters was examined. The presence of the ANCA was also assessed by ELISA specific for MPO and proteinase 3 (PR3) and indirect immunofluorescence (IIF), followed by assessing the differences in clinical parameters with and without the ANCA.

Results: Serum MPO-DNA complex levels were significantly higher in patients with IgA vasculitis than those in healthy controls. A significant positive correlation between the serum MPO-DNA complex and IgA levels was noted. Interestingly, 63.6% of IgA vasculitis patients were ANCA-positive in IIF with an atypical pattern, whereas neither MPO-ANCA nor PR3-ANCA was detected by ELISA. These findings indicated that some IgA vasculitis patients possessed the so called minor ANCA. Serum IgA and MPO-DNA complex levels and the frequency of hematuria in the minor ANCA-positive group were significantly higher than in the minor ANCA-negative group.

Conclusion: The collective findings suggested that NETs are certainly involved in the pathogenesis of IgA vasculitis.
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http://dx.doi.org/10.1159/000519869DOI Listing
November 2021

Dermatomyositis-like eruptions and fasciitis with novel compound heterozygous MEFV mutations: Newly recognized features of a variant of familial Mediterranean fever.

J Dermatol 2021 Sep 17;48(9):1453-1456. Epub 2021 Jun 17.

Department of Dermatology, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.

Familial Mediterranean fever (FMF) is an autoinflammatory disease characterized by recurrent febrile attacks and serositis. The diagnosis of FMF has been based on clinical criteria, including frequent symptoms and good response to the treatment with colchicine. Some patients with FMF show skin or muscle manifestations, which may be confused with other cutaneous or muscle disorders. Here we report a female in her 40s with periodic fever, migratory myalgia, dermatomyositis-like dermatitis, arthralgia, pharyngalgia, and lymphadenopathy. The initial clinical differential diagnosis included dermatomyositis, malignant lymphoma, and adult-onset Still's disease. However, the following examinations could not explain her pathological condition with such diseases. In particular, findings from muscle and fascial biopsy demonstrated severe inflammatory cell infiltrate in the fascia, suggesting fasciitis as a possible cause of migratory myalgia. We examined the possibility of autoinflammatory diseases by genetic testing. Accordingly, she was found to have novel compound heterozygous mutations (L110P, E148Q, and P369S) in the MEFV gene. Given her genetic mutations and favorable response to colchicine, she was finally diagnosed as a variant of FMF with myalgia and previously unprecedented skin eruptions.
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http://dx.doi.org/10.1111/1346-8138.16031DOI Listing
September 2021

Stewart-Treves syndrome associated with disuse edema in amyotrophic lateral sclerosis.

J Dermatol 2021 Sep 31;48(9):e443-e444. Epub 2021 May 31.

Department of Dermatology, St. Marianna University School of Medicine, Kawasaki, Japan.

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http://dx.doi.org/10.1111/1346-8138.16004DOI Listing
September 2021

Complete pruritus relief by oren-gedoku-to in eruptive pruritic papular porokeratosis.

J Dermatol 2021 Aug 13;48(8):e378-e379. Epub 2021 May 13.

Department of Dermatology, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan.

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http://dx.doi.org/10.1111/1346-8138.15947DOI Listing
August 2021

Japanese Dermatological Association Guidelines: Outlines of Guidelines for Cutaneous Squamous Cell Carcinoma 2020.

J Dermatol 2021 Jul 7;48(7):e288-e311. Epub 2021 May 7.

Department of Dermatology, International University of Health and Welfare, Narita, Japan.

In consideration of the development of treatment options for squamous cell carcinoma (SCC), the Japanese Skin Cancer Society issued the first guidelines of SCC in 2007 and revised them in 2015. Here, we report the English version of the 2020 edition of the Japanese SCC guidelines. The first half of this article is an overview of SCC including actinic keratosis and Bowen's disease, and the second half discusses three clinical questions: (i) treatment of actinic keratosis; (ii) determination of the resection margin of the primary lesion; and (iii) treatment of radically incurable cases, as contemporary problems encountered in treating SCC. In these evaluations, all processes were implemented according to the Grading of Recommendations, Assessment, Development, Evaluation system. Also, items of recommendation concerning each clinical question were determined by a multidisciplinary expert panel consisting of dermatologists, plastic/reconstructive surgeons, radiologists, and oncologists through a comprehensive literature search and systematic reviews.
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http://dx.doi.org/10.1111/1346-8138.15889DOI Listing
July 2021

Arthritis and enthesitis during dupilumab therapy completely remitted by celecoxib.

J Dermatol 2021 Jun 28;48(6):e279-e280. Epub 2021 Mar 28.

Department of Dermatology, St Marianna University School of Medicine, Kawasaki, Japan.

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http://dx.doi.org/10.1111/1346-8138.15872DOI Listing
June 2021

A case of facial redness in atopic dermatitis occurring during dupilumab treatment successfully treated with topical delgocitinib ointment.

Dermatol Ther 2021 03 25;34(2):e14888. Epub 2021 Feb 25.

Department of Dermatology, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan.

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http://dx.doi.org/10.1111/dth.14888DOI Listing
March 2021

Intravascular large B-cell lymphoma mimicking erythema nodosum: A case report and review of published works.

J Dermatol 2021 Apr 7;48(4):e184-e185. Epub 2021 Feb 7.

Department of Dermatology, St Marianna University School of Medicine, Kawasaki, Japan.

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http://dx.doi.org/10.1111/1346-8138.15792DOI Listing
April 2021

Atrophic erythema in a patient with immunoglobulin G4-related sclerosing sialadenitis.

J Dermatol 2020 Oct 19;47(10):e360-e362. Epub 2020 Jul 19.

Department of Dermatology, St Marianna University School of Medicine, Kawasaki, Japan.

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http://dx.doi.org/10.1111/1346-8138.15518DOI Listing
October 2020

Wound, pressure ulcer and burn guidelines - 1: Guidelines for wounds in general, second edition.

J Dermatol 2020 Aug 2;47(8):807-833. Epub 2020 Jul 2.

Department of Dermatology, JCHO Chukyo Hospital, Nagoya, Japan.

The Japanese Dermatological Association prepared the clinical guidelines for the "Wound, pressure ulcer and burn guidelines", second edition, focusing on treatments. Among them, "Guidelines for wounds in general" is intended to provide the knowledge necessary to heal wounds, without focusing on particular disorders. It informs the basic principles of wound treatment, before explanations are provided in individual chapters of the guidelines. We updated all sections by collecting references published since the publication of the first edition. In particular, we included new wound dressings and topical medications. Additionally, we added "Question 6: How should wound-related pain be considered, and what should be done to control it?" as a new section addressing wound pain, which was not included in the first edition.
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http://dx.doi.org/10.1111/1346-8138.15401DOI Listing
August 2020

Increase of lymphocytes and eosinophils, and decrease of neutrophils at an early stage of anti-PD-1 antibody treatment is a favorable sign for advanced malignant melanoma.

Drug Discov Ther 2020 Jul 27;14(3):117-121. Epub 2020 Jun 27.

Department of Dermatology, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan.

The advent of immune checkpoint inhibitors such as anti-PD-1 antibodies had a striking impact on the treatment for advanced malignant melanoma. However, less than half of the patients benefited from those antibodies, and biomarkers that could sensitively differentiate responders from non-responders are urgently needed. Herein, we explored such biomarkers by retrospectively analyzing clinical data from patients with advanced malignant melanoma treated with nivolumab and pembrolizumab. We found that anti-PD-1 antibody was especially effective for those with metastasis only to soft tissues. Although no significant difference was found in the baseline value of relative neutrophil count (RNC), relative lymphocyte count (RLC), neutrophil to lymphocyte ratio (NLR), and relative eosinophil count (REC) between responders and non-responders, responders after anti-PD-1 therapy revealed the increase of lymphocytes and eosinophils and the decrease of neutrophils within the first 6 weeks of the treatment. We also calculated the change of RNC and RLC 3 weeks and 6 weeks after the initiation of the therapy and designated as NΔ3-LΔ3 and NΔ6-LΔ6 respectively. NΔ3-LΔ3 was significantly decreased in responders, which suggest that the neutrophil decrease and lymphocyte increase after as early as 3 weeks of anti-PD-1 therapy might be a useful clinical indicator. In addition, the difference of NΔ6-LΔ6 between responders and non-responders was even more robust. These data suggest that change of RNC, RLC, and REC together with the combination of NΔ3-LΔ3 and NΔ6-LΔ6 might be a useful tool for early and sensitive biomarkers for anti-PD-1 therapy.
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http://dx.doi.org/10.5582/ddt.2020.03043DOI Listing
July 2020

Wound, pressure ulcer and burn guidelines - 6: Guidelines for the management of burns, second edition.

J Dermatol 2020 Nov 28;47(11):1207-1235. Epub 2020 Apr 28.

Department of Geriatric and Environmental Dermatology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Japan.

"Wound, pressure ulcer and burn guidelines - 6: Guidelines for the management of burns, second edition" is revised from the first edition which was published in the Japanese Journal of Dermatology in 2016. The guidelines were drafted by the Wound, Pressure Ulcer and Burn Guidelines Drafting Committee delegated by the Japanese Dermatological Association, and intend to facilitate physicians' clinical decisions in preventing, diagnosing and treating burn injury. All sections are updated by collecting documents published since the publication of the first edition. Especially, the recommendation levels of dressing materials newly covered by the Japanese national health insurance are mentioned. In addition, the clinical questions (CQ) regarding the initial treatment of electrical (CQ15) and chemical burns (CQ16), and also the use of escharotomy (CQ22), are newly created.
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http://dx.doi.org/10.1111/1346-8138.15335DOI Listing
November 2020

Wound, pressure ulcer and burn guidelines - 4: Guidelines for the management of connective tissue disease/vasculitis-associated skin ulcers.

J Dermatol 2020 Oct 21;47(10):1071-1109. Epub 2020 Jan 21.

Tanioka Dermatology Clinic, Kyoto, Japan.

The Japanese Dermatological Association prepared guidelines focused on the treatment of skin ulcers associated with connective tissue disease/vasculitis practical in clinical settings of dermatological care. Skin ulcers associated with connective tissue diseases or vasculitis occur on the background of a wide variety of diseases including, typically, systemic sclerosis but also systemic lupus erythematosus (SLE), dermatomyositis, rheumatoid arthritis (RA), various vasculitides and antiphospholipid antibody syndrome (APS). Therefore, in preparing the present guidelines, we considered diagnostic/therapeutic approaches appropriate for each of these disorders to be necessary and developed algorithms and clinical questions for systemic sclerosis, SLE, dermatomyositis, RA, vasculitis and APS.
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http://dx.doi.org/10.1111/1346-8138.15186DOI Listing
October 2020

Regulation of skin fibrosis by RALDH1-producing dermal dendritic cells via retinoic acid-mediated regulatory T cell induction: A role in scleroderma.

J Dermatol Sci 2020 Feb 15;97(2):125-134. Epub 2020 Jan 15.

Department of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan; Department of Dermatology, St Marianna University School of Medicine, Kanagawa, Japan. Electronic address:

Background: Skin fibrosis of systemic sclerosis (SSc) is believed to be driven by complex processes including immune abnormalities, but the underlying immune response remains enigmatic. In particular, the role of dermal dendritic cells (DCs) is totally unknown.

Objective: We investigated the impact of CD103 loss on bleomycin-induced skin fibrosis because CD103 is a critical molecule determining DC phenotypes.

Methods: Bleomycin-induced skin fibrosis was generated with Cd103 mice. The alterations of tissue fibrosis and related inflammation were investigated by histologic examination, hydroxyproline assay, quantitative reverse transcription PCR and flow cytometry. SSc skin samples were evaluated by immunofluorescence.

Results: CD103 loss decreased bleomycin-induced dermal thickness and collagen contents, along with TGF-β1 and CTGF suppression. Treg proportion was increased, while Th1/Th2/Th17 cell proportions were decreased in the skin of bleomycin-treated Cd103 mice. Bleomycin injection enhanced CD11bCD103 DC proportion in wild-type mice, which was further augmented in Cd103 mice. Importantly, RALDH1/ALDH1A1 enzyme oxidizing retinaldehyde to retinoic acid, an inducer of Tregs, was preferentially expressed by CD11bCD103 DCs and its expression levels were elevated in bleomycin-injected skin lesions, to a greater extent in Cd103 mice than in wild-type mice. Importantly, the number of RALDH1-positive DCs was decreased in the lesional skin of SSc patients and tended to inversely correlate with skin fibrosis severity.

Conclusion: This study identified a critical role of dermal DCs as a regulator of Treg development through RALDH1 in bleomycin-treated mice and possibly in human SSc. This finding sheds new light on dermal DCs as a new therapeutic target of SSc.
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http://dx.doi.org/10.1016/j.jdermsci.2020.01.002DOI Listing
February 2020

The contribution of IL-17 to the development of autoimmunity in psoriasis.

Innate Immun 2019 08 24;25(6):337-343. Epub 2019 May 24.

2 Department of Dermatology, St. Marianna University School of Medicine, Kawasaki, Japan.

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http://dx.doi.org/10.1177/1753425919852156DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7103612PMC
August 2019

Sudden elevation of plasma D-dimer levels induced by the combination therapy of dabrafenib and trametinib: Report of two cases.

J Dermatol 2019 Apr 5;46(4):358-360. Epub 2019 Feb 5.

Department of Dermatology, St Marianna University School of Medicine, Kawasaki, Japan.

The combination therapy of dabrafenib and trametinib revolutionized the treatment for BRAF V600-mutated melanoma. Various adverse events have been reported for this treatment, most notably fever. Herein, we report two cases of novel an adverse event, namely sudden and significant elevation of plasma D-dimer level induced by this therapy. In the first case, the remarkable elevation of plasma D-dimer level up to 87.4 mg/dL was noted on day 11, and in the second case, the plasma D-dimer level reached 125.5 mg/dL on day 25. In both cases, D-dimer levels gradually decreased after the cessation of this therapy. Although the exact cause is not clear, we assume two possible hypotheses: the first is that the combination therapy may induce disseminated intravascular coagulation, and the second is that the therapy induced pathological condition of secondary thrombotic microangiopathies. Our cases suggest that this thrombotic adverse event should not be overlooked, and coagulation parameters need to be monitored during the course of this treatment.
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http://dx.doi.org/10.1111/1346-8138.14798DOI Listing
April 2019

Psoriasis and the TNF/IL23/IL17 axis.

G Ital Dermatol Venereol 2019 Aug 15;154(4):418-424. Epub 2019 Jan 15.

Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan -

The excellent response of psoriasis to anti-TNF-α(TNF)/IL23/IL17A biologics implies a crucial role for the TNF/IL23/IL17 axis in developing psoriasis. In addition to the TNF/IL23/IL17 axis provided by immune cells, current evidence points to an important contribution of TNF, IL23 and IL17C produced from non-hematopoietic keratinocytes. Therefore, crosstalk between immune cells and keratinocytes forms a multilayered feed-forward loop to accelerate the TNF/IL23/IL17A axis. Many biologics have already been licensed or are under clinical trials. Given that the IL-17 signature is more upregulated in the skin than in synovium in psoriatic arthritis, anti-IL-23/IL-17 agents seem to be superior to anti-TNF-α remedies in the treatment of skin lesions. In this review, we summarize recent topics in psoriasis and the TNF/IL23/IL17 axis.
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http://dx.doi.org/10.23736/S0392-0488.18.06202-8DOI Listing
August 2019

The vitamin D analog, maxacalcitol, reduces psoriasiform skin inflammation by inducing regulatory T cells and downregulating IL-23 and IL-17 production.

J Dermatol Sci 2018 Nov 24;92(2):117-126. Epub 2018 Aug 24.

Department of Dermatology, Teikyo University School of Medicine, Tokyo, Japan.

Background: Psoriasis is a Th1/Th17-mediated inflammatory dermatosis treated with topical corticosteroids and vitamin D analogs (VD3 As).

Objective: To compare the effects of a VD3 A maxacalcitol and betamethasone valerate (BV) steroid lotion on topical imiquimod (IMQ)-induced psoriasiform skin inflammation.

Methods: Female BALB/c mice were treated with vehicle, maxacalcitol or BV lotion on the skin for 3 days, and IMQ cream for 6 days. q-PCR, H&E, immunohistochemistry and immunofluorescence studies were performed on skin samples. Additionally, mice were treated with vehicle, maxacalcitol or BV lotion for 3 days and CD4CD25 regulatory T cells (Tregs) and CD4CD25 cells from each group were isolated from lymph nodes. Adoptive transfer of the cells was performed on recipient mice which were treated with IMQ cream for 6 days, and skin samples were obtained for q-PCR and H&E staining.

Results: Maxacalcitol and BV were comparable in regards clinical improvement, although maxacalcitol reduced the MHC Class II inflammatory cell infiltration more than BV in IMQ skin. While both treatments downregulated IL-17 A, IL-17 F, IL-22, IL-12p40, TNF-α and IL-6 mRNA expression levels, only maxacalcitol downregulated IL-23p19 expression. Significantly increased Foxp3 cell infiltrations and IL-10 expression were noted in maxacalcitol-treated IMQ skin. Adoptive transfer of Treg cells from maxacalcitol-treated donor mice improved IMQ-induced inflammation clinically and histopathologically more than the recipients of Treg cells from BV-treated donor groups, showing reduced levels of inflammatory cytokines and increased IL-10 expression.

Conclusion: These results indicate that maxacalcitol reduces psoriasiform skin inflammation by inducing Treg cells as well as downregulating IL-23 and IL-17 production.
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http://dx.doi.org/10.1016/j.jdermsci.2018.08.007DOI Listing
November 2018

Melanoma and Immune Checkpoint Inhibitors.

Curr Oncol Rep 2018 03 23;20(3):29. Epub 2018 Mar 23.

Department of Dermatology, Kyushu University, Maidashi 3-1-1, Higashiku, Fukuoka, 812-8582, Japan.

Purpose Of Review: Prognosis of patients with advanced melanoma is dismal with a median overall survival of about 8 months and 5-year overall survival from a diagnosis of metastatic disease of roughly 10%. However, immune checkpoint inhibitors have brought indispensable benefits to melanoma patients. Here we will review the recent clinical efficacy and adverse events of immune checkpoint inhibitors for melanoma patients.

Recent Findings: The immune checkpoint inhibitors increase confirmed objective response and prolong progression-free and overall survival of the afflicted patients in association with maintaining their quality of life. Although diverse immune-related adverse events occur, most of them are manageable by appropriate immunomodulating agents. Clinical efficacy of immune checkpoint inhibitors continues even after discontinuation of drugs. Compared with conventional therapeutic options, the immune checkpoint inhibitors appear to prolong the survival of patients with advanced melanoma. Further clinical trials are warranted to determine whether their combinatory use with other treatment options may augment benefits or not.
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http://dx.doi.org/10.1007/s11912-018-0676-zDOI Listing
March 2018

Autoimmunity and autoimmune co-morbidities in psoriasis.

Immunology 2018 05 6;154(1):21-27. Epub 2018 Feb 6.

Department of Dermatology, Kyushu University, Fukuoka, Japan.

Psoriasis is characterized by widespread scaly erythematous plaques that cause significant physical and psychological burdens for the affected individuals. Accelerated inflammation driven by the tumour necrosis factor-α/interleukin-23/interleukin-17 axis is now known to be the major mechanism in the development of psoriasis. In addition, psoriasis has an autoimmune nature that manifests as autoreactive T cells and is co-morbid with other autoimmune diseases, such as autoimmune bullous diseases, vitiligo, alopecia and thyroiditis. In this article, we review the recent topics on autoimmunity and autoimmune co-morbidities in psoriasis.
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http://dx.doi.org/10.1111/imm.12891DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5904708PMC
May 2018

Lymphangiosarkom der Hüfte in einem nicht bestrahlten kongenitalen Lymphangiom.

J Dtsch Dermatol Ges 2017 Dec;15(12):1235-1237

Department of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.

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http://dx.doi.org/10.1111/ddg.13356_gDOI Listing
December 2017

Lymphangiosarcoma of the hip arising in a congenital non-irradiated lymphangioma.

J Dtsch Dermatol Ges 2017 Dec 25;15(12):1235-1237. Epub 2017 Oct 25.

Department of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.

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http://dx.doi.org/10.1111/ddg.13356DOI Listing
December 2017

Topical E6005/RVT-501, a novel phosphodiesterase 4 inhibitor, for the treatment of atopic dermatitis.

Expert Opin Investig Drugs 2017 Dec 31;26(12):1403-1408. Epub 2017 Oct 31.

c Research and Clinical Center for Yusho and Dioxin , Kyushu University , Fukuoka , Japan.

Introduction: Local adverse effects of steroid use and the burning sensation of calcineurin inhibitors impair patients' adherence to treatment and decrease the treatment response in atopic dermatitis (AD). Steroid phobia appears to be a psychological problem in patients with AD. Topical non-steroidal remedies are in demand. Areas covered: This manuscript reviews the current literature on preclinical and clinical studies regarding topical E6005/RVT-501, a novel phosphodiesterase 4 inhibitor. We also discuss the mechanistic background of E6005/RVT-501 in the treatment of AD. Expert opinion: Topical E6005/RVT-501 improves skin eruption and pruritus of pediatric and adult AD patients without any serious side effects. It is useful for mild to moderate lesions of AD in pediatric and adult patients. Topical E6005/RVT-501 is non-steroidal agent but its potency is equal to that of mild rank topical steroid, therefore, it may fit the demand of patients with steroid phobia. Its steroid-sparing effects may also be investigated in future clinical trials and may minimize the dose and frequency of topical steroids.
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http://dx.doi.org/10.1080/13543784.2017.1397626DOI Listing
December 2017

A possible implication of reduced levels of LIF, LIFR, and gp130 in vasculopathy related to systemic sclerosis.

Arch Dermatol Res 2017 Dec 16;309(10):833-842. Epub 2017 Oct 16.

Department of Dermatology, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.

Leukemia inhibitory factor (LIF) is a member of IL-6 family, which serves as a potent chemoattractant for neutrophils as well as a potent angiostatic factor. LIF has been implicated in various autoimmune inflammatory diseases, but its role still remains elusive in systemic sclerosis (SSc). Therefore, we investigated the potential role of LIF in the development of SSc by evaluating the clinical correlation of serum LIF levels, the expression of LIF and its receptors in skin samples, and in vitro experiments with human dermal microvascular endothelial cells. Serum LIF levels were significantly decreased in patients with SSc, especially in those with disease duration of < 1 year compared with healthy controls. As for clinical correlation, SSc patients with digital ulcers exhibited serum LIF levels significantly lower than those without. In immunohistochemistry, the expression of LIF and its receptors, LIF receptor and gp130, was remarkably decreased in dermal blood vessels of SSc lesional skin relative to those of healthy control skin. Furthermore, gene silencing of transcription factor Fli1, whose deficiency is involved in the development of SSc vasculopathy, suppressed the expression of LIF, LIF receptor, and gp130 and Fli1 bound to the promoters of those genes in human dermal microvascular endothelial cells. Collectively, these results suggest that decreased serum LIF levels may be associated with vasculopathy in SSc and that Fli1 deficiency may contribute to the inhibition of LIF-dependent biological effects on SSc endothelial cells by suppressing the expression of LIF, LIF receptor, and gp130.
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http://dx.doi.org/10.1007/s00403-017-1786-4DOI Listing
December 2017

Disseminated erythema with intense and selective inflammation of sweat gland and lichenoid drug eruption during nivolumab therapy.

J Dermatol 2018 Feb 6;45(2):e33-e34. Epub 2017 Oct 6.

Department of Dermatology, St Marianna University School of Medicine, Kawasaki, Japan.

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http://dx.doi.org/10.1111/1346-8138.14091DOI Listing
February 2018

Highlighting Interleukin-36 Signalling in Plaque Psoriasis and Pustular Psoriasis.

Acta Derm Venereol 2018 Jan;98(1):5-13

Department of Dermatology, Kyushu University, Maidashi 3-1-1, Higashiku, Fukuoka, 812-8582, Japan.

Plaque psoriasis and pustular psoriasis are overlapping, but distinct, disorders. The therapeutic response to biologics supports the pivotal role of the tumour necrosis alpha (TNF-?)/ interleukin (IL)-23/IL-17/IL-22 axis in the pathogenesis of these disorders. Recently, functional activation of the IL-36 receptor (IL-36R) was discovered to be another driving force in the pathogenesis of psoriasis. This was first highlighted by the discovery that a loss-of-function mutation of the IL-36R antagonist (IL-36Ra) causes pustular psoriasis. Although the TNF-?/IL-23/IL-17/IL-22 axis and the functional activation of IL-36R are fundamentally involved in plaque psoriasis and pustular psoriasis, respectively, the 2 pathways are closely related and mutually reinforced, resulting in full-blown clinical manifestations. This review summarizes current topics on how IL-36 agonists (IL-36?, IL-36?, IL-36?) signal IL-36R, the pathological expression of IL-36 agonists and IL-36Ra in plaque and pustular psoriatic lesions, and the cross-talk between the TNF-?/IL-23/IL-17/IL-22 axis and the functional activation of IL-36R in the epidermal milieu.
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http://dx.doi.org/10.2340/00015555-2808DOI Listing
January 2018

Nivolumab-induced vitiligo successfully treated with narrowband UVB phototherapy.

Eur J Dermatol 2017 12;27(6):656-658

Department of Dermatology, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.

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http://dx.doi.org/10.1684/ejd.2017.3096DOI Listing
December 2017

Cardiovascular and Metabolic Diseases Comorbid with Psoriasis: Beyond the Skin.

Intern Med 2017 1;56(13):1613-1619. Epub 2017 Jul 1.

Department of Dermatology, St. Marianna University School of Medicine, Japan.

A close association of systemic inflammation with cardiovascular diseases and metabolic syndrome is recently a popular topic in medicine. Psoriasis is a chronic inflammatory skin disease with a prevalence of approximately 0.1-0.5% in Asians. It is characterized by widespread scaly erythematous macules that cause significant physical and psychological burdens for the affected individuals. The accelerated inflammation driven by the TNF-α/IL-23/IL-17A axis is now known to be the major mechanism in the development of psoriasis. Psoriasis is not a mere skin disease; it is significantly associated with cardiovascular diseases and metabolic syndrome, which suggests that the chronic skin inflammation extends the systemic inflammation beyond the skin. In this article, we review the epidemiological and pathological aspects of psoriasis and its comorbidities.
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http://dx.doi.org/10.2169/internalmedicine.56.8209DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5519460PMC
January 2018

Multiple-opposing rotation flaps for the scalp defect including hair whorl.

J Dermatol 2017 Nov 21;44(11):e302-e303. Epub 2017 Jun 21.

Department of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.

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http://dx.doi.org/10.1111/1346-8138.13952DOI Listing
November 2017
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