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

We herein report a 45-year-old-man with multiple foreign body granulomas in the lungs caused by polytetrafluoroethylene (PTFE). A mass in the right lower lobe of the lung and bilateral centrilobular lung nodules were found unexpectedly during the patient's visit to a hospital for a respiratory infection. The patient's occupation for 26 years involved spraying PTFE. A lung biopsy using bronchoscopy revealed granulomatous lesions and giant cells. The presence of fluorine in the granulomatous lesions was confirmed using an electron probe microanalyzer with wavelength dispersive spectrometer. Fluorine is a component of PTFE and is not found in normal lung tissue.

DOI： 10.2169/internalmedicine.9008-21

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DOI： 10.1016/j.jaci.2021.02.006

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Intractable chronic inflammatory diseases, including autoimmune diseases, autoinflammatory diseases and allergic diseases, are caused by disruption or failure of the immune system. Pathogenic immune cells are presumed to be closely related to the pathogenesis of intractable diseases, but the precise cellular and molecular mechanisms underlying the pathogenesis of these diseases remain unclear. The balance between the T helper type 1 (Th1) and Th2 cell fractions has been believed to be responsible for the differences among inflammatory diseases. However, an analysis of the cells infiltrating inflammatory lesions in mice and humans revealed the generation of pathogenic Th cells with different characteristics at the memory T-cell stage in the peripheral tissues in various inflammatory diseases. In this review, we will summarize and discuss recent progress regarding the characteristics of pathogenic Th cells, their mode of action, and the molecular mechanisms that regulate the pathology of intractable chronic inflammatory diseases, particularly those with tissue fibrosis. We hope this article will help clarify the pathogenesis of these diseases and propose a future direction for research.

DOI： 10.1016/j.alit.2021.02.001

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Eosinophils are multifunctional leukocytes, being involved in the host defense against helminth infection, tissue homeostasis and repair of injured tissue. However, eosinophils also play critical roles in shaping the pathogenesis of allergic diseases, including fibrotic responses in allergic diseases. Eosinophils consist of various granules that are a source of cytokines, chemokines, enzymes, extracellular matrix and growth factors. Recent studies have revealed that eosinophil extracellular trap cell death (EETosis) exacerbates eosinophilic inflammation by releasing the products, including Charcot-Leyden crystals (CLCs). In type 2 inflammatory diseases, memory-type pathogenic helper T (Tpath) cells are involved in shaping the pathogenesis of eosinophilic inflammation by recruiting and activating eosinophils in vivo. We herein review the molecular mechanisms underlying the development of eosinophils and the various functions of granules, including CLCs, during eosinophilic inflammation. We also discuss the double-edged roles of eosinophils in tissue repair and type 2 immune inflammation.

DOI： 10.1016/j.alit.2020.09.002

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Memory T cells are crucial for both local and systemic protection against pathogens over a long period of time. Three major subsets of memory T cells; effector memory T (TEM) cells, central memory T (TCM) cells, and tissue-resident memory T (TRM) cells have been identified. The most recently identified subset, TRM cells, is characterized by the expression of the C-type lectin CD69 and/or the integrin CD103. TRM cells persist locally at sites of mucosal tissue, such as the lung, where they provide frontline defense against various pathogens. Importantly, however, TRM cells are also involved in shaping the pathology of inflammatory diseases. A number of pioneering studies revealed important roles of CD8+ TRM cells, particularly those in the local control of viral infection. However, the protective function and pathogenic role of CD4+ TRM cells that reside within the mucosal tissue remain largely unknown. In this review, we discuss the ambivalent feature of CD4+ TRM cells in the protective and pathological immune responses. We also review the transcriptional and epigenetic characteristics of CD4+ TRM cells in the lung that have been elucidated by recent technical approaches. A better understanding of the function of CD4+ TRM cells is crucial for the development of both effective vaccination against pathogens and new therapeutic strategies for intractable inflammatory diseases, such as inflammatory bowel diseases and chronic allergic diseases.

DOI： 10.3389/fimmu.2021.616309

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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INTRODUCTION/OBJECTIVES: Interstitial lung disease (ILD) is a significant cause of mortality among patients with dermatomyositis (DM) or polymyositis (PM). There are two subtypes of PM and DM often complicated with ILD: those with anti-aminoacyl-tRNA synthetase (anti-ARS) antibodies and those with anti-MDA-5-associated amyopathic DM (ADM). Our aim is to clarify the inflammatory and immunological differences between the disorders. METHODS: We retrospectively collected consecutive patients with anti-ARS-ILD and those with anti-MDA-5 antibody-positive ADM-ILD. The serum concentration of 38 cytokines was measured using a cytokine panel. The relative risks for anti-MDA-5 antibody-positive ADM-ILD were examined with univariate and multivariate logistic regression models. Spearman's rank correlation coefficient was calculated between cytokine levels and clinical parameters in the disease. Levels of cytokines were compared between anti-ARS-ILD and anti-MDA-5-positive ADM-ILD patients (alive or dead) using Dunnett's test. RESULTS: Twenty-three patients with anti-ARS-ILD and the same number of patients with anti-MDA-5-positive ADM-ILD were enrolled. The anti-MDA-5 group had poor survival (p = 0.025). Univariate logistic regression models showed that eotaxin, IL-10, IP-10, and MCP-1 were associated with the diagnosis of anti-MDA-5-positive ADM-ILD. Multivariate logistic regression models revealed that IP-10 was the most significantly associated (p = 0.001). Relationship analyses showed that IL-10 had significant positive correlations with CK (r = 0.5267, p = 0.009) and ferritin (r = 0.4528, p = 0.045). A comparison of the cytokine levels found that IP-10 was elevated in both patients who were alive and patients who had died with ADM-ILD compared with the levels in those with ARS-ILD (p = 0.003 and p = 0.001, respectively). CONCLUSIONS: Anti-MDA-5-positive ADM-ILD had poorer survival than anti-ARS-ILD. IP-10 seems to be most deeply involved in the pathophysiology of anti-MDA-5-associated ADM-ILD.Key Points• To clarify differences in the inflammatory and immunological features of anti-MDA-5-positive ADM-ILD and anti-ARS-ILD, we performed an observational study to measure serum cytokine concentrations before treatment using a multiplex immunoassay system.• Multivariate logistic regression models revealed that IP-10 was associated with the most significant relative risk for ADM-ILD with anti-MDA-5 antibodies.• Levels of IP-10 were elevated considerably in anti-MDA-5-positive survivors and nonsurvivors compared with the levels in anti-ARS patients.• These results suggest that IP-10 is the most deeply involved in the pathophysiology of anti-MDA-5-positive ADM-ILD.

DOI： 10.1007/s10067-020-04984-x

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Language：Japanese   Publisher：(有)科学評論社  

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PURPOSE: In the past decade, the relationship between naturally occurring interferon-γ-neutralizing autoantibodies (IFNγ-Ab) and disseminated non-tuberculous mycobacteria (NTM) infection has been established. Furthermore, immune suppressive therapy aimed at the suppression of antibody production has shown efficacy as a supportive treatment. However, the nature of antibody behavior and antibody titer during the course of this disease, as well as the pathophysiological significance of IFNγ-Ab, has not yet been fully elucidated. METHODS: Thirteen Japanese subjects suffering from disseminated NTM (dNTM) infection with IFNγ-Ab were evaluated. The fluctuation of IFNγ-Ab titer and the neutralizing capacity against IFN-γ during the course of the disease were retrospectively analyzed. IFNγ-Ab titers in the sera were quantified using an enzyme-linked immunosorbent assay; neutralizing capacity was evaluated via flow cytometry. RESULTS: Serum antibody titers were not constant during the treatment period and varied over the course of the disease. The antibody titer decreased when the disease was improved by anti-mycobacterial treatment (p < 0.01) and increased as the disease progressed (p < 0.05). Even after the antibody titer decreased, the neutralizing capacity against IFN-γ was maintained by individual sera. CONCLUSIONS: Despite the improvement in the pathological condition via treatment, the patients' sera maintained neutralizing capacity against IFN-γ. Antibody titer fluctuated over the course of the disease and exhibited potential as a biomarker for judgment of the disease state.

DOI： 10.1007/s10875-020-00762-1

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Very recently, a modest but significant efficacy of granulocyte-macrophage colony-stimulating factor (GM-CSF) inhalation therapy for the treatment of mild to moderate autoimmune pulmonary alveolar proteinosis (aPAP) has been reported. As the ability to measure the level of GM-CSF autoantibody (GMAb) in the serum is required to decide the indication for this therapy, we developed a high-performance GMAb testing kit for clinical use. As the kit succeeded in reducing nonspecific IgG binding to the ELISA plate, the predictive performance shown in the training study to discriminate aPAP patients from healthy subjects was perfect, providing a cut-off value of 1.65 U·mL-1 in 78 patients with aPAP and 90 healthy subjects in an operator-blinded manner using logistic regression analysis. As in the validation study, serum samples from another 213 patients with aPAP were also blinded and evaluated in an operator-blinded manner against external 207 samples from patients with other types of PAP and patients exhibiting various ground-glass opacities on chest high-resolution computed tomography that require discrimination from PAP. The logistic regression analysis of these validation data sets revealed values of 97.6% and 100% for specificity and sensitivity, respectively. Thus, this new GMAb testing kit is reliable for the diagnosis of aPAP and differential diagnosis of other lung diseases.

DOI： 10.1183/23120541.00259-2019

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Tissue-resident memory T cells (TRM cells) are crucial mediators of adaptive immunity in nonlymphoid tissues. However, the functional heterogeneity and pathogenic roles of CD4+ TRM cells that reside within chronic inflammatory lesions remain unknown. We found that CD69hiCD103lo CD4+ TRM cells produced effector cytokines and promoted the inflammation and fibrotic responses induced by chronic exposure to Aspergillus fumigatus. Simultaneously, immunosuppressive CD69hiCD103hiFoxp3+ CD4+ regulatory T cells were induced and constrained the ability of pathogenic CD103lo TRM cells to cause fibrosis. Thus, lung tissue-resident CD4+ T cells play crucial roles in the pathology of chronic lung inflammation, and CD103 expression defines pathogenic effector and immunosuppressive tissue-resident cell subpopulations in the inflamed lung.

DOI： 10.1038/s41590-019-0494-y

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BACKGROUND: Natural killer T (NKT) cells express a T-cell receptor that recognizes endogenous and environmental glycolipid antigens. Several subsets of NKT cells have been identified, including IFN-γ-producing NKT1 cells, IL-4-producing NKT2 cells, and IL-17-producing NKT17 cells. However, little is known about the factors that regulate their differentiation and respective functions within the immune system. OBJECTIVE: We sought to determine whether the polycomb repressive complex 2 protein enhancer of zeste homolog 2 (Ezh2) restrains pathogenicity of NKT cells in the context of asthma-like lung disease. METHODS: Numbers of invariant natural killer T (iNKT) 1, iNKT2, and iNKT17 cells and tissue distribution, cytokine production, lymphoid tissue localization, and transcriptional profiles of iNKT cells from wild-type and Ezh2 knockout (KO) iNKT mice were determined. The contribution of NKT cells to development of spontaneous and house dust mite-induced airways pathology, including airways hyperreactivity (AHR) to methacholine, was also assessed in wild-type, Ezh2 KO, and Ezh2 KO mice lacking NKT cells. RESULTS: Ezh2 restrains development of pathogenic NKT cells, which induce spontaneous asthma-like disease in mice. Deletion of Ezh2 increased production of IL-4 and IL-13 and induced spontaneous AHR, lung inflammation, mucus production, and IgE. Increased IL-4 and IL-13 levels, AHR, lung inflammation, and IgE levels were all dependent on iNKT cells. In house dust mite-exposed animals Ezh2 KO resulted in enhanced AHR that was also dependent on iNKT cells. CONCLUSION: Ezh2 is a central regulator of iNKT pathogenicity and suppresses the ability of iNKT cells to induce asthma-like pathology.

DOI： 10.1016/j.jaci.2019.02.024

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DOI： 10.1007/s00281-019-00735-6

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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House dust mites (HDMs), Dermatophagoides sp., are one of the most widespread aeroallergens worldwide and cause various allergic diseases, including asthma. The pathophysiology of asthma has been intensively investigated using murine models of allergic airway inflammation induced by exposure to D. pteronyssinus. However, the pathogenic roles of D. farinae in the allergic airway inflammation remains unclear. We herein report that repetitive exposure to D. farinae resulted in neutrophil-dominant airway inflammation together with fibrotic changes and the formation of lymphoid clusters. Both type 1 and type 2 inflammatory cytokines were induced. The pathogenic changes in the airway were dependent on both the frequency and dose of D. farinae exposure. Our study provides novel procedures and insight into the pathogenesis of D. farinae-induced airway inflammation in vivo.

DOI： 10.1016/j.jim.2018.12.003

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We report a case of non-AIDS (acquired immunodeficiency syndrome), non-CAPD (Continuous Ambulatory Peritoneal Dialysis), non-cirrhotic, Mycobacterium avium peritonitis, which is a rare form of mycobacterial infection. A 66-year-old Japanese man who had been treated previously for angioimmunoblastic T-cell lymphoma (AITL), had developed disseminated M. avium infection. Antimycobacterial regimen improved his symptoms; however, following an interruption in treatment, he developed chylous ascites. The patient died of uncontrolled peritonitis despite intensive treatment. Anti-interferon-γ autoantibody was positive, and AITL was presumed to be involved in autoantibody production. A rare coexistence of chylous ascites, autoantibody, and AITL taught us an intriguing lesson on the pathogenesis of M. avium infection. Particularly, we conclude that treatment strategies for M. avium infection should aim to restore immunity.

DOI： 10.1007/s00430-018-0555-0

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The primary function of the lung is efficient gas exchange between alveolar air and alveolar capillary blood. At the same time, the lung protects the host from continuous invasion of harmful viruses and bacteria by developing unique epithelial barrier systems. Thus, the lung has a complex architecture comprising a mixture of various types of cells including epithelial cells, mesenchymal cells, and immune cells. Recent studies have revealed that Interleukin (IL-)33, a member of the IL-1 family of cytokines, is a key environmental cytokine that is derived from epithelial cells and induces type 2 inflammation in the barrier organs, including the lung. IL-33 induces allergic diseases, such as asthma, through the activation of various immune cells that express an IL-33 receptor, ST2, including ST2+ memory (CD62LlowCD44hi) CD4+ T cells. ST2+ memory CD4+ T cells have the capacity to produce high levels of IL-5 and Amphiregulin and are involved in the pathology of asthma. ST2+ memory CD4+ T cells are maintained by IL-7- and IL-33-produced lymphatic endothelial cells within inducible bronchus-associated lymphoid tissue (iBALT) around the bronchioles during chronic lung inflammation. In this review, we will discuss the impact of these immune cells-epithelial/mesenchymal interaction on shaping the pathology of chronic allergic inflammation. A better understanding of pathogenic roles of the cellular and molecular interaction between immune cells and non-immune cells is crucial for the development of new therapeutic strategies for intractable allergic diseases.

DOI： 10.3389/fimmu.2019.00570

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A 63-year-old woman presented with a fever, eruption, and sterile pyuria. A cystoscopic examination revealed submucosal nodular lesions in the trigone of the bladder, and a biopsy specimen showed epithelioid cell granulomas in the lamina propria of the bladder. Mycobacterium avium grew in the urine culture. Other organ involvement, such as the lungs, spleen, bones, muscles, and pelvic lymph nodes, was observed on radiological examinations, and M. avium was isolated from some organ lesions. Interferon-γ-neutralizing autoantibodies were detected in the patient's serum. Therefore, the patient was diagnosed with disseminated M. avium infection, which was resolved with antimycobacterial treatment.

DOI： 10.2169/internalmedicine.0965-18

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Background: Interferon-γ neutralizing autoantibodies (nIFNγ-autoAbs) are reported in patients with disseminated nontuberculous mycobacteria (NTM) infection and may function by increasing the infection risk. Notwithstanding, the prevalence of nIFNγ-autoAbs as well as the clinical presentation, diagnosis, and natural history of disseminated NTM infection in these patients is poorly understood. Methods: In this retrospective observational study, data and sera for 331 Japanese subjects with mycobacterial infection were collected and analyzed. IFNγ-autoAb titers in sera were quantified using an enzyme-linked immunosorbent assay; neutralizing capacity was evaluated via flow cytometry. Results: Disseminated NTM was identified in 50 human immunodeficiency virus-uninfected patients. Of these, 30 of 37 (81%) immunocompetent patients had an increased nIFNγ-autoAb titer whereas only 1 of 13 (7.7%) immunodeficient patients had an increased nIFNγ-autoAb titer (P < .0001, χ2 test). Presenting symptoms were nonspecific and NTM infection was not included in the differential diagnosis in most cases. All patients with disseminated NTM and an increased serum nIFNγ-autoAb level received prolonged antimicrobial therapy. In 6 cases when antibiotic treatment was discontinued, NTM infection recurred and required resumption of antibiotic therapy for infection control. The mortality rate was 3.2% in disseminated NTM patients with nIFNγ-autoAbs and 21% in those without. Conclusions: nIFNγ-autoAbs were present in most patients with disseminated NTM infection without a diagnosis of clinical immunodeficiency. Diagnosis of disseminated NTM requires a high degree of suspicion and can be improved by measuring serum nIFNγ-autoAb titer. Long-term antibiotic therapy helps prevent recrudescent NTM infection.

DOI： 10.1093/cid/cix996

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A 59-year-old Japanese man diagnosed with interstitial lung disease associated with amyopathic dermatomyositis with anti-melanoma differentiation-associated gene 5 (MDA-5) antibodies was treated with intravenous methyl prednisolone (PSL) 1000 mg, oral PSL 1 mg/kg, and oral cyclosporin 200 mg daily. His respiratory condition worsened after treatment with two times of intravenous cyclophosphamide and another steroid pulse therapy as well as PSL and cyclosporin. Addition of mycophenolate mofetil (MMF), 1.5 g daily improved PaO2/FiO2 (PF) ratio of the patient from 294 to 360 at 4 weeks and 416 at 15 weeks after addition of MMF. We measured cytokine concentration in preserved serum taken at 11 and 7 weeks before addition of MMF and at 4, 11, and 15 weeks after MMF administration. Of the 28 cytokines evaluated, the concentrations of fibroblast growth factors-2 (FGF-2), chemokine (C-X3-C motif) ligand 1 (CX3CL1), interleukin (IL)-1ra, IL-17A, inducible protein 10 (IP-10), and monocyte chemotactic protein-1 (MCP-1) decreased after addition of MMF. These results suggest that MMF may be beneficial to patients with interstitial lung disease by modification of the cytokine/growth factor protein expression.

DOI： 10.1002/rcr2.235

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：W B SAUNDERS CO LTD  

Background: Patients with amyopathic dermatomyositis (ADM) sometimes develop rapidly progressive interstitial lung disease (ILD) predominantly in Asia. Although anti-CADM-140/MDA5 antibody titer could correlate with disease activity and predict the course of ILD associated with ADM, it is not clear how this antibody is involved in the pathogenesis of ILD in ADM.
Methods: We retrospectively collected clinical records and preserved serum before treatment of consecutive patients with ADM-ILD treated in the Niigata University Medical and Dental Hospital since 2000. We measured anti-CADM-140/MDA5 antibody titer and compared it between survivors and non-survivors. Serum cytokine/growth factor protein concentration was measured using a multiplex immunoassay system. The associations between anti-CADM-140/MDA5 antibody titer and each cytokine/growth factor protein concentration were evaluated.
Results: Thirteen patients were enrolled into the study. Among them, four patients did not respond to intensive immunosuppressive therapy and died. The mean anti-CADM-140/MDA5 antibody titer was significantly higher in patients who did not responded to therapy than in those who survived (p &lt; 0.05). Relationship analyses between the antibody titer and each cytokine/GF protein concentration revealed that Spearman's rank correlation coefficients were more than 0.4 in thirteen cytokine/GF proteins. In particular, the strongest correlation was found between anti-CADM-140/MDA5 antibody titer and CX3CL1 (r = 0.8897).
Conclusions: These results confirmed that anti-CADM-140/MDA5 antibody levels could predict outcomes of ADM-ILD. Relationship analyses suggested that CX3CL1 might be involved in the pathogenesis of anti-CADM-140/MDA5 antibody positive ADM-ILD. (C) 2015 Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.rmed.2015.07.004

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：SAGE PUBLICATIONS LTD  

A 23-year-old man was admitted to our hospital with severe thrombocytopaenia. He had unprotected sexual contact 6 weeks earlier. He was diagnosed with acute HIV infection by means of HIV RNA viral load testing and HIV-associated thrombocytopaenia. Although his thrombocytopaenia improved immediately with short-term dexamethasone therapy, this effect was not sustained after cessation of therapy. Antiretroviral therapy including raltegravir was initiated, and the patient recovered from severe thrombocytopaenia within several days. The findings from this case suggest that acute HIV infection should be suspected with unexplained thrombocytopaenia, and that antiretroviral therapy is the treatment of choice for severe HIV-associated thrombocytopaenia, even when in the early period following acquisition of the virus.

DOI： 10.1177/0956462414531937

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Language：Japanese   Publisher：(株)羊土社  

CD4陽性T細胞(ヘルパーT細胞;Th細胞)は外来異物に対する宿主防御機構として獲得免疫応答の中心を担う一方、多くのアレルギー疾患の発症や病態形成に関与している。かつては1型Th細胞(Th1)と2型Th細胞(Th2)の不均衡がアレルギー疾患をはじめとする慢性炎症疾患の発症メカニズムとして理解されてきた。しかし近年、Th細胞が多様なサブセットと可塑性を有することが明らかになるにあたり、古典的なTh1/Th2バランス破綻モデルではアレルギー疾患の発症機序を十分説明することができないことがわかってきた。では、Th細胞はどのように働き、アレルギーに関与するのだろうか。筆者らは病原性の高いTh細胞がアレルギー疾患の発症に深く関与するという「病原性Th細胞(Tpath)疾患誘導モデル」を提唱した。(著者抄録)

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(公社)日本医学放射線学会  

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Language：Japanese   Publisher：(株)医学書院  

＜文献概要＞Point ・肺外非結核性抗酸菌(NTM)症は,限局型と播種型(全身型)から成り,好発部位は皮膚やリンパ節,骨などである.・限局型は,宿主要因に関係なく発症し,外科的切除などの局所治療で治癒することがある.・播種型は,宿主要因を背景に発症し,抗菌薬治療だけでは不十分なこともある.

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Other Link： https://search-tp.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2018&ichushi_jid=J06862&link_issn=&doc_id=20181025210023&doc_link_id=10.11477%2Fmf.1437200202&url=https%3A%2F%2Fdoi.org%2F10.11477%2Fmf.1437200202&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：(一社)日本感染症学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本CT検診学会  

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Language：English   Publishing type：Research paper, summary (international conference)   Publisher：AMER THORACIC SOC  

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Language：Japanese   Publisher：(一社)日本結核病学会  

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

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Language：Japanese   Publisher：(株)へるす出版  

症例は9歳男児で、そり遊び中用水路に落ち、泥水に顔をつけて倒れ、母親に発見され人工呼吸で自発呼吸は再開し救急搬送された。血液検査で異常はなく、X線で両側肺門中心の透過性低下を認め、CTでは両側上肺優位に気管支周囲のスリガラス影、斑状影が認められた。その後意識レベルの低下で気管挿管し人工呼吸管理でICU入室した。肺炎合併を考慮し抗菌薬投与を開始した。入室30時間後に呼気CO2分圧の急激な上昇で酸素化不良となり、X線で両側肺門陰影の増強と右下肺野の浸潤影を認め、呼吸状態悪化で高頻度振動換気を導入するも心停止となり、カプノモニター波形が末梢気道閉塞パターンを示した。心拍再開後気管支拡張薬を投与したが2回目の心停止となり、経皮的心肺補助を導入した。挿管チューブから泡沫状分泌物が増加し、血管内脱水徴候が続き、大量輸液、アルブミン剤投与を行うもICU入室48時間後に死亡した。喀痰培養でAeromonas hydrophilaが検出された。

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Language：Japanese   Publisher：新潟市民病院  

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Language：Japanese   Publisher：新潟市民病院  

症例は突然死と肥大型心筋症の家族歴がある45歳の男性。8年前に閉塞性肥大型心筋症と診断された。薬物治療(β遮断薬、カルシウム拮抗薬、抗不整脈薬Ia群)が行われたが、左室流出路圧較差及び労作時息切れの改善は認められなかった。今回、心房細動から心室細動になり、自動体外式除細動器で蘇生された。心臓カテーテル検査で左室流出路圧較差が130mmHgあり、ICD(implantable cardioverter defibrillator)植え込みを行った後に経皮的心筋中隔焼灼術(percutaneous transluminal septal myocardial ablation:PTSMA)を施行され、左室流出路圧較差は110mmHgから26mmHgへ改善した。その後息切れ等なく経過し、6ヵ月後の心臓カテーテル検査で左室流出路圧較差を認められなかった。本症例はPTSMAが奏効した経過良好な症例である。また、PTSMAを施行した後であっても頻脈性不整脈による心停止のリスクはあると報告されており、閉塞性肥大型心筋症で心停止をきたした症例に対してはPTSMAに加えてICDを植え込む必要があると考える。(著者抄録)

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Language：Japanese   Publisher：東北救急医学会  

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