Language：Japanese   Publisher：(株)協和企画  

＜文献概要＞症例のポイント ・左半側の分節性多汗症と温痛覚異常がみられ,脳幹部腫瘍および脊髄空洞症の診断に至った1例を経験した.・神経障害を伴う発汗異常では,その原因として腫瘍性病変や脳脊髄障害を念頭に置いた画像評価を行うことが重要である.

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Language：English   Publishing type：Research paper (scientific journal)  

Although rare, paradoxical eczema (PE) is an adverse event associated with the use of biological agents to treat psoriasis, particularly in patients with atopic predispositions. We report the first case of severe PE induced by secukinumab in a patient with generalized pustular psoriasis (GPP) and asthma. A woman in her 50s with a history of interstitial nephritis attributable to Sjogren's syndrome experienced a flare-up of GPP after discontinuing mycophenolate mofetil and was hospitalized. Treatment with secukinumab accompanied by an increased prednisolone level afforded rapid improvement, but she subsequently developed widespread, itchy, serous papules and erythema. A biopsy confirmed that the erythema was an eczematous reaction, thus PE. Her condition improved after switching from secukinumab to deucravacitinib with a temporary increase in the prednisolone level; no recurrence of GPP or PE was observed for 11 months. Elevated serum levels of interleukin (IL)-17A, IL-22, and the Th2 chemokine TARC recorded at the onset time of PE suggested that these mediators contributed to the observed pathology. Our case highlights the need for careful consideration when prescribing IL-17 inhibitors to patients with GPP, particularly those with atopic predispositions, given the potential activation of the Th2 axis and thus severe eczematous reactions. Further research is required to understand the essential nature of PE in patients with GPP and the roles of IL-17A and IL-22 in this context.

DOI： 10.7759/cureus.64680

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Language：Japanese   Publisher：(株)協和企画  

＜文献概要＞症例のポイント ・経過中に作用波長が変化した日光蕁麻疹の1例を経験した.・寛解誘導療法(hardening療法)とは,光線過敏症患者において少量の光線曝露を繰り返すことで皮膚が不反応状態となり,逆に皮疹が生じにくくなる治療である.・日光蕁麻疹は経過中に作用波長が変化する可能性があり,治療に難渋する場合は光線照射テストを再検することも必要である.

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Language：English   Publishing type：Research paper (scientific journal)  

Psoriasis vulgaris, also known as plaque-type psoriasis, is the most common form of psoriasis. It is characterized by erythematous plaques covered with scales. Among the available treatments, the fully human monoclonal antibodies ustekinumab (UST) and guselkumab (GUS) have low immunogenicity. Additionally, GUS has not been found to have a significant risk of inducing the development of clinically relevant neutralizing antibodies. Therefore, we sometimes consider switching to GUS when UST is insufficiently effective. However, switching to another biological agent usually requires an induction phase, potentially incurring additional costs. We herein present the first case of a successful transition from UST 90 mg to an extended dosing interval of GUS without an induction phase. This approach may be a viable and cost-saving option, especially for patients with relatively low disease activity.

DOI： 10.7759/cureus.61567

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Language：Japanese   Publisher：(株)医学書院  

＜文献概要＞68歳,女性.当科初診2ヵ月前から咽頭の違和感を自覚した.その後,口腔内にびらん・潰瘍が出現し,皮膚にも水疱・びらんを認め,前医を受診した.尋常性天疱瘡が疑われ当科を紹介され受診した.抗デスモグレイン(Dsg)1および3抗体価が高値であり,生検組織で基底膜直上に表皮内水疱を認め,内部に好酸球浸潤・棘融解細胞がみられた.蛍光抗体直接法では表皮細胞間にIgG・C3の沈着を認め,粘膜皮膚型尋常性天疱瘡と診断した.ステロイドパルス,プレドニゾロン,アザチオプリン,血漿交換,免疫グロブリン大量静注療法で一時寛解するも,8ヵ月後皮疹が再燃した.再燃時は粘膜疹を欠き抗Dsg1抗体価のみ上昇していたことから落葉状天疱瘡に移行したと判断した.治療再開で寛解するもプレドニゾロン減量で再燃したため,2回目の再燃時にリツキシマブ(RTX)を併用し,病勢は良好にコントロールされプレドニゾロンの減量が可能となった.RTXの効果持続期間は6ヵ月から12ヵ月とされるため効果減弱前に再投与を検討している.自験例のようにPSL減量困難な難治性天疱瘡に対してはRTX投与を積極的に検討すべきと考える.

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Publishing type：Research paper (scientific journal)   Publisher：JLE  

DOI： 10.1684/ejd.2024.4680

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Publishing type：Research paper (scientific journal)   Publisher：JLE  

DOI： 10.1684/ejd.2024.4677

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Language：Japanese   Publisher：日本皮膚科学会-西部支部  

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Publishing type：Research paper (scientific journal)   Publisher：Frontiers Media SA  

DOI： 10.3389/jcia.2024.12575

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Sweat is an essential protection system for the body, but its failure can result in pathologic conditions, including several skin diseases, such as palmoplantar pustulosis (PPP). As reduced intraepidermal E-cadherin expression in skin lesions was confirmed in PPP skin lesions, a role for interleukin (IL)-1-rich sweat in PPP has been proposed, and IL-1 has been implicated in the altered E-cadherin expression observed in both cultured keratinocytes and mice epidermis. For further investigation, live imaging of sweat perspiration on a mouse toe-pad under two-photon excitation microscopy was performed using a novel fluorescent dye cocktail (which we named JSAC). Finally, intraepidermal vesicle formation which is the main cause of PPP pathogenesis was successfully induced using our "LASER-snipe" technique with JSAC. "LASER-snipe" is a type of laser ablation technique that uses two-photon absorption of fluorescent material to destroy a few acrosyringium cells at a pinpoint location in three-dimensional space of living tissue to cause eccrine sweat leakage. These observatory techniques and this mouse model may be useful not only in live imaging for physiological phenomena in vivo such as PPP pathomechanism investigation, but also for the field of functional physiological morphology.

DOI： 10.1038/s41598-023-50875-x

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Publishing type：Research paper (scientific journal)   Publisher：The Japanese Skin Cancer Society  

DOI： 10.5227/skincancer.39.152

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Publishing type：Research paper (scientific journal)   Publisher：Wiley  

DOI： 10.1111/1346-8138.17063

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Language：English   Publishing type：Research paper (scientific journal)  

Nuclear IL-33 levels are high at the epidermal edges of skin wounds and facilitate wound healing. However, IL-33-mediated regulation of keratinocyte (KC) biology during wound healing remains poorly understood. During skin-wound healing, KC migration and re-epithelialization are mediated predominantly by EGFR signaling activation and depend on the function of signal transducer and activator of transcription 3 (STAT3). We found that migrating KCs at the leading edges of mouse skin wounds exhibited concomitant induction and nuclear colocalization of IL-33 and phosphorylated STAT3. In cultured human KCs, activation of EGFR signaling caused rapid elevation of nuclear IL-33, which directly interacts with phosphorylated STAT3, promoting STAT3 activation. In vitro KC migration and wound-healing assays revealed that high nuclear IL-33 levels were required for KC migration and wound closure. KC mobility associated with a lack of suprabasal epidermal keratins and extracellular matrix degradation mediated by matrix metalloproteinases (MMPs) control cell migration at the intracellular and extracellular levels, respectively. In EGFR-activated KCs, nuclear IL-33 mediated keratin 1 and 10 downregulation and MMP9 upregulation by promoting STAT3 activation and limited MMP1, MMP3, and MMP10 induction by suppressing NF-κB transactivation. Thus, epidermal nuclear IL-33 is involved in KC migration and wound closure by regulating the STAT3 and NF-κB pathways.

DOI： 10.1016/j.xjidi.2023.100205

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Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

Abstract

Trehalose is the nonreducing disaccharide of glucose, evolutionarily conserved in invertebrates. The living skin equivalent (LSE) is an organotypic coculture containing keratinocytes cultivated on fibroblast-populated dermal substitutes. We demonstrated that human primary fibroblasts treated with highly concentrated trehalose promote significantly extensive spread of the epidermal layer of LSE without any deleterious effects. The RNA-seq analysis of trehalose-treated 2D and 3D fibroblasts at early time points revealed the involvement of the CDKN1A pathway, the knockdown of which significantly suppressed the upregulation of DPT, ANGPT2, VEGFA, EREG, and FGF2. The trehalose-treated fibroblasts were positive for senescence-associated β-galactosidase. Finally, transplantation of the dermal substitute with trehalose-treated fibroblasts accelerated wound closure and increased capillary formation significantly in the experimental mouse wounds in vivo, which was canceled by the CDKN1A knockdown. These data indicate that high-concentration trehalose can induce the senescence-like state in fibroblasts via CDKN1A/p21, which may be therapeutically useful for optimal wound repair.

DOI： 10.1038/s42003-022-04408-3

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Other Link： https://www.nature.com/articles/s42003-022-04408-3

Publishing type：Research paper (scientific journal)   Publisher：The Japanese Skin Cancer Society  

DOI： 10.5227/skincancer.38.142

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Language：Japanese   Publisher：日本皮膚科学会-西部支部  

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Publishing type：Research paper (scientific journal)   Publisher：Wiley  

DOI： 10.1002/cia2.12262

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Other Link： https://onlinelibrary.wiley.com/doi/full-xml/10.1002/cia2.12262

Language：English   Publishing type：Research paper (scientific journal)  

Various epidermal growth factor receptor (EGFR) ligands are highly expressed in the epidermis of psoriasis lesions, and abnormal EGFR activation appears to be involved in the pathogenesis of psoriasis. However, how EGFR signaling contributes to the development of psoriasis is unclear. Interleukin (IL)-17A, a critical effector of the IL-23/IL-17A pathway, increases the expression of psoriasis signature genes in keratinocytes and plays an essential role in the pathogenesis of psoriasis by inducing IκBζ, a critical transcriptional regulator in psoriasis. In this study, we stimulated primary human keratinocytes with IL-17A and various EGFR ligands to investigate whether EGFR ligands regulate the expression of psoriasis signature genes. In cultured normal human keratinocytes and a living skin equivalent, EGFR ligands did not induce psoriasis-related gene expression, but significantly enhanced the IL-17A-mediated induction of various psoriasis signature genes, including antimicrobial peptides, cytokines, and chemokines. This was dependent on an EGFR activation-mediated synergistic increase in IL-17A-induced IκBζ expression and was partially mediated by the EGFR-dependent upregulation of Bcl3. Therefore, EGFR ligands can act as synergistic agents of IL-17A signaling by stimulating the epidermal production of psoriasis signature genes in psoriasis lesions. This study reveals a potential mechanism by which EGFR signaling contributes to the pathogenesis of psoriasis. This article is protected by copyright. All rights reserved.

DOI： 10.1002/eji.202149706

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Generalized pustular psoriasis (GPP) is characterized by acute flare-ups induced by various factors, but few reports have described GPP onset or flare-up induced by vaccination. To our knowledge, only three such cases following coronavirus disease 2019 (COVID-19) vaccination have been reported. We herein report a case of GPP flare-up after COVID-19 mRNA vaccination. A 65-year-old man with GPP controlled by infliximab presented with widespread pustular erythema, fever, and malaise following his second COVID-19 mRNA vaccination. A skin eruption was apparent at the injection site. He also exhibited systemic capillary leak syndrome (SCLS), which responded rapidly to secukinumab and systemic corticosteroids. Two biopsies, one of which was of the injection site, revealed not only findings typical of GPP, but also a dermal mixed-cell infiltration with eosinophils, and microthrombi in the small dermal vessels. The latter findings have been observed in cutaneous lesions induced by both COVID-19 infection and vaccination. This is the first case of a GPP flare-up accompanied by SCLS induced by a COVID-19 mRNA vaccine. Also, this is the first flare-up induced by the second vaccine dose, and the first such report including detailed histological data, including for the injection site.

DOI： 10.1111/1346-8138.16271

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Atopic dermatitis (AD) is an inflammatory skin disease characterized by skin barrier dysfunction. Although T helper type 2 cytokines downregulate the expression of epidermal barrier proteins, the signaling mechanism underlying these effects remains unclear. IL-33, a chromatin-associated cytokine, is highly expressed in the nuclei of epidermal keratinocytes in AD skin; however, it is unclear whether this expression promotes the development of AD. TSLP, an epithelial cells-derived pro‒T helper type 2 cytokine, is elevated in the epidermis of patients with AD. TSLP affects the pathogenesis of AD by activating T helper type 2 responses and impairing epidermal barrier integrity. In this study, we stimulated postconfluent human keratinocytes and living skin equivalent with TSLP to investigate the role of nuclear IL-33 in TSLP-induced epidermal barrier defects. We observed that TSLP reduced the levels of FLG, hBD2, S100A7, and claudin-1, which required nuclear IL-33 expression. Similar to the T helper type 2 cytokines IL-4, IL-13, and IL-31, TSLP was shown to upregulate IL-33 expression and triggered the formation of nuclear IL-33/phosphorylated signal transducer and activator of transcription 3 complex, which bound to the FLG promoter, thereby inhibiting transcription. Moreover, nuclear IL-33 acted as a cofactor of signal transducer and activator of transcription 3 in the TSLP-induced transcriptional repression of hBD2, S100A7, and claudin-1. Therefore, epidermal nuclear IL-33 may be a key regulator of TSLP-mediated epidermal barrier dysfunction.

DOI： 10.1016/j.jid.2022.01.005

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IL-33, a chromatin-associated multifunctional cytokine, is implicated in the pathogenesis of atopic dermatitis (AD), an inflammatory skin disorder characterized by skin barrier dysfunction. IL-33 accumulates in the nuclei of epidermal keratinocytes (KCs) in AD lesions. However, it is unclear whether nuclear IL-33 directly contributes to the pathogenesis of AD. IL-31, a pruritogenic cytokine primarily produced by T helper type 2 cells, is elevated in AD lesions and promotes AD development by suppressing KC differentiation and inducing itching. In this study, we investigated the involvement of nuclear IL-33 in IL-31‒mediated suppression of KC differentiation. In monolayer cultures and living skin equivalent, IL-31 increased the expression of full-length IL-33 and the phosphorylation of signal transducer and activator of transcription 3 (STAT3) in the nuclei of human KCs, which in turn downregulated the expression of differentiation markers. We found that IL-31 and IL-4/IL-13 use very similar mechanisms to inhibit KC differentiation: nuclear IL-33 combines with phosphorylated STAT3 and functions as a STAT3 transcription cofactor, promoting phosphorylated STAT3 binding to the FLG promoter to inhibit its transcription; moreover, the nuclear IL-33/phosphorylated STAT3 complex drives the downregulation of keratin 1 and keratin 10 by reducing the availability of the transcription factor RunX1. Therefore, nuclear IL-33 plays an important role in IL-31‒mediated differentiation suppression by regulating STAT3 activation in human KCs.

DOI： 10.1016/j.jid.2021.05.033

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Publishing type：Research paper (scientific journal)   Publisher：The Japanese Skin Cancer Society  

DOI： 10.5227/skincancer.37.187

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Language：English   Publishing type：Research paper (scientific journal)  

IL-33 is a chromatin-associated multifunctional cytokine implicated in the pathogenesis of atopic dermatitis (AD), an inflammatory skin disorder characterized by skin barrier dysfunction. The previous reports show that IL-33 is highly detected in the nucleus of epidermal keratinocytes in AD lesions compared with that in unaffected or normal skin. However, it is unclear whether intracellular IL-33 directly contributes to the pathogenesis of AD. T helper type 2 cytokines IL-4 and IL-13 that are elevated in AD lesions suppress keratinocyte differentiation to impair skin barrier function. We investigated whether intracellular IL-33 is involved in IL-4 and IL-13 function. In monolayer culture and living skin equivalent analyses, IL-4 and IL-13 increased the expression of full-length IL-33 in the nucleus of keratinocytes by activating the MAPK/extracellular signal‒regulated kinase kinase/extracellular signal‒regulated kinase signaling pathway, which is necessary for the inhibition of differentiation markers FLG, LOR, keratin 1, and keratin 10. The nuclear IL-33 functions as a transcription cofactor of signal transducer and activator of transcription 3, increasing the binding of phosphorylated signal transducer and activator of transcription 3 to FLG promoter, thereby inhibiting its transcription, and it inhibits the expression of transcription factor RUNX1 by signal transducer and activator of transcription 3 and signal transducer and activator of transcription 6, thereby downregulating LOR, keratin 1, and keratin 10. Thus, the elevated nuclear IL-33 in the epidermis of AD lesions may be involved in the pathogenesis of AD by inhibiting keratinocyte differentiation and skin barrier function.

DOI： 10.1016/j.jid.2021.04.002

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Language：English  

DOI： 10.1111/ced.14900

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Language：English  

DOI： 10.1016/j.jdermsci.2021.06.002

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Publishing type：Research paper (scientific journal)   Publisher：Wiley  

DOI： 10.1002/cia2.12165

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Other Link： https://onlinelibrary.wiley.com/doi/full-xml/10.1002/cia2.12165

Language：Japanese   Publisher：日本皮膚科学会-西部支部  

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Language：English  

DOI： 10.1111/1346-8138.15631

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DOI： 10.1111/bjd.18261

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DOI： 10.1111/1346-8138.15005

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DOI： 10.1016/j.jdcr.2019.03.024

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A 76-year-old Japanese woman was admitted due to uncontrolled cellulitis of the right lower leg. She had deep vein thrombosis on the right limb. Moreover, she had a long history of rheumatoid arthritis treated with corticosteroids. Skin biopsy and lumbar puncture were performed to diagnose disseminated cryptococcosis. She was administered antifungal agents (liposomal amphotericin B and 5-fluorocytosine). On treatment day 14, debridement was performed, and cryptococcosis was controlled. However, she developed toxic megacolon due to Clostridioides difficile infection (CDI). On day 32, she was transferred to the intensive care unit due to severe acidosis and acute kidney injury secondary to CDI-related toxic megacolon. Vancomycin, metronidazole, and tigecycline were administered for treatment of CDI. After several weeks of intensive care, toxic megacolon was improved, but renal replacement therapy was discontinued according to the patient's will. On day 73, she died of renal failure. We experienced a complex of rare diseases, Cryptococcus neoformans cellulitis and Clostridioides difficile-related toxic megacolon. Both diseases were presumed to be the result of corticosteroid and methotrexate use. Hence, careful monitoring is required when treating immunocompromised hosts to reduce the risk of developing complications.

DOI： 10.1016/j.jiac.2018.12.003

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Hyaluronan (HA), a linear non-sulfated glycosaminoglycan, participates in a variety of biological processes in the skin, such as cell-matrix interactions and activation of chemokines/cytokines, enzymes, and growth factors. In these activation events, HA acts as a damage-associated molecular pattern (DAMP). This review discusses the progress in functional research on HA, and its associated factors, in several aspects of cutaneous biology; e.g., immunity and wound repair.

DOI： 10.1016/j.jdermsci.2019.01.009

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DOI： 10.1111/1346-8138.14649

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DOI： 10.2340/00015555-3010

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DOI： 10.1684/ejd.2018.3329

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Tumor necrosis factor (TNF)-α inhibitors target TNF-α to effectively treat autoimmune inflammatory conditions, such as rheumatoid arthritis. However, many cases of cutaneous and systemic vasculitis related to TNF-α inhibitors have been reported in the literature. Here, the authors report the first case of a 61-year-old Japanese woman who developed leukocytoclastic vasculitis with cutaneous perivascular hemophagocytosis, which was related to elevated cytokines and immune complexes after initiating adalimumab for rheumatoid arthritis without evidence of hemophagocytic syndrome and rarely encountered in the skin. The patient was successfully treated by discontinuing adalimumab and initiating corticosteroid therapy, which should be considered as the treatment of choice. We believe that our case confirms and adds to the evidence pertaining to the involvement of TNF-α in dermal perivascular hemophagocytosis, a histologic finding rarely observed in the skin.

DOI： 10.1097/DAD.0000000000000959

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DOI： 10.1111/ced.13104

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Pili torti is an extremely rare hair phenotype characterized by short length of hairs with hair shafts being easily broken. However, the mechanism of fragility in pili torti is unclear. In this study, we examined the underlying morphological features responsible for pili torti formation using transmission electron microscopy (TEM). We used pili torti samples from a patient with Björnstad syndrome and normal hairs from a healthy subject as a comparison. The macroscopic morphological features of the samples agreed with the results of a previous study showing that pili torti is twisted, flattened, thin and with partial trichorrhexis. Young's modulus of the samples was lower than that of normal hairs. Because the cross-sectional area of the pili torti samples was also smaller than that of normal hairs, it was clarified that the tensile strength of pili torti is 2.1-times lower than that of normal hair. Assessment of morphological features by TEM showed that the cuticle layers of the samples had wavy shapes with different thicknesses. Additionally, the cortex in the samples showed loose keratin intermediate filaments (IF). Our results suggested that these abnormalities in pili torti had already occurred below the infundibulum. Thus, the weakness of pili torti in tensile strength is thought to result from loose IF because of dysformation of disulfide bonds.

DOI： 10.1111/1346-8138.13700

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BACKGROUND: Neutrophil elastase plays an important role in skin inflammation induced by neutrophil infiltration. Elafin is an inducible elastase inhibitor expressed by keratinocytes, and is known to be involved in pathogenesis of neutrophilic skin disorders such as psoriasis. METHODS: Immunohistochemical studies of elafin expression in the cases of vasculitis were performed. Induction of elafin expression in cultured vascular cells and its effect on neutrophil migration were studied in vitro. RESULTS: A positive immunoreactivity was detected in polyarteritis nodosa, giant cell arteritis and Schönlein-Henoch purpura, but no immunoreactivity was found in Churg-Strauss syndrome. Elafin expression in cultured venous endothelial cells and arterial smooth muscle cells was undetectable, but induced by interleukin-1β (IL-1β) and IL-8. Elafin inhibited the elastin peptide-induced neutrophil chemotaxis at the concentration of 10(-8) -10(-5) mol/L. CONCLUSION: Elafin deposition induced by cytokines (IL-1β or IL-8) will be an important regulator for the progress of leucocytoclastic vasculitis by functioning as an inhibitor for neutrophil chemotaxis as well as for vascular elastin degradation.

DOI： 10.1111/jdv.13650

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Although macrophages can be polarized to distinct phenotypes in vitro with individual ligands, in vivo they encounter multiple signals that control their varied functions in homeostasis, immunity, and disease. Here, we identify roles of Rev-erb nuclear receptors in regulating responses of mouse macrophages to complex tissue damage signals and wound repair. Rather than reinforcing a specific program of macrophage polarization, Rev-erbs repress subsets of genes that are activated by TLR ligands, IL4, TGFβ, and damage-associated molecular patterns (DAMPS). Unexpectedly, a complex damage signal promotes co-localization of NF-κB, Smad3, and Nrf2 at Rev-erb-sensitive enhancers and drives expression of genes characteristic of multiple polarization states in the same cells. Rev-erb-sensitive enhancers thereby integrate multiple damage-activated signaling pathways to promote a wound repair phenotype.

DOI： 10.7554/eLife.13024

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Genes related to the parathyroid hormone (PTH) influence cutaneous immune defense and development, but the full functions of the PTH family in cutaneous biology remain incompletely understood. In this study, we examined the expression and potential functions of the PTH second receptor (PTH2R) and its ligand, the tuberoinfundibular peptide of 39 residues (TIP39), in the skin. TIP39 and PTH2R mRNA and protein were detectable in both human and mouse skin, and in cultured keratinocytes and adipocytes. TIP39 was observed in the basal layer of human skin, whereas PTH2R was detected in the spinous to granular layer. The subcellular localization of TIP39 in keratinocytes changed during calcium-induced differentiation and shifted to colocalize with PTH2R at the membrane. The addition of recombinant TIP39 to normal human keratinocytes in culture induced an increase in intercellular calcium and triggered aspects of terminal differentiation including decreased keratin-14 and increased involucrin expression. Consistent with these observations, PTH2R(-/-) mice were observed to have increased epidermal thickness. In summary, identification of TIP39 and its receptor in the epidermis reveals an additional PTH family member that is expressed in the skin and may influence keratinocyte function.

DOI： 10.1016/j.jid.2016.02.814

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Language：Japanese   Publishing type：Research paper (scientific journal)  

A 76-year-old man presented with many bullous lesions and erythema over his whole body in August 2014. Blood examination showed an elevation of the anti-BP180 antibody (658 U/mL) and a biopsied specimen of the skin lesions showed subepidermal bulla. A diagnosis of bullous pemphigoid was made based on the clinical and histological findings. Although 20 mg/day of prednisolone was administered, there was a poor response and consequently the dose of steroid was increased to 70 mg/day after 2 weeks. Bullous pemphigoid related to a malignant tumor was suspected. Colonic endoscopic examination revealed a sigmoid colon cancer and he underwent a sigmoidectomy with lymphodenectomy. The histopathological findings revealed a moderately-differentiated adenocarcinoma, pT1b, pN1, pStage Ⅲa, and he received adjuvant chemotherapy(UFT/ LV). The dermatological findings were rapidly relieved after tumor resection and anti-BP180 antibody was normalized. He has had no signs or symptoms of recurrence, both of the cancer and the bullous pemphigoid, for 9 months after the operation.

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Group A Streptococcus (GAS) commonly infects human skin and occasionally causes severe and life-threatening invasive diseases. The hyaluronan (HA) capsule of GAS has been proposed to protect GAS from host defense by mimicking endogenous HA, a large and abundant glycosaminoglycan in the skin. However, HA is degraded during tissue injury, and the functions of short-chain HA that is generated during infection have not been studied. To examine the impact of the molecular mass of HA on GAS infection, we established infection models in vitro and in vivo in which the size of HA was defined by enzymatic digestion or custom synthesis. We discovered that conversion of high molecular mass HA to low molecular mass HA facilitated GAS phagocytosis by macrophages and limited the severity of infection in mice. In contrast, native high molecular mass HA significantly impaired internalization by macrophages and increased GAS survival in murine blood. Thus, our data demonstrate that GAS virulence can be influenced by the size of HA derived from both the bacterium and host and suggest that high molecular mass HA facilitates GAS deep tissue infections, whereas the generation of short-chain HA can be protective.

DOI： 10.1074/jbc.M114.575621

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The breakdown and release of hyaluronan (HA) from the extracellular matrix has been hypothesized to act as an endogenous signal of injury. To test this hypothesis, we generated mice that conditionally overexpressed human hyaluronidase 1 (HYAL1). Mice expressing HYAL1 in skin either during early development or by inducible transient expression exhibited extensive HA degradation, yet displayed no evidence of spontaneous inflammation. Further, HYAL1 expression activated migration and promoted loss of DCs from the skin. We subsequently determined that induction of HYAL1 expression prior to topical antigen application resulted in a lack of an antigenic response due to the depletion of DCs from the skin. In contrast, induction of HYAL1 expression concurrent with antigen exposure accelerated allergic sensitization. Administration of HA tetrasaccharides, before or simultaneously with antigen application, recapitulated phenotypes observed in HYAL1-expressing animals, suggesting that the generation of small HA fragments, rather than the loss of large HA molecules, promotes DC migration and subsequent modification of allergic responses. Furthermore, mice lacking TLR4 did not exhibit HA-associated phenotypes, indicating that TLR4 mediates these responses. This study provides direct evidence that HA breakdown controls the capacity of the skin to present antigen. These events may influence DC function in injury or disease and have potential to be exploited therapeutically for modification of allergic responses.

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Language：English   Publishing type：Research paper (scientific journal)  

The release of endogenous molecules from the skin after injury has been proposed to influence inflammation. Recent studies have found that pro-inflammatory signals can be generated by damaged endogenous self-RNA, and this event is detected by TLR3. Conversely, release of endogenous fragments of hyaluronic acid (HA) after injury has been proposed to inhibit LPS induced inflammation driven by TLR4. In this study we investigated if HA oligomers could also influence inflammation mediated by TLR3. A tetramer form of HA (oligo-HA) was added to MH-S cells (mouse alveolar macrophage cell line) that were then activated by poly(I:C). ELISA analysis of culture supernatants showed that the presence of oligo-HA suppressed the poly(I:C) induced release of IL-6 and TNFα. IL-6 mRNA expression was also suppressed as measured by quantitative RT-PCR. To determine the mechanism of action for oligo-HA to inhibit poly(I:C), macrophages derived from wild-type (WT), Tlr2-/- or Tlr4-/- mice were treated with oligo-HA and poly(I:C). Similar to WT cells, Tlr2-/- macrophages were inhibited by oligo-HA and retained suppression of cytokine release. In contrast, Tlr4-/- macrophages lost the capacity to be suppressed by oligo-HA. An increase in Traf1 (TLR negative regulator) mRNA was observed after oligo-HA treatment of WT but not in Tlr4-/- macrophages, and oligo-HA did not suppress cytokine responsiveness in Traf1-/- macrophages. These results show that oligo-HA acts through TLR4 and TRAF1 to inhibit TLR3-dependent inflammation. This observation illustrates the complex immunomodulatory action of endogenous products released after injury.

DOI： 10.1371/journal.pone.0072421

PubMed

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Language：English   Publishing type：Research paper (scientific journal)  

Exposure to ultraviolet B (UVB) radiation from the sun can result in sunburn, premature aging and carcinogenesis, but the mechanism responsible for acute inflammation of the skin is not well understood. Here we show that RNA is released from keratinocytes after UVB exposure and that this stimulates production of the inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) from nonirradiated keratinocytes and peripheral blood mononuclear cells (PBMCs). Whole-transcriptome sequencing revealed that UVB irradiation of keratinocytes induced alterations in the double-stranded domains of some noncoding RNAs. We found that this UVB-damaged RNA was sufficient to induce cytokine production from nonirradiated cells, as UVB irradiation of a purified noncoding RNA (U1 RNA) reproduced the same response as the one we observed to UVB-damaged keratinocytes. The responses to both UVB-damaged self-RNAs and UVB-damaged keratinocytes were dependent on Toll-like receptor 3 (TLR3) and Toll-like receptor adaptor molecule 1 (TRIF). In response to UVB exposure, Tlr3(-/-) mice did not upregulate TNF-α in the skin. Moreover, TLR3 was also necessary for UVB-radiation-induced immune suppression. These findings establish that UVB damage is detected by TLR3 and that self-RNA is a damage-associated molecular pattern that serves as an endogenous signal of solar injury.

DOI： 10.1038/nm.2861

PubMed

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Language：English   Publishing type：Research paper (scientific journal)  

As C-Xyloside has been suggested to be an initiator of glycosaminoglycan (GAG) synthesis, and GAGs such as Dermatan sulfate (DS) are potent enhancers of fibroblast growth factor (FGF)--10 action, we investigated if a C-Xylopyranoside derivative, (C-β-D-xylopyranoside-2-hydroxy-propane, C-Xyloside), could promote DS production by cultured normal human keratinocytes, how this occurs and if C-Xyloside could also stimulate FGF-dependent cell migration and proliferation. C-Xyloside-treated keratinocytes greatly increased secretion of total sulfated GAGs. Majority of the induced GAG was chondroitin sulfate/dermatan sulfate (CS/DS) of which the major secreted GAG was DS. Cells lacking xylosyltransferase enzymatic activity demonstrated that C-Xyloside was able to stimulate GAG synthesis without addition to core proteins. Consistent with the observed increase in DS, keratinocytes treated with C-Xyloside showed enhanced migration in response to FGF-10 and secreted into their culture media GAGs that promoted FGF-10-dependent cellular proliferation. These results indicate that C-Xyloside may enhance epithelial repair by serving as an initiator of DS synthesis.

DOI： 10.1371/journal.pone.0025480

PubMed

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Language：English   Publishing type：Research paper (scientific journal)  

Antimicrobial peptides play an important role in host defense against pathogens. Recently, phenol-soluble modulins (PSMs) from Staphylococcus epidermidis (S. epidermidis) were shown to interact with lipid membranes, form complexes, and exert antimicrobial activity. Based on the abundance and innocuity of the cutaneous resident S. epidermidis, we hypothesized that their PSMs contribute to host defense. Here we show that S. epidermidis delta-toxin (PSMgamma) is normally present in the epidermis and sparsely in the dermis of human skin using immunohistochemistry. Synthetic delta-toxin interacted with neutrophil extracellular traps (NETs) and colocalized with cathelicidin while also inducing NET formation in human neutrophils. In antimicrobial assays against Group A Streptococcus (GAS), delta-toxin cooperated with CRAMP, hBD2, and hBD3. In whole blood, addition of delta-toxin exerted a bacteriostatic effect on GAS, and in NETs, delta-toxin increased their killing capacity against this pathogen. Coimmunoprecipitation and tryptophan spectroscopy demonstrated direct binding of delta-toxin to host antimicrobial peptides LL-37, CRAMP, hBD2, and hBD3. Finally, in a mouse wound model, GAS survival was reduced (along with Mip-2 cytokine levels) when the wounds were pretreated with delta-toxin. Thus, these data suggest that S. epidermidis-derived delta-toxin cooperates with the host-derived antimicrobial peptides in the innate immune system to reduce survival of an important human bacterial pathogen.

DOI： 10.1371/journal.pone.0008557

PubMed

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Fragments of hyaluronan released after injury bind and activate TLR4 in a complex with CD44. Here we investigated if the recognition of hyaluronan by CD44 and TLR4 alters lipopolysaccharide (LPS) responsiveness and thus could alter the septic response. In contrast to mice injected with LPS, mice exposed to hyaluronan prior to LPS had greatly decreased serum IL-6 and TNFalpha and were protected from symptoms of sepsis. The protective effect of HA was not seen in Cd44(-/-) mice. Consistent with our findings in vivo, addition of hyaluronan to macrophages before LPS exposure significantly decreased the release of IL-6 and TNFalpha and this effect was not seen in macrophages from Cd44(-/-) mice. Investigation of the mechanism responsible for inhibition of LPS activation showed hyaluronan treatment resulted in an increase in peritoneal macrophage A20 mRNA expression, and that this was significantly reduced in macrophages from Cd44(-/-) mice and Tlr4(-/-) mice. Suppression of the A20 response with siRNA inhibited the ability of hyaluronan to protect against the cytokine response to LPS. Therefore, our results show that hyaluronan acts through TLR4, CD44 and A20 to stimulate a unique cellular response that can protect against the septic response to LPS.

DOI： 10.1016/j.molimm.2009.08.026

PubMed

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Inflammation under sterile conditions is a key event in autoimmunity and following trauma. Hyaluronan, a glycosaminoglycan released from the extracellular matrix after injury, acts as an endogenous signal of trauma and can trigger chemokine release in injured tissue. Here, we investigated whether NLRP3/cryopyrin, a component of the inflammasome, participates in the inflammatory response to injury or the cytokine response to hyaluronan. Mice with a targeted deletion in cryopyrin showed a normal increase in Cxcl2 in response to sterile injuries but had decreased inflammation and release of interleukin-1beta (IL-1beta). Similarly, the addition of hyaluronan to macrophages derived from cryopyrin-deficient mice increased release of Cxcl2 but did not increase IL-1beta release. To define the mechanism of hyaluronan-mediated activation of cryopyrin, elements of the hyaluronan recognition process were studied in detail. IL-1beta release was inhibited in peritoneal macrophages derived from CD44-deficient mice, in an MH-S macrophage cell line treated with antibodies to CD44, or by inhibitors of lysosome function. The requirement for CD44 binding and hyaluronan internalization could be bypassed by intracellular administration of hyaluronan oligosaccharides (10-18-mer) in lipopolysaccharide-primed macrophages. Therefore, the action of CD44 and subsequent hyaluronan catabolism trigger the intracellular cryopyrin --> IL-1beta pathway. These findings support the hypothesis that hyaluronan works through IL-1beta and the cryopyrin system to signal sterile inflammation.

DOI： 10.1074/jbc.M806084200

PubMed

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We reported a 23-year-old female who was treated for rash due to hand, foot, and mouth disease (HFMD). On day 4 of hospitalization, the patient showed opsoclonus (jerky eye movements in all directions), myoclonus of the neck, trunk, and extremities, and cerebellar ataxia. Based on the changes in serum viral antibody titer, the patient was diagnosed as enterovirus 71 infection. No obvious abnormal findings were noted in head MRI. Immunoglobulin 5 g/day was administered for 3 days in the early stages of infection, and administration of methylprednisolone 500 mg/day for 3 days was repeated twice. Afterwards, oral corticosteroids were given, resulting in neurological improvements a month. Including our case, there are only 2 cases within opsoclonus myoclonica associated with enterovirus 71 infection. Our case suggests, based on the course of treatment, possible involvement of direct viral action or autoimmune response in opsoclonus myoclonica.

PubMed

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Elafin has a primary structure with two functional domains; a transglutaminase substrate domain at the N-terminus and a protease inhibitor domain at the C-terminus. Elafin expression has so far been reported only for epithelial tissues. Accumulation of elafin was immunohistochemically detected in the actinic elastosis of sun-damaged skin. Exposure of normal skin to UVA induced elafin expression that colocalized with elastic fibers. Incubation of synthetic transglutaminase substrate domain of elafin and elastin molecules in the presence of tissue transglutaminase in vitro resulted in the formation of a higher molecular complex on SDS-PAGE. Elafin expression was not detected in normal cultured skin fibroblasts, but was induced by UVA irradiation at both messenger RNA and protein levels. When radiolabeled insoluble elastin was incubated with recombinant full-length elafin and tissue transglutaminase, insoluble elastin became more resistant to neutrophil elastase digestion. These results indicate that (1) dermal fibroblasts potentially express elafin on UV irradiation, (2) UV-mediated elafin interacts with elastin, and (3) the elafin-elastin complex protects elastic fibers from elastolytic degradation, leading to the accumulation of elastic fibers in the actinic elastosis of sun-damaged skin. The transglutaminase substrate moiety of elafin plays an important role in anchoring elafin at its proper sites of action during UV-induced aging processes.

PubMed

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Language：English   Publishing type：Research paper (scientific journal)  

PubMed

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Language：English   Publisher：BLACKWELL PUBLISHING LTD  

Web of Science

PubMed

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Language：Japanese   Publisher：(株)日本医事新報社  

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Language：Japanese   Publisher：日本結合組織学会  

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Language：Japanese   Publisher：日本皮膚科学会-西部支部  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(一社)日本救急医学会  

プロカルシトニン(procalcitonin:PCT)は、細菌感染症の診断に有用であるが、外傷後や熱傷後などで血清PCT濃度が上昇した症例報告もあり、決定的ではない。今回、コンパートメント症候群を呈し、高PCT血症を認めた皮膚筋型結節性多発動脈炎(cutaneous and muscular polyarteritis nodosa:CMPAN)の1例を経験したので報告する。症例は76歳の日本人男性。手指、足趾、足背に進行性の紫斑や壊疽を生じ、さらに右下腿に発赤と重度の腫脹を認めた。右下腿の前方コンパートメント内圧と浅後方コンパートメント内圧でそれぞれ30mmHg以上であり、コンパートメント症候群と診断し、緊急皮膚切開と筋膜切開を行った。C-reactive protein(CRP)、PCTの上昇を伴ったため、軟部組織感染症を疑い抗生物質を投与したが、臨床症状の改善はみられなかった。皮膚生検では筋肉内の好中球浸潤と皮下脂肪織の小動脈に壊死性血管炎を認め、CMPANと診断した。ステロイドパルス療法後、臨床症状は著明に改善した。自験例は血管炎に伴う循環障害によりコンパートメント症候群を生じ、コンパートメント症候群によりPCT高値に至ったと考えられた。(著者抄録)

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Language：Japanese   Publisher：金原出版(株)  

＜文献概要＞62歳,女性。左側胸部の黒色結節を伴う茶褐色局面を主訴に受診した。ダーモスコピー所見では黒色結節の部にlarge blue-gray ovoid nestsを認めたが,arborizing vesselsはみられなかった。結節部の皮膚生検にて,基底細胞癌と診断し,全摘した。病理組織学的に脂漏性角化症と連続して基底細胞癌を認めた。自験例では脂漏性角化症の病変と連続して基底細胞癌が共存していたが,脂漏性角化症においてダーモスコピー等で非典型的な所見がある場合は皮膚生検も検討することが望ましいと考えた。

DOI： 10.18888/hi.0000001880

CiNii Research

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Other Link： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2020&ichushi_jid=J01266&link_issn=&doc_id=20200512100010&doc_link_id=10.18888%2Fhi.0000001880&url=https%3A%2F%2Fdoi.org%2F10.18888%2Fhi.0000001880&type=%88%E3%8F%91.jp_%83I%81%5B%83%8B%83A%83N%83Z%83X&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00024_2.gif

Language：Japanese   Publisher：日本臨床皮膚科医会  

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Language：Japanese   Publisher：日本臨床皮膚科医会  

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Language：Japanese   Publisher：(一社)日本皮膚悪性腫瘍学会  

75歳、男性。陰茎癌術後、陰嚢にリンパ浮腫を認めていた。陰嚢の腫脹、外尿道口周囲の硬結を主訴に当科紹介受診。初診時、陰嚢表面には出血および紫斑を混じていた。硬結部の病理組織は、angiosarcomaの所見であった。治療は放射線療法を選択し、計45Gy照射後、陰嚢の潰瘍、紫斑は完全に消退した。Angiosarcomaは体中どこにでも生じうるが、外陰部に発生したangiosarcomaは報告例が少なく極めて稀である。陰嚢に発生した誘因として、術後リンパ浮腫を生じていたことからStewart-Treves症候群として発症した可能性と、転倒後に陰嚢の腫脹、硬結を生じていたことから外傷を契機に発症した可能性が考えられた。(著者抄録)

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：金原出版(株)  

＜文献概要＞26歳,女性。4ヵ月前より両側上腕,両側大腿に皮疹が出現し,他院にてカルシポトリオール水和物混合軟膏で加療するも改善しなかった。四肢の紅斑,紅色丘疹が拡大したため,精査加療目的で当科を紹介受診した。皮膚生検では表皮に正常角化と不全角化の交互の配列,毛孔に一致して角栓,真皮の血管周囲にリンパ球浸潤を認め毛孔性紅色粃糠疹(PRP)と診断した。セクキヌマブ投与で皮疹は著明に軽快した。PRPは自然軽快することが多いが難治例や再発例が存在する。過去にTNF-α阻害薬やIL-12/23p40阻害薬などの生物学的製剤を使用し奏効した報告があり,今回の症例からセクキヌマブも難治なPRPの治療選択肢のひとつして有用と考えられた。

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Language：Japanese   Publisher：金原出版(株)  

＜文献概要＞53歳,男性。心筋梗塞後に投与されたロスバスタチンカルシウム内服開始22日後より紅斑が出現し,当科を紹介受診した。38℃台の発熱があり,皮疹は体幹でtarget lesionを呈し,四肢に水疱と口唇のびらんがみられた。入院後ステロイドパルス療法を施行したが,全身に広範囲の表皮剥離とNikolsky現象がみられ中毒性表皮壊死症(TEN)と診断した。ステロイドパルス療法施行後も病勢が進行したため,免疫グロブリン大量静注療法を追加し皮疹は徐々に軽快した。薬剤リンパ球刺激試験でロスバスタンチンカルシウムが陽性であった。これまで本邦においてロスバスタチンカルシウムなどのHMG-CoA還元酵素阻害薬によるTENの症例報告はなく,まれと考えられた。

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(一社)日本皮膚悪性腫瘍学会  

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Language：Japanese   Publisher：日本臨床皮膚科医会  

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Language：Japanese   Publisher：日本臨床皮膚科医会  

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Language：Japanese   Publisher：金原出版(株)  

＜文献概要＞15歳,女児。3ヵ月前に右眉毛上部に紅色の小結節が出現した。増大傾向であったため当科を紹介受診した。ダーモスコピーで,蛇行し拡張した毛細血管がみられた。生検でcellular neurothekeomaと診断し,全摘術を施行した。病理組織学的に,粘液様の間質を背景として類円形核と好酸性胞体を有する腫瘍細胞(CD68+,S100-,αSMA-,NSE-,MIB-1indx<20%)が真皮内で胞巣を形成しながら増生していた。Cellular neurothekeomaの定義や腫瘍細胞の起源については一定の見解はなく,若干の文献的考察を含めて報告する。

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＜文献概要＞69歳,男性。数ヵ月前から右中指背面に潰瘍を伴う15mm大の黒色結節があった。5mm離して,伸筋腱上で切除術を施行した。病理組織学的に角化傾向を示す異型細胞が真皮内で充実性に増殖し,浸潤する異型細胞間に樹枝状のメラノサイトと色素伝達障害性メラノサイトがみられた。以上より自験例を色素性有棘細胞癌と診断した。切除断端は陰性で,術後1年経過したが再燃は認めていない。手指に生じた色素性有棘細胞癌はこれまで報告がなく,まれと考えられた。

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(一社)日本皮膚免疫アレルギー学会  

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Language：Japanese   Publisher：(一社)日本皮膚免疫アレルギー学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：金原出版(株)  

2歳女児。当科受診の2ヵ月前に両手に強いそう痒を伴う紅色丘疹が出現し、徐々に全身に拡大した。近医でジフルプレドナート軟膏とオロパタジン塩酸塩を処方されたが改善に乏しく、当科受診した。腋窩部のダーモスコピー検査で疥癬トンネルの先端に三角の黒点と白色の胴部が観察できた。KOH直接鏡検法で疥癬虫の虫体を検出し、疥癬と診断した。治療はフェノトリンローション(スミスリンローション5%)を1週間間隔で2回使用し、全身の皮疹は改善した。その後、鏡検を1週間間隔で2回行い、疥癬虫の虫体・虫卵がともにないことを確認した。

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：金原出版(株)  

爪白癬患者51例(男性23例、女性28例、平均年齢69.1歳)を対象にエフィナコナゾールを1日1回外用し、その治療効果と患者アンケートによる治療満足度を評価した。罹病期間は平均7.7年で、エフィナコナゾールの平均投与期間は3.1ヵ月であった。患者全体の治療効果では、感染面積は平均75.7%から平均62.8%へ、新生爪の伸長は平均1.76mmから平均2.86mmへ、有意な改善が認められた。感染面積50%以上の重症例29例による解析では、感染面積は平均91.4%から平均74.6%、新生爪の伸長は平均0.43mmから平均1.77mmと、重症例においても有意な改善が確認された。アンケート調査では、患者の治療満足度は約70%で高い満足感が得られ、また約80%の患者は治療開始6ヵ月以内の比較的早期に治療効果を実感していることが明らかになった。

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Language：Japanese   Publisher：日本皮膚病理組織学会  

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Language：Japanese   Publisher：日本皮膚科学会-大阪地方会・京滋地方会  

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42歳,女性.既往として多発性嚢胞腎がある.2007年7月上旬,慢性腎不全が急速に悪化したため,右大腿静脈よりUKカテーテルを挿入し血液透析を開始した.経過中,両総腸骨静脈および下大静脈の閉塞・狭細化を認めた.カテーテルを抜去し,末梢よりヘパリンの持続点滴静注を開始したが,両総腸骨静脈および下大静脈の閉塞は改善しなかった.経過からヘパリン起因性血小板減少症を疑い,抗ヘパリン-PF4複合体抗体を測定したところ,陽性だった.末梢点滴ルートとして使用していた両側下腿の点滴刺入部は,抜針後徐々に潰瘍化したが,デブリードマンとスルファジアジン銀外用にてほぼ上皮化した.日常広く使用されているへパリンの副作用として,出血傾向ではなく,ヘパリン起因性血小板減少症の存在を知ることは重要である.(著者抄録)

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78歳男性。患者は急性心筋梗塞で内科ヘ入院中に重症不整脈が生じ、約1ヵ月間、塩酸ニフェカラント点滴投与が行われた。しかし、留置針刺入部の両前腕・左下腿の3ヶ所に皮下硬結を認められたため、著者らの皮膚科へ紹介となった。受診時、当該3ヶ所には拇指大でやや紅色調の皮下硬結がみられ、局所麻酔下にこの3ヶ所の皮下硬結を切開・切除すると、右前腕には皮下硬結が2つ連なり、これらと連続して中枢側に索状の浸潤が触れられた。そして、更に切開すると皮下静脈部に一致して白色で索状の固形物がみられた。また、左下腿の皮下硬結の病理所見では皮下に好酸性で針状の結晶(塩酸ニフェカラントの結晶)が認められ、結晶周囲には好酸球、好中球、リンパ球、形質細胞の浸潤を伴った肉芽組織がみられた。尚、組織の一般細菌、抗酸菌、真菌は培養を行うも、すべて陰性であった。

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27歳,男性.臍部の疼痛を伴う結節を主訴に来院した.MRI上,臍から連続して腹壁内に突出する嚢胞性腫瘤と,それに連続して膀胱前上部に伸びる索状構造を認めた.尿膜管膿瘍の診断で炎症の鎮静化をはかった後,尿膜管摘出術を施行した.病理組織学的に尿膜管膿瘍で,悪性所見は認められなかった.臨床的に臍部結節をみた場合,尿膜管遺残を考慮し,早期に画像診断を行うことが重要であると思われた.(著者抄録)

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67歳女性。患者は約40年前より両下腿に自覚症状のない夏季に増悪する紅斑があったが放置し、約半年前より腹部、四肢に皮疹が拡大し、そう痒を伴うため著者らの施設へ初診となった。また、同時期より両足、膝関節痛が出現し、初診時は歩行困難な状態であった。所見では体幹・四肢には爪甲大までの落屑を伴う紅斑が播種状に多発し、病理組織学的に滴状乾癬を考え、抗生剤内服とステロイド、ビタミンD3軟膏外用を開始した。治療開始後、約1ヵ月で皮疹は平坦化したが、病理組織像にてcornoid lamella、好酸球性海綿状態を認め、炎症を伴った播種状表在性汗孔角化症と診断された。現在、そう痒は消失したが、褐色斑は残存している。尚、関節痛は関節リウマチと診断され、ステロイド内服などにより軽快した。

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Language：Japanese   Publisher：(一社)日本研究皮膚科学会  

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73歳男。患者は約40年間、両鼠径部および腋窩部にHailey-Hailey病(HHD)による紅斑局面があり、ステロイド軟膏外用で加療していた。今回、皮疹による疼痛で、自己判断により1ヵ月間入浴しなかったところ、体幹から四肢にかけて膿疱の混じる角化性紅斑と発熱が同時に出現した。受診時所見では、腋窩および鼠径部では浸軟した痂皮、亀裂、糜爛を伴う局面を呈し、悪臭、疼痛を伴っていた。治療としてアジスロマイシン500mg/日を3日間内服したが、初診5日後に皮疹は紅皮症化して敗血症が疑われた。4ヶ所の皮膚生検を施行したところ、表皮基底層直上から表皮上層にかけての棘融解を認め、解離した表皮細胞は崩れかかった煉瓦壁様の所見を呈していた。また、この棘融解した表皮裂隙中には好中球の集簇を認め、咽頭部からメチシリン感受性の黄色ブドウ球菌が検出された。以上より、汎発化したHHDに敗血症が合併したものと診断し、ペントシリンを主体とした抗菌薬加療を行った結果、皮疹と全身症状は軽快した。

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62歳男。患者は健康診断で2型糖尿病と診断され、近医でグリペンクラミド内服による加療を受けるも、血糖コントロールは不良であった。その後、転院となり、ノボラピッド、イノレット Nによるインスリン療法が開始されたが、インスリン注射部位のそう痒を伴う膨疹が出現し、精査目的で著者らの施設へ紹介となった。所見では、ヒトインスリン特異IgE抗体価は8.69UA/ml と高値、インスリン抗体80.0%と陽性で、インスリンに対して抵抗性であった。インスリンに対する即時型アレルギーを疑い、プリックテストを施行した結果、ヒューマリン R、ヒューマリン N、イノレット N、ノボラピッドで陽性であった。ヒトインスリンに対する即時型アレルギーと診断し、減感作療法を勧めたが、患者が希望せず、厳格な食事療法と経口血糖降下薬による治療を再開し、血糖コントロールがほぼ可能となった。

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Language：Japanese   Publisher：日本皮膚科学会-西部支部  

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61歳女.患者は35年前にシリコン注入による豊胸術を受けた.1992年頃から徐々に両乳房の硬化,変形が進行し,2002年にシリコン除去術を受けたが,シリコンは胸壁まで浸潤し完全な除去はできなかった.2004年1月,Raynaud現象が出現し,3月から手指の硬化を自覚した.5月から皮膚硬化が急速に進行し,受診となった.シリコン豊胸術の既往から,全身性強皮症を呈したヒトアジュバント病(HAD)と診断し,プレドニゾロン 30mg内服とプロスタグランディンの点滴を開始したところ,皮膚硬化は速やかに改善した

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25歳女.右耳前部から頸部にかけて表面萎縮性の白斑が散在し一部融合し白色になっていた.右耳前部はびらんを伴う紅斑があり,わずかに浸潤を触れた.疼痛,そう痒の自覚症状はなかった.特徴的な臨床・病理組織像より硬化性萎縮性苔癬(LSA)と診断した.ミノサイクリンを生検後から内服開始したところ,びらんが急速に上皮化したため,このままミノサイクリン内服を継続し,酪酸ヒドロコルチゾンの外用を加えて経過観察した.その後,鼻尖部にも一時皮疹の新生を認めたが約3ヵ月で軽快しほぼ正常の外観を呈するようになった.原因は明らかではないが抗核抗体陽性であったため免疫学的機序が考えられた.また,皮疹の分布が顔面神経の頬骨枝,頬筋枝の分布に沿って拡大しており,皮膚神経の関与も考えられた

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59歳女.顔面神経麻痺の既往があった.上口唇中央から右側にかけて自覚症状のない腫脹があり,口唇右側に小豆大で弾性硬,下床と癒着する紅色結節を認めた.舌に異常はなく,上顎前歯の歯肉移行部は一部腫脹し,圧痛を伴っていた.結節の生検病理所見で真皮全層に類上皮細胞肉芽腫を認め,周囲にはリンパ球が著明に浸潤していた.一部では拡張する脈管の周囲に肉芽腫の形成およびリンパ球浸潤がみられ,筋層間にも肉芽腫が散見された.金属のパッチテストで重クロム酸カリウムが陽性であり,口腔内に多数の義歯,金属冠を認めたため,その1つで金属成分分析を行ったがクロムは検出されなかった.Melkersson-Rosenthal症候群と診断し,金属アレルギーの関与を否定できず,金属除去などの歯科治療,ミノサイクリン内服で経過観察した.しかし症状は遷延し,歯科治療に伴って増悪する傾向を認めたため,プレドニゾロン30mg/日を開始した.その結果,腫脹は著明に軽快し,プレドニゾロンを中止した

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67歳男.20年以上前より徐々に増大してきた腫瘍を左第II趾背側に認め,腫瘍は16×24×12mm,淡紅色で広基性であった.弾性軟で腫瘍辺縁は一部顆粒状の外観を呈し,びらんを伴っていた.皮膚生検で悪性所見は認められず,2mm離して全摘した.腫瘍は表皮と連続性に周囲皮膚よりも上方に突出する形で認められた.腫瘍細胞は互いに結合しつつ索状構造を呈し増殖していた.腫瘍基部では一部腫瘍細胞が網目状構造を形成していた.腫瘍を構成する主な細胞は核が類円形,小さめの立方状細胞で,一部に管腔様構造を認めた.胞巣辺縁部に柵状配列はみられなかった.間質は浮腫性で一部にリンパ球の浸潤を伴っていた.胞巣の一部に異型性や核分裂像を認め,また胞体の明るい細胞が多くみられる部分も存在した.以上よりエクリン汗孔腫と診断した.全層植皮術を施行し,術後6ヵ月経過したが,局所再発は認めていない

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57歳男.左第IV〜V間の足背側から足底側にかけ1.3×1.0cm大,白色調で角化の強い局面を認め,表面は平坦で乳頭腫状の変化はなかった.骨との癒着はなかったが,趾間軟部組織の深いところまで一塊として浸潤を触れた.生検で疣贅か腫瘍か鑑別できず,局所麻酔下に角化局面より2mm離して一塊に切除し,人工真皮で欠損部をおおった.組織学的に完全に切除できているのを確認し,約2週間後肉芽の形成が見られてから全層植皮術を施行した.病理組織学的には著明な角質増生と著しい表皮突起の下方延長と乳頭層の上方延長を認め,腫瘍細胞の境界明瞭な圧排性の増殖がみられた.腫瘍は外方性,内方性に増殖し,疣贅にみられるような中心部へ向かう角化は見られなかった.基底層近くに構築の乱れがみられたものの,核異型はほとんど認めず,疣状癌と診断した.40年近く安全靴を着用しており,過度の圧迫が発症の誘因となった可能性が考えられた

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56歳女.糖尿病でアマリールの内服を開始したが,2週後より皮疹が出現し,内服中止後も皮疹は拡大した.右臀部より大腿後面・前脛骨部から足背にかけて扁平隆起性の紫紅色丘疹が多発し,帯状あるいは線状に配列していた.一部融合し,掻痒を伴っていた.生検病理所見で,軽度の角質増生,顆粒層の肥厚と真皮上層にリンパ球が主体で帯状の稠密な細胞浸潤を認めた.更に基底層の液状変性,コロイド小体が散見された.金属および薬剤の貼付試験ではニッケルのみ陽性であった.酪酸プロピオン酸ベタメタゾンなど副腎皮質ホルモン剤外用を2ヵ月間行ったが無効であり,歯科金属を除去すると共にミノマイシン200mg/日内服を開始したところ,皮疹は3日後には色素沈着化し著明に軽快した

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49歳女.顔面浮腫と高度の蛋白尿のため内科にてネフローゼ症候群と診断され入院中であった.左・右頬部に爪甲大で軽度浸潤を触れる紅斑を認め,血液検査で抗核抗体陽性,白血球低下を認めた.皮膚の病理所見で表皮基底層に液状変性を,真皮浅層の血管・附属器周囲にリンパ球浸潤を認め,蛍光抗体直接法で基底膜部にIgMの沈着を認めた.腎生検組織所見は光顕で糸球体が14個含まれていたが,いずれも硝子体変化はなく半月形成も認めなかった.糸球体はメサンギウムの肥厚や係蹄壁の異常,基底膜の肥厚はなかった.wire loopの所見もなく,蛍光抗体法も陰性で,微小糸球体変化と考えられた.電顕ではメサンギウムの分割した軽度の増殖を認めた.SLEと診断し,メチルプレドニゾロンのステロイドパルス療法を3日間行い,後療法としてプレドニゾロン内服を開始した.一時腎機能が悪化し,血液透析を導入したが,その後腎機能は改善し3週間で透析離脱となり,尿蛋白も陰性化した.現在,外来で経過観察中である

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Language：Japanese   Publisher：金原出版(株)  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(一社)日本神経学会  

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Language：Japanese   Publisher：(株)医学書院  

48歳女.Evans症候群と診断され,ステロイド剤や免疫抑制剤を内服し,脾臓摘出術を施行されている.プレドニゾロン(PSL)の内服で加療していたが,血小板減少や貧血が軽快したため漸減中止した.しかし,再び貧血が進行し,下肢の浮腫とともに左手掌に紅斑が出現した.皮疹の性状および組織所見から紅斑性狼瘡を疑い精査を行ったところ,血液検査で抗核抗陽性,抗ds-DNA抗体陽性であった.胸部X線写真で心拡大を認めたため心臓超音波検査を施行したところ心嚢液の貯留から心外膜炎の合併も診断した.また,甲状腺ホルモン,頸部超音波検査および甲状腺シンチグラフィ所見からBasedow病合併も判明した.よって,皮疹,貧血,抗核抗体陽性,抗ds-DNA抗体陽性,心外膜炎の合併からSLEと診断し,PSLの内服を開始したところ,貧血とともに皮疹も軽快.以後漸減した.Basedow病に対してはチアマゾールの内服で経過観察中である

DOI： 10.11477/mf.1412100429

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(株)協和企画  

55歳女.両下腿の腫脹,発赤を主訴とした.右下腿に発赤と浮腫を認め,軽度の掻痒感も認めた.一部で毛孔が開大し,いわゆる"オレンジ皮様外観"を呈していた.浮腫局面内には丘疹が散在性に認められた.軽度であるが,左下腿にも発赤,腫脹を認めた.病理組織学的所見では,真皮は著明に肥厚し,全層にわたり膠原線維が離解,浮腫性となっていた.膠原線維間には無構造物質の沈着が認められた.これはAlcian blue染色にて青染するため,沈着している物質は酸性ムコ多糖類と考えられた.脛骨前粘液水腫と診断し,潜在的な甲状腺機能異常症の合併を考え精査を行った.その結果,甲状腺機能亢進症であることが判明した.甲状腺シンチグラムより,甲状腺機能亢進症はGraves病によるもので,皮疹はそれに合併した脛骨前粘液水腫と診断した.発疹に対してはvery strong classのステロイド外用を,Graves病に対してはチアマゾール内服のみを行った.皮疹は約1週間でほぼ消失し,以後再発をみていない

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Language：Japanese   Publisher：(株)医学書院  

73歳女.肺癌でゲフィチニブ250mgを内服開始し,10日後に下痢と毛嚢炎様の皮疹が出現したが,一時軽快し,2ヵ月後から皮疹の増悪と共に膀胱炎症状,肝機能障害を認め同剤内服を中止した.悪化時,全身の皮膚は乾燥症状を呈し,毛孔一致性の小丘疹や膿疱,びらん,痂皮を混じた暗赤色紅斑が上肢,頸部で多発し融合していた.病理組織学的に角層下膿瘍を伴い,不全角化やexocytosisを認め,真皮では毛嚢は萎縮し周囲にリンパ球,好中球の浸潤を認めた.ミノマイシンの内服,トレチノイン軟膏を外用し,皮疹は乾燥症状を残して軽快した.ゲフィチニブのパッチテスト及びDLSTは陰性で,ゲフィチニブは上皮成長因子受容体(EGFR)のチロシンキナーゼ阻害剤であり,薬疹の機序としてEGFRへの直接的な関与が考えられた

DOI： 10.11477/mf.1412101475

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Language：Japanese   Publisher：(株)医学書院  

55歳女.約1年前から口腔内アフタ,下肢の有痛性紅斑が出没し,近医で加療を受けていたが難治であった.その後,左下肢に突然腫脹,発赤,疼痛が出現した.静脈造影で,左大腿から外腸骨静脈にかけて途絶を認め,深部静脈血栓症と診断した.ヘパリン,ウロキナーゼの点滴による凝固・線溶療法を施行した.腫脹は徐々に軽快し,ワーファリン経口投与と弾性ストッキングによる圧迫療法に切り替え,退院となった.胸痛・呼吸困難等肺塞栓を思わせる症状は認めなかった.3ヵ月後の静脈造影では閉塞は残存するが,側副路の発達がみられた.下腿の紅斑は血栓性静脈炎に合致し,経過中に外陰部潰瘍も認められたことから,半年以上続く口腔内アフタと併せ,不完全型ベーチェット病が基礎疾患と考えられた

DOI： 10.11477/mf.1412101397

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Language：Japanese   Publisher：(株)医学書院  

43歳男性.Fibroma of tendon sheath(FTS)の1例を経験した.患者は数年前からの左第1趾基部の無症候性皮下結節が徐々に増大したため著者らの施設へ紹介受診となった.所見では,左第1趾基部の趾間側に1×2cm大の弾性硬で下床とやや癒着し半球状に隆起した皮下結節を認め,皮膚超音波では腱と連続する境界明瞭な充実性腫瘍影が認められた.MRIではT1およびT2強調像ともに筋肉より低信号で,ガドリニウム造影での増強効果は微弱であった.局麻下に全摘術を施行したところ,病理所見では線維性被膜を有する境界明瞭な腫瘍で,硝子化・膨化し,かつ増生した線維束間に紡錘形の線維芽細胞様細胞が散在していた.さらに特殊染色では腫瘍細胞は線維芽細胞で,繊維束は膠原線維と思われ,この膠原線維間にはムチンの沈着も認められた.これらのことから著者らはFTSと診断したが,本症例のような足趾に生じる軟部腫瘍の診断と伸展度の評価にはMRIが有用であると考えられた

DOI： 10.11477/mf.1412101303

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Other Link： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2003&ichushi_jid=J01559&link_issn=&doc_id=20030620120017&doc_link_id=10.11477%2Fmf.1412101303&url=https%3A%2F%2Fdoi.org%2F10.11477%2Fmf.1412101303&type=%88%E3%8F%91.jp_%83I%81%5B%83%8B%83A%83N%83Z%83X&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00024_2.gif

Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：日本内科学会-関東地方会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(株)医学書院  

ケラトアカントーマ(KA)の臨床像は非常に特徴的であり,中心臍窩を有する噴火口に似た角化性丘疹が急速に増大し,数ヵ月後にはしばしば自然退縮する.しかしながら,KAと高分化型有棘細胞癌(SCC)は病理組織像が類似し,鑑別が困難な場合が時にある.そこで,著者等が経験した上口唇に生じたKAの症例を供覧すると共に,KAの治療方針について述べた.自験例のごとく臨床及び病理組織像からKAと考えられてもSCCとの鑑別が難しい症例では,放置して自然退縮を期待する経過観察ではなく,SCCに準じて治療すべきであると考えられた

DOI： 10.11477/mf.1412101248

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(株)医学書院  

Giant cell tumor of tendon sheath(GCTTS)の2例を経験した.症例1は60歳男性で,左第3趾末節骨背側の皮下結節で紹介受診した.同部に1.4cm大の弾性硬で下床と癒着し半球状に隆起した多房性皮下結節を認めた.一方,症例2は13歳女性で,左拇指MP関節尺側の皮下結節の増大で受診した.同部に1cm大の弾性硬で下床との可動性良好ななだらかに隆起する皮下結節を認めた.両症例ともMRIでT1強調,T2強調にて筋組織よりも低信号を呈し,ガドリニウム造影でまだら状に染まる腫瘍像を認めたが,骨侵食像は認めなかった.全摘術を施行した.病理学的には組織球類似細胞が胞巣を形成し,胞巣内に複数の核を持つ巨細胞が散在しており,辺縁に泡沫細胞やヘモジデリンの沈着を認め,GCTTSと診断した.いずれも再発を認めていない.GCTTSのような皮下腫瘍は診断が困難であるが,MRIは術前の診断に有用と考えられた

DOI： 10.11477/mf.1412904119

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Language：Japanese  

CiNii Books

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Other Link： http://search.jamas.or.jp/link/ui/2003020686

Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(株)医学書院  

57歳男.背部の紅色小結節を主訴とした.上背部に4mm大の広基性有茎性の紅色小結節を認め,pyogenic granulomaを疑い単純切除を行った.病理組織学的所見では,真皮内に異型性に富む類円形の腫瘍細胞が増生し,表皮直下にgrenz zoneを認めた.これら細胞はメラニン顆粒に乏しく,S-100強陽性,散在性にHMB-45陽性であった.以上より有茎性amelanotic malignant melanomaと診断し,拡大切除術を施行した.術後1年11ヵ月経過した現在,再発・転移はみられない

DOI： 10.11477/mf.1412904094

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：日本皮膚科学会-西部支部  

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Language：Japanese   Publisher：(一社)日本透析医学会  

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Language：Japanese   Publisher：(株)協和企画  

症例は40歳女で,手足の浮腫が出現し,その後皮膚の硬化が急速に拡大した.全身の皮膚はび漫性に硬化して蝋様光沢を有し,色素沈着と色素脱失の混在した局面を認めた.手指は浮腫が著明で屈曲拘縮を呈した.顔面は仮面様顔貌を呈し,舌小帯の短縮を認めた.大腿部は発赤し熱感を帯び,痒疹様の丘疹を伴っていた.左右肘部伸側には各々7×7mmと14×4mmの打ち抜き状で白苔の付着する潰瘍を認めた.Raynaud現象は認めず,嚥下障害や眼・口腔内の乾燥症状もなかった.病理組織所見で,表皮突起は消失し,表皮の菲薄化を認めた.真皮全層に密な線維化を認め,皮下脂肪織上層にまで及んでいた.毛包,汗腺は萎縮性で,周囲に軽度の小円形細胞浸潤を伴っていた.血液検査で抗Scl-70抗体陽性であること,肺線維症を合併していることと併せ全身性硬化症と診断した.PSL内服により皮膚症状は軽減したが,その後筋力低下が出現し,入院加療中である

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Language：Japanese   Publisher：鳥居薬品(株)  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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