The influence of the Great East Japan earthquake on microscopic polyangiitis: A retrospective observational study

Takeuchi, Yoichi; Saito, Ayako; Ojima, Yoshie; Kagaya, Saeko; Fukami, Hirotaka; Sato, Hiroyuki; Matsuda, Ken; Nagasawa, Tasuku

doi:10.1371/journal.pone.0177482

Cited by 21 publications

(10 citation statements)

References 33 publications

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“…An association between silica exposure and MPO-AAV has been consistently observed 24,25 . The high prevalence of silica in the natural environment (for example, in cement) is one proposed explanation for the apparent upsurge in AAV incidence following major earthquakes in 1995 and 2011 in Japan 26,27 . However, this correlation was not replicated in the aftermath of the 2011 earthquake in Christchurch, New Zealand 28 , a discordance that highlights the potential importance of AAV gene-environment interactions.…”

Section: Risk Factors and Disease Determinantsmentioning

confidence: 99%

ANCA-associated vasculitis

Kitching

Anders

Basu

et al. 2020

Nat Rev Dis Primers

632

507

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The anti-neutrophil cytoplasmic antibody (ANCA)associated vasculitides (AAVs) are diseases characterized by inflammation of blood vessels, endothelial injury and tissue damage. The three types of small-vessel vasculitis, namely granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA) and eosinophilic GPA (EGPA; previously known as Churg-Strauss syndrome), feature a loss of tolerance to neutrophil primary granule proteins, most often leukocyte proteinase 3 (PR3; also known as myeloblastin) or myeloperoxidase (MPO) (Table 1). The vessels involved in AAV are typically capillaries, arterioles and venules but small arteries and veins may also be affected. Autoimmunity is documented clinically by serum ANCAs to PR3 (PR3-ANCA) or MPO (MPO-ANCA), which are generally associated with the main syndromic AAV presentations (box 1). AAVs collectively represent one of several types of autoimmune vasculitis (Fig. 1). GPA and MPA can involve small blood vessels in any organ or tissue but commonly affect the upper and lower respiratory tract and the kidneys (box 2). Patients with AAV typically present with severe organ-threatening or life-threatening disease, although less severe presentations also occur. GPA is predominantly associated with PR3-ANCA and its clinical features typically include sinonasal disease, lower respiratory tract involvement with pulmonary haemorrhage and granulomatous inflammation, and glomerulonephritis. MPA is usually associated with MPO-ANCA and clinical features include more severe renal disease and some of the manifestations of GPA but without granulomatous inflammation. EGPA is characterized by asthma, eosinophilia and, in many (but not all) cases, vasculitis. EGPA is less common than GPA or MPA and, in some cases, is associated with ANCAs, mainly MPO-ANCA (Table 1). Although categorized as a form of AAV, EGPA has less overlap with the other AAVs than that between GPA and MPA with regard to its genetic, pathogenetic, and clinical features and its management and is typically considered a separate entity. Improvements in treatment and prognosis for patients with AAV have resulted from the translation of both preclinical and clinical research findings. Here, we provide an updated overview of the clinical and

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Section: Risk Factors and Disease Determinantsmentioning

confidence: 99%

ANCA-associated vasculitis

Kitching

Anders

Basu

et al. 2020

Nat Rev Dis Primers

632

507

View full text Add to dashboard Cite

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“…These observations suggest that silica dust in the air, caused by the massive destruction and subsequent reconstruction of the cities 22 and by the marine sludge and sediments deposited in the subsequent tsunami disaster, 23 might have affected the presentation of AAV, especially its respiratory manifestations such as pulmonary haemorrhage and interstitial pneumonitis. However, in a contrasting study, no difference in the incidence of AAV was observed before versus after the February 2011 earthquake in Christchurch, New Zealand.…”

Section: [H2] Environmental Factorsmentioning

confidence: 99%

“…20 Although the association of silica with AAV has been intensely debated, a systematic review and meta-analysis confirmed the association between silica dust exposure and development of AAV. 21 Moreover, morbidity and disease severity increased substantially in patients with AAV after the great earthquakes in Japan (Hanshin-Awaji in 1995 22 and East Japan in 2011 23 ).…”

Section: [H2] Environmental Factorsmentioning

confidence: 99%

Pathogenesis and therapeutic interventions for ANCA-associated vasculitis

et al. 2018

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Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a vasculitis that affects systemic small vessels, accompanied by the presence of ANCAs in the serum. This disease entity includes microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis and drug-induced AAV. Similar to other autoimmune diseases, AAV develops in patients with a predisposing genetic background who have been exposed to causative environmental factors. The mechanism by which ANCAs cause vasculitis involves ANCA-mediated excessive activation of neutrophils that subsequently release inflammatory cytokines, reactive oxygen species and lytic enzymes. In addition, this excessive activation of neutrophils by ANCAs induces formation of neutrophil extracellular traps (NETs). Although NETs are essential elements in the innate immunity, excessive NET formation is harmful to small vessels. Moreover, NETs are involved not only in ANCA-mediated vascular injury but also in the production of ANCAs themselves. Therefore, a vicious cycle of NET formation and ANCA production is considered to be involved in the pathogenesis of AAV.

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“…Takeuchi et al. showed evacuation of silica influenced by the development of ANCA-associated vasculitis after the Great East Japan earthquake 15 . Although the causes of vasculitis are largely unknown, CCR8-mediated allergic stimuli could be part of the pathogenesis in pauci-immune types of vasculitis.…”

Section: Discussionmentioning

confidence: 99%

Chemokine Receptor 8 Can Distinguish Antineutrophil Cytoplasmic Antibody–Associated Vasculitis From Infectious Complications

Sanada

Akiyama

Sato

et al. 2019

Kidney International Reports

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Introduction Diagnosing vasculitis is frequently difficult because its clinical symptoms are similar to those of common infectious diseases and other inflammatory disorders. This study focused on chemokine receptor 8 (CCR8) in peripheral blood mononuclear cells to find a new biomarker that distinguishes vasculitis from infectious complications. Methods A cross-sectional study was conducted among 113 patients with systemic vasculitis who were referred to Japan Health Care Organization Sendai Hospital from 2014 to 2016, including those with antineutrophil cytoplasmic antibody (ANCA)−associated vasculitis, anti−glomerular basement membrane disease, lupus nephritis, and Henoch-Schonlein purpura. Peripheral blood mononuclear cells were extracted from blood, and CCR8 expression was examined by real time polymerase chain reaction and flow cytometry. Results CCR8 gene expression was significantly higher in patients with ANCA-associated vasculitis, which was confirmed by upregulated CCR8 protein expression in flow cytometry ( P < 0.001 and P = 0.01, respectively). Neither lupus nephritis nor Henoch-Schonlein purpura showed upregulated CCR8. Elevated CCR8 in the active phase decreased significantly in remission ( P = 0.002), which was correlated with decreased serum inflammatory markers. Despite elevated serological inflammatory markers, the CCR8 levels at the time of infection, including bacterial, viral, and fungal, did not increase, indicating that infectious complications did not affect CCR8 expression ( P = 0.02). Conclusion CCR8 in peripheral blood mononuclear cells may be a useful diagnostic marker for ANCA-associated vasculitis to differentiate between active vasculitis and infectious inflammation.

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The influence of the Great East Japan earthquake on microscopic polyangiitis: A retrospective observational study

Cited by 21 publications

References 33 publications

ANCA-associated vasculitis

ANCA-associated vasculitis

Pathogenesis and therapeutic interventions for ANCA-associated vasculitis

Chemokine Receptor 8 Can Distinguish Antineutrophil Cytoplasmic Antibody–Associated Vasculitis From Infectious Complications

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