Trichophyton verrucosum(T.verrucosum)感染症は，主にウシからヒトへと接触感染する人畜共通感染症として知られ，ヒトに感染した場合には一時的に激しい皮膚症状を来すことがある。小膿疱が多発融合して隆起し，中心治癒傾向の乏しい浸潤性紅斑局面をとることもあり，診断に苦慮する例も多い。今回，診断が遅れた結果，ステロイド外用剤により難治となった，いわゆる生毛部急性深在性白癬と小児のケルスス禿瘡を経験したので報告する。症例 1：50 歳，男性。畜産農家。左前腕伸側に小膿疱を伴う暗赤色の紅斑性局面を認めた。痂皮の KOH 標本にて分枝した糸状菌を認めたため，いわゆる生毛部急性深在性白癬と診断し，イトラコナゾール(以下 ITCZ) 125 mg/日の内服とネチコナゾール塩酸塩(以下 NCZ)の外用を約 9 週間行い軽快した。症例 2：7 歳，男児。自宅の流し台の棚の開き戸で頭部を受傷し，生じた潰瘍は難治で排膿を認めた。母子ともにウシとの直接的な接触歴はないが，母親の勤務先には牛舎があった。病変部の毛髪の KOH 標本にて菌糸，胞子を認めたため，ケルスス禿瘡と診断し，テルビナフィン塩酸塩 60 mg/日の内服，NCZ の外用にて加療を約 4 週間継続したが，効果が乏しく，ITCZ 150 mg/日の内服と白色ワセリン外用を約 16 週間継続し軽快した。形態学的特徴と遺伝子解析にて症例 1，2 ともに原因菌は T.verrucosum と同定した。

90 歳，女性。左頰部の紅色結節を主訴に，前医を受診し，生検でメルケル細胞癌(Merkel cell carcinoma ； MCC)が疑われる組織像であった。当科紹介時には，径 2 cm のドーム状に隆起した潰瘍を伴う鮮紅色腫瘤がみられた。側方マージン 1 cm，superficial muscular aponeurotic system(SMAS)を含める深さで腫瘍を切除した。病理組織では，真皮内で異型を示す N/C 比のやや低い好塩基性細胞が索状に配列し，浸潤性に増殖していた。CK20 は陰性だったが，その他神経系腫瘍マーカー所見(synaptophysin 陽性，chromogranin A 陽性，CD56 陽性)から MCC と診断した。Merkel cell polyoma virus(MCPyV)は陰性であった。一方，腫瘍内には，淡好酸性の細胞質と不整形な核を有する異型扁平上皮(有棘細胞癌〈squamous cell carcinoma ； SCC〉)が混在しており，両者に移行像を認めた。SCC を合併した MCC の過去の報告例では，MCPyV は16 例中 15 例で陰性であり，MCPyV が発癌に関与せず，MCPyV 陽性 MCC と比較して発症機序がより複雑であると考えた。

Epiplakin is a versatile cytolinker protein that is expressed in the epithelium, including the epidermis, several glands, and digestive organs [ [1] Fujiwara S. Takeo N. Otani Y. Parry D.A.D. Kunimatsu M. Lu R. et al. Epiplakin, a novel member of the plakin family originally identified as a 450-kDa human epidermal autoantigen: Structure and tissue localizatio. J. Biol. Chem. 2001; 276: 13340-13347 Crossref PubMed Scopus (50) Google Scholar ]. Human epiplakin consists of 13 B domains that are homologous to the B domain found in the carboxy-terminal region of desmoplakin; the last five B domains at the carboxy-terminal end, together with their associated linker regions, are highly conserved [ [1] Fujiwara S. Takeo N. Otani Y. Parry D.A.D. Kunimatsu M. Lu R. et al. Epiplakin, a novel member of the plakin family originally identified as a 450-kDa human epidermal autoantigen: Structure and tissue localizatio. J. Biol. Chem. 2001; 276: 13340-13347 Crossref PubMed Scopus (50) Google Scholar ] (Fig. 1A). The mRNA of epiplakin is transcribed from the third exon of the epiplakin gene (EPPK1) [ 2 https://www.ncbi.nlm.nih.gov/gene/83481 updated on 20-Apr-2017. Google Scholar , 3 Takeo N. Wang W. Matsuo N. Sumiyoshi H. Yoshioka H. Fujiwara S. Structure and heterogeneity of the human gene for epiplakin (EPPK1). J. Invest. Dermatol. 2003; 121: 1224-1226 Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar ] (Fig. 1B). The molecular size of epiplakin is estimated to be about 555 kDa, which is 25 amino acids longer than previously reported [ 1 Fujiwara S. Takeo N. Otani Y. Parry D.A.D. Kunimatsu M. Lu R. et al. Epiplakin, a novel member of the plakin family originally identified as a 450-kDa human epidermal autoantigen: Structure and tissue localizatio. J. Biol. Chem. 2001; 276: 13340-13347 Crossref PubMed Scopus (50) Google Scholar , 2 https://www.ncbi.nlm.nih.gov/gene/83481 updated on 20-Apr-2017. Google Scholar ]. However, in previous studies, immunoblot analysis of epidermal extracts and cell lysates revealed additional protein bands above and below the primary epiplakin band at 555 kDa [ 4 Fujiwara S. Shinkai H. Takayasu S. Owaribe K. Tsukita S. Kageshita T. A case of subepidermal blister disease associated with autoantibody against 450 kD protein. J. Dermatol. 1992; 19: 610-613 Crossref PubMed Scopus (20) Google Scholar , 5 Jang S.I. Kalinin A. Takahashi K. Marekov L.N. Steinert P.M. Characterization of human epiplakin: RNAi-mediated epiplakin depletion leads to the disruption of keratin and vimentin IF networks. J. Cell Sci. 2005; 118: 781-793 Crossref PubMed Scopus (42) Google Scholar , 6 Tsuchisaka A. Numata S. Teye K. Natsuaki Y. Kawakami T. Takeda Y. et al. Epiplakin is a paraneoplastic pemphigus autoantigen and related to bronchiolitis obliterans in Japanese patients. J. Invest. Dermatol. 2016; 136: 399-408 Abstract Full Text Full Text PDF PubMed Scopus (38) Google Scholar ]. Spazierer et al. estimated the size of human epiplakin to be 725 kDa, which is similar to mouse epiplakin that contains 16 B domains [ [7] Spazierer D. Fuchs P. Pröll V. Janda L. Oehler S. Fischer I. et al. Epiplakin gene analysis in mouse reveals a single exon encoding a 725-kDa protein with expression restricted to epithelial tissues. J. Biol. Chem. 2003; 278: 31657-31666 Crossref PubMed Scopus (31) Google Scholar ].

EJD, vol. 27, n◦ 6, November-December 2017 PG associated with arteriovenous dialysis shunts have been reported to date [6, 7]. We speculate that the debridement for the stasis ulcers or the transcatheter arterial microembolization provoked PG in our case. It is known that PG rarely occurs at the sites of surgical incision, which is described as postoperative PG. Operative trauma and pathergy seem to induce postoperative PG through up-regulation of neutrophils [1]. Pathergy is considered as a condition of altered tissue reactivity occurring in response to the trauma [8]. Although surgical debridement probably induced PG through pathergy, we cannot exclude the possibility that transcatheter arterial microembolization provoked this PG, although no reports have been published regarding an association between PG and transcatheter arterial microembolization. Since transcatheter arterial microembolization using imipenem/cilastatin sodium is a recently proposed approach for management [9], the number of cases treated in this way will increase as will those of PG using this method.

症例は 85 歳，女性。2011 年 1 月に転倒して打撲したのを契機に左腰部に皮下腫瘤を形成した。腫瘤が徐々に増大してきたため，同年 3 月に近医を受診し，当初皮下血腫の診断にて加療されていたが，同年 8 月頃より急激な皮下腫瘤の増大を認めたため，同年 9 月に当科を紹介され受診した。初診時，左腰部に熱感を伴う 15×12 cm で高さが 8 cm の表面に光沢を伴った弾性軟の皮下腫瘤を認めた。皮膚生検で脂肪肉腫を疑われ，腫瘍辺縁より 3 cm マージンにて腫瘍切除術を施行した。術中所見で腸骨との癒着を認めたため，腸骨稜全体を切除した。腹壁形成後に有茎前外側大腿皮弁と分層植皮による再建術を施行した。その後，皮弁部・植皮部の潰瘍および欠損部に対して計 3 回植皮術を施行して治癒したため，自宅退院とした。病理組織検査の結果，最終的に粘液線維肉腫 (myxofibrosarcoma) と診断した。画像による定期的経過フォローを行い，再発転移を認めていなかったが，2015 年3 月療養所で死亡した。

Nivolumab is a monoclonal antibody directed against PD1 (programmed cell death 1) that can improve survival in patients with metastatic melanoma. Such immune checkpoint inhibitors have been known to induce type 1 diabetes mellitus (T1D) [1, 2].A 54-year-old woman reported enlarging black nodules on her left sole, which had been present for seven months (figure 1A). CT imaging revealed swollen lymph nodes in the left inguinal and pelvic regions (figure 1B). After clinical diagnosis of malignant melanoma [...]

Hereditary lactate dehydrogenase (LDH) M-subunit deficiency is very rare and we have found reports of close to a dozen cases in the published work, two of which were associated with pustular psoriasis-like lesions. We report a third case of pustular psoriasis-like eruptions associated with LDH M-subunit deficiency, which occurred 24 years after the diagnosis of LDH M-subunit deficiency. These cases indicate that abnormal activity of LDH can induce pustular psoriatic lesions in the long term. Some patients with symptoms of hereditary LDH M-subunit deficiency have antecedent annular scaly plaque lesions, that resemble psoriatic lesions. We discuss a hypothesis to explain this scenario.

The incidence of tuberculosis in Japan remains higher than in western countries and more than 20,000 new patients were registered with this disease in Japan in 2011 [1]. We report the case of an 84-year-old female who presented with a subcutaneous nodule in her nose that provided a clue to diagnosing miliary tuberculosis.In September 2014, the patient complained of a symptomless nodule on the left side of the root of her nose. She had suffered from rib caries when she was 28 years old. She had lost [...]

Pigmented cosmetic dermatitis‐like (Riehl's melanosis‐like) pigmentation was reported in three of 27 patients with primary Sjögren's syndrome. But case reports of such eruptions are rare. We describe three cases of such eruptions associated with primary Sjögren's syndrome or anti‐SSA antibody and possible associations with specific types of human leukocyte antigen (HLA) and infiltrating lymphocytes. These middle‐aged Japanese women had reticular facial pigmentation and histopathological examination revealed interface dermatitis, melanophages, and dense lymphocytic infiltration around hair follicles and sweat ducts. HLA typing revealed common antigenic equivalents or genetic typing of HLA‐A2, DR52, DPA1(02:02) and DPB1(05:01). Immunohistochemical staining revealed major subsets of T cells to be CD8 and CD45RO. Some Foxp3‐ and few IL17‐positive cells were found in strong contrast to the major CD4 subset of infiltrated T cells in annular erythema associated with Sjögren's syndrome. Apparently, our patients' pigmentation represented a specific etiology associated with primary Sjögren's syndrome or anti‐SSA antibody.

Pemetrexed, which is used for the treatment of non‐small cell lung carcinoma and malignant mesothelioma, induces cutaneous adverse reactions in approximately 20% of patients. There are also reports of the induction of fibrosing disorders. We describe a case of pemetrexed‐induced scleroderma‐like conditions in the lower legs of a patient whose pulmonary carcinoma has been relatively well controlled, with prolongation of the dose interval, in spite of the discomfort in both his legs. Skin biopsy revealed dermal fibrosis and dilated lymph vessels in the dermis, but lymphocytic infiltration around the lymph vessels, in contrast to the blood vessels, was minimal. Immunohistochemical staining revealed that the major subsets of T cells that had infiltrated around blood vessels were CD3 and CD45Ro, but no B cells were detected. High serum levels of interleukin (IL)‐4 and IL‐6 suggested that T cells, which secrete these cytokines, may be involved in the pathogenesis of this condition. Magnetic resonance imaging of the lower extremities revealed muscular and fascial involvement. Several chemotherapeutic agents, such as taxanes, gemcitabine and bleomycin, are known to induce scleroderma‐like changes, and we should also keep the side‐effects of pemetrexed in mind when we encounter patients with fibrosing conditions.

Mucoepidermoid carcinoma (MEC) is histologically characterised as low-, intermediate-, and high-grade [1]. Low-grade tumours rarely transform into high-grade tumours (dedifferentiation) [2, 3] and the latter very rarely produce granulocyte colony stimulating factor (G-CSF) [4, 5]. MEC harbours a characteristic t(11;19)(q21;p13) translocation; this rearrangement results from the fusion between exon 1 of the gene for CRTC1 (cyclic AMP/cyclic AMP-responsive element-binding protein-regulated transcription [...]

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All plakin family proteins are known to be autoantigens in paraneoplastic pemphigus (PNP). In this study, we first examined whether PNP sera also react with epiplakin, another plakin protein, by various immunological methods using 48 Japanese PNP sera. Immunofluorescence confirmed that cultured keratinocytes expressed epiplakin. Epiplakin was detected by 72.9% of PNP sera by immunoprecipitation-immunoblotting with KU-8 cell extract, but not by immunoblotting of either normal human epidermal extract or KU-8 cell extract. Epiplakin was essentially not detected by 95 disease and normal control sera. Statistical analyses of various clinical and immunological findings revealed a significant correlation of the presence of anti-epiplakin antibodies with both bronchiolitis obliterans and mortality. No epiplakin-negative PNP case developed bronchiolitis obliterans. However, although 29.4% of European patients with PNP had bronchiolitis obliterans, significant correlation with anti-epiplakin autoantibodies was not observed. In further studies for lung, immunofluorescence showed the presence of epiplakin in normal human lung, particularly respiratory bronchiole, immunoprecipitation-immunoblotting showed that PNP sera reacted with epiplakin in cultured lung cells, and mice injected with polyclonal antibody specific to epiplakin histopathologically showed abnormal changes in small airway epithelia. These results indicated that epiplakin is one of the major PNP autoantigens and is related to PNP-related bronchiolitis obliterans.

成人 T 細胞白血病/リンパ腫（adult T-cell leukemia/lymphoma；ATLL）慢性型・リンパ腫型と診断されており，急性増悪の約半年前に突然全身に紅斑が多発した症例である。ATLL の皮膚浸潤を疑い 4 回皮膚生検を施行したが，いずれも interface dermatitis を呈し，異型は目立たなかった。薬疹の可能性を考えて，内服薬を全て中止しステロイドの全身投与をしたところ，皮疹は軽快傾向を示すものの消退しなかった。皮疹出現後半年で急性増悪し，予後不良の転帰をとった。後日追加の免疫染色を行ったところ，1 回目の生検組織では CD3，CD4，CCR4，Foxp3，CD25，CD30 陽性の少数の大型異型リンパ球がみられた。2，3 回目の生検組織では異型リンパ球はほとんどなく，CD4/8 比が低下した。4 回目生検組織には少数の大型異型リンパ球が真皮浅層にみられたが 1 回目より少なく，CD8 陽性細胞も多く，ATLL の病変が免疫反応で修飾されたものと考えられた。全経過を通して皮疹が消退することはなく，紅斑性局面は ATLL 急性増悪の予兆と考えられた。

We performed skin cancer screenings for 2 or 3 days annually from 2006 through 2013 in Oita Prefecture, Japan. Screening of approximately 3000 people in total allowed us to identify and treat several skin cancers, including five cases of malignant melanoma, four of squamous cell carcinoma, 16 of basal cell carcinoma, 11 of Bowen's disease, 17 of actinic keratosis, one of extramammary Paget's disease and one of metastatic breast carcinoma. The sensitivity and specificity for the category defined by an identified lesion associated with risk of cancer and requiring further examination (category C) were 92.7% and 95%, respectively. We cannot estimate the outcome of our skin cancer screenings in terms of cancer mortality because of the small number of subjects examined and the brief follow-up period. However, we did estimate the effectiveness of these screenings in terms of stages or sizes of cancerous lesions. The relative numbers of subjects with malignant melanoma at various clinical stages, identified during skin cancer screenings and during a routine visit to our hospital, were significantly different. We also compared, statistically, the sizes of lesions in Bowen's disease that were found during cancer screenings and during a direct visit to our hospital. The former lesions were smaller than the latter. Our data suggest the benefits of our skin cancer screenings and the importance of campaigns and education to encourage people to visit dermatologists for the detection of skin cancers at an early stage.

Background: Human leukocyte antigen (HLA) genotypes in lamotrigine -induced (LTG-induced) cutaneous adverse drug reactions (cADRs) have been described in several reports but controversy remains even for a given ethnic group. We attempted to clarify a possible association between LTG-induced cADRs and HLA alleles in Japanese patients.Method: Sixteen subjects, including eight patients with LTG-induced cADRs and eight LTG-tolerant controls were included in this study. All eight patients with LTG-induced cADRs gave positive results in a drug-induced lymphocyte stimulation test (DLST) with LTG. We performed HLA-typing for HLA-A, -B, -C, -DRB1, -DQA1, -DQB1, -DPA1 and -DPB1, using PCR with sequence-specific oligonucleotide probes and multiple analyte profiling (xMAP) technology (Luminex System; Luminex Corporation, Austin, TX).We examined differences between allele frequencies in our two groups of subjects and the allele frequencies in the general Japanese population.Results: The frequencies of HLA-DRB1*0405, and HLA-DQB1*0401 alleles were higher in our LTG-cADRs patients than the reference frequencies in the general Japanese population. We also detected HLADQA1*0303 frequently in our LTG-cADRs patients, but data for this allele in the Japanese population was not available. Our observation was presumably due to the linkage disequilibrium among the three alleles. The haplotype frequency of HLA-DRB1*0405. DQB1*0401 and DQA1*0303 in our LTG-cADRs subjects was also different from the corresponding haplotype frequency in the database for the Japanese population and the difference was statistically significant. One patient with the HLA-DRB1*0405, -DQB1*0401 and DQA1*0303 haplotype was safely re-treated with LTG after results of a DLST with LTG ceased to be positive about 4 months after discontinuation of LTG.Limitations: Our analysis included only 16 patients. Associations between LTG-induced cADRs and specific HLA loci will have to be confirmed in larger studies.Conclusions: LTG-induced cADRs are associated with HLA-DRB1'0405, -DQB1*0401 and -DQA10303. (C) 2015 Elsevier By. All rights reserved.