Relevant bibliographies by topics / Anti-neutrophil cytoplasm antibody

Academic literature on the topic 'Anti-neutrophil cytoplasm antibody'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Anti-neutrophil cytoplasm antibody"

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Hewins, Peter, and Caroline Savage. "Anti-neutrophil cytoplasm antibody associated vasculitis." International Journal of Biochemistry & Cell Biology 35, no. 3 (March 2003): 277–82. http://dx.doi.org/10.1016/s1357-2725(02)00094-8.

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Holle, J. U. "ANCA („anti-neutrophil cytoplasm antibody“)-assoziierte Vaskulitiden." Zeitschrift für Rheumatologie 72, no. 5 (June 2013): 445–56. http://dx.doi.org/10.1007/s00393-013-1211-0.

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NAGASAWA, TOSHIHIKO. "Anti-blood neutrophil cytoplasm antibody (ANCA) and glomerulonephritis." Nihon Naika Gakkai Zasshi 83, no. 12 (1994): 2173–78. http://dx.doi.org/10.2169/naika.83.2173.

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Salama, A. D., and A. J. Rees. "Autoantibodies in anti-neutrophil cytoplasm antibody-associated vasculitis." Nephrology Dialysis Transplantation 29, no. 6 (January 23, 2014): 1105–7. http://dx.doi.org/10.1093/ndt/gft526.

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Ferraro, Alastair J., Basma Hassan, and Caroline O. Savage. "Pathogenic mechanisms of anti-neutrophil cytoplasm antibody-associated vasculitis." Expert Review of Clinical Immunology 3, no. 4 (July 2007): 543–55. http://dx.doi.org/10.1586/1744666x.3.4.543.

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Salama, Alan D. "Relapse in Anti-Neutrophil Cytoplasm Antibody (ANCA)–Associated Vasculitis." Kidney International Reports 5, no. 1 (January 2020): 7–12. http://dx.doi.org/10.1016/j.ekir.2019.10.005.

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7

McAdoo, S. P., C. Densem, A. Salama, and C. D. Pusey. "Bacterial endocarditis associated with proteinase 3 anti-neutrophil cytoplasm antibody." Clinical Kidney Journal 4, no. 3 (April 2, 2011): 208–10. http://dx.doi.org/10.1093/ndtplus/sfr030.

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YOSHIDA, Masaharu, Motoaki SAITO, and Toshihiko NAGASAWA. "Studies on anti-neutrophil cytoplasm antibody(ANCA) in Wegener's granulomatosis." Nihon Naika Gakkai Zasshi 78, no. 11 (1989): 1581–85. http://dx.doi.org/10.2169/naika.78.1581.

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Jones, Rachel B. "Rituximab in the Treatment of Anti-Neutrophil Cytoplasm Antibody-Associated Vasculitis." Nephron Clinical Practice 128, no. 3-4 (November 14, 2014): 243–49. http://dx.doi.org/10.1159/000368580.

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Chapman, Gavin B., Andrew E. Leitch, Rashmi Lahiri, Peter Reid, and Neeraj Dhaun. "Strawberry carina as a presentation of anti-neutrophil cytoplasm antibody–associated vasculitis." Rheumatology 61, no. 3 (October 20, 2021): e59-e61. http://dx.doi.org/10.1093/rheumatology/keab783.

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Dissertations / Theses on the topic "Anti-neutrophil cytoplasm antibody"

1

Pankhurst, Tanya. "Heterogeneity of injury in vasculitis : influence of anti neutrophil cytoplasm antibody IgG subclass and endothelial susceptibility." Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/718/.

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This study examined IgG subclass in ANCA associated vasculitis and glomerular endothelial cell (GEC) phenotype predisposes to injury. Using the flow model, interaction of neutrophils with normal immunoglobulin subclasses was compared to interaction with subclasses of ANCA IgG. Neutrophils were captured by normal IgG3>IgG1>IgG2/IgG4. Blockade of CD32 affected IgG3, CD16, IgG1/2. Neutrophils exposed to soluble ANCA IgG1/3 adhered to cytokine-activated endothelial cells, as did IgG4, not previously thought to bind constitutively expressed CD16/CD32. Fc blockade reduced binding. GEC were compared with human umbilical vein endothelial cells. Surface VCAM-1 was reduced on GEC and GEC demonstrated reduced leukocyte capture. RNA array analysis demonstrated a reduction in the GEC gene responsible for post translational modification of VCAM-1 to a sialoglycoprotein. VCAM-1 expression by GEC may be a protective mechanism to reduce inflammatory responses, potentially disrupted in disease. ANCA subclass and endothelial phenotype are important vasculitis pathogenesis: this may be useful in designing targeted therapy reducing overall immunsuppressive load. Additionally modification of specific adhesion molecule profiles on endothelial cells may enable alteration of conditions of one vascular bed whilst reducing impact on unaffected sites.
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Durant, Stéphanie. "Etude moléculaire et fonctionnelle de la protéinase 3 du neutrophile, cible des ANCA : implications physiopathologiques dans les vascularites." Paris 6, 2003. http://www.theses.fr/2003PA066526.

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李瑞山 and Shui-shan Lee. "Anti-neutrophil cytoplasmic antibody: a clinical & experimental study." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1993. http://hub.hku.hk/bib/B31981513.

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Lee, Shui-shan. "Anti-neutrophil cytoplasmic antibody : a clinical & experimental study /." [Hong Kong : University of Hong Kong], 1993. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13762679.

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Rajp, Amit. "The immunogenetics of anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis." Thesis, University of Birmingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273729.

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6

Bansi, Devinder Singh. "Immunologyical mechanisms in primary primary sclerosing cholangitis : the role of the anti-neutrophil cytoplasmic antibody." Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242304.

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Govender, Ramona. "Anti-neutrophil cytoplasmic antibody (ANCA) testing at Groote Schuur Hospital: Adherence to indications for testing." Master's thesis, Faculty of Health Sciences, 2021. http://hdl.handle.net/11427/33700.

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Appropriate use of laboratory investigations is increasingly important in resource-constrained environments. We receive the anti-neutrophil cytoplasmic antibody (ANCA) testing practices in a tertiary hospital in South Africa.
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Basu, Neil. "The characterisation and determinants of quality of life in ANCA associated vasculitis." Thesis, University of Aberdeen, 2012. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=189406.

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Background: The enhancement of quality of life (QOL) is a principal health care objective. Surprisingly, few studies have investigated this outcome in ANCA associated vasculitis (AAV), a complex chronic disease. Existing studies have, however, identified fatigue as a specific problem amongst this population. Although its aetiology is unknown, there is evidence, from other populations, to support a neural basis for this symptom. Aims: This study aimed to characterise QOL and its determinants amongst patients with AAV. A secondary study examined the association of AAV related fatigue with alterations of the brain. Methods: An AAV case-control study was conducted, incorporating a comparison and within-case analysis, using two groups of population and chronic disease controls. All participants completed a questionnaire comprising measures of QOL and putative determinants of QOL impairment. Concurrently, putative clinical determinants were collected from cases. The secondary study recruited AAV cases based on fatigue status. A further group with idiopathic fatigue was recruited from the general population. All subjects underwent magnetic resonance (MR) brain scanning incorporating structural and physiological imaging. Results: Compared to population controls, cases were substantially more likely to report low QOL and levels were equable to disease controls. Potentially modifiable biological and psycho-social factors were independently associated with poor QOL, of which fatigue was found to be of principal importance. In the secondary study, structural and physiological differences were observed between AAV patients with and without fatigue, as well as fatigued population subjects. Conclusions: AAV patients experienced significant QOL impairment. A bio-psychosocial approach to AAV health care is likely to improve QOL outcomes, although a better understanding of specific mechanisms is necessary to fully manage these problems. MR techniques have suggested a neural basis for AAV related fatigue. In the future they may help delineate the mechanisms of fatigue and consequently improve QOL in AAV.
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Bensalem, Amina. "Pharmacocinétique et relation dose-concentration-effet du rituximab dans la polyartrite rhumatoïde et les vascularités associées aux anticorps anti-cytoplasme des neutrophiles." Thesis, Tours, 2019. http://www.theses.fr/2019TOUR3302.

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Le rituximab est un anticorps monoclonal (AcMo) IgG1 chimérique qui cible le CD20, une protéine présente à la surface de la plupart des lymphocytes B. Il est indiqué dans la polyarthrite rhumatoïde (PR) et est utilisé dans les vascularites associées aux anticorps (ANCA) anti-cytoplasme des neutrophiles (AAV). Il existe une grande variabilité interindividuelle de la pharmacocinétique (PK) du rituximab et de sa relation concentration-réponse. Le rituximab se lie au CD20, et les complexes rituximab-CD20 formés sont éliminés par le système immunitaire. L’élimination médiée par la cible n'a jamais été décrite dans les maladies inflammatoires auto-immunes. Ce travail de thèse visait à étudier la PK et la relation concentration-réponse du rituximab par modélisation PK et pharmacocinétique-pharmacodynamique (PK-PD) de population. Ces travaux ont été réalisés grâce à : - 52 patients atteints de PR, suivis dans le Service de rhumatologie du CHRU de Tours, où les concentrations de rituximab, la numération CD4+ et le score d'activité de la maladie sur 28 articulations (DAS28) ont été mesurés. - 92 patients de l'essai RAVE, où les concentrations de rituximab, d'anticorps anti-protéinase 3 (PR3-ANCA) et d’anti-myéloperoxydase (MPO-ANCA) ont été mesurées. Chez les patients atteints de PR, la PK du rituximab a été décrite à l'aide d'un modèle à bicompartimental. Aucune élimination médiée par la cible n'a été détectée. Cela peut être dû à (i) une faible quantité d'antigène-cible par rapport à l’oncologie, et/ou (ii) à des données de PK peu denses. Chez les patients atteints d’AAV, une élimination non-linéaire médiée par la cible a été détectée au début du suivi. Un modèle TMDD simplifié a été utilisé, où le rituximab se fixait de façon irréversible sur le CD20, modélisé en tant que variable «latente». La variable latente peut être en partie interprétée comme la fraction de CD20 (circulante ou exprimée sur la membrane des cellules B) et disponible pour la liaison au rituximab. L'élimination médiée par la cible, négligeable, à la fin du suivi dans les AAV, peut être due aux numérations de cellules B faibles à la fin du suivi. La relation quantitative entre la déplétion des cellules B du sang, des cellules immunitaires, et la réponse clinique reste floue, aussi bien dans la PR que dans les AAV. De plus, cette relation, très variable selon les patients, n’a jamais été quantifiée à l’aide de la modélisation PK-PD. - Dans la PR, les relations entre les concentrations de rituximab et les numérations CD19+, entre les numérations CD19+ et CD4+, et entre les numérations CD4+ et le DAS28 ont respectivement été décrites à l'aide de modèles de durée de vie cellulaire « cell lifespan », de réponse indirecte et directs (Emax). Cette étude a montré que (i) l’amplitude de la déplétion CD19+ n’était pas associée à une déplétion CD4+ ou à une diminution du DAS28, et (ii) que la diminution du DAS28 était doublée en présence de déplétion des CD4+ comparé à son absence, et (iii) des concentrations plus élevées de rituximab étaient liées à une meilleure réponse clinique. - Dans les AAV, la relation entre les concentrations de rituximab et les niveaux d'ANCA a été décrite à l'aide d'un modèle de transit semi-mécanistique avec rétrocontrôle négatif. Ce modèle a montré que (i) la diminution des niveaux d'ANCA induite par le rituximab était profonde mais retardée et plus soutenue chez les patients avec MPO-ANCA que chez ceux avec PR3-ANCA, et (ii) des concentrations plus élevées de rituximab étaient associées à une diminution plus importante des niveaux d'ANCA. Des administrations répétées de rituximab seraient susceptibles d’améliorer la réponse clinique au rituximab et diminuer le risque de rechute. En conclusion, ce travail a été le premier à montrer une PK non linéaire du rituximab dans une maladie auto-immune (AAV), et à quantifier la relation complexe entre la déplétion des cellules B induite par le rituximab, la diminution des CD4+, et son efficacité clinique
Rituximab is a chimeric IgG1 monoclonal antibody (mAb) that targets CD20, a protein on the surface of most B lymphocytes. It is approved as a second line treatment in rheumatoid arthritis (RA) patients, and is used in anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). There is a large interindividual variability in rituximab pharmacokinetics (PK), and its concentration–response relationship. Rituximab binds to CD20 with high affinity and specificity and form mAb-target complexes which are eliminated by immune system. This elimination is usually described using target-mediated drug disposition (TMDD) models. For rituximab, TMDD was never reported in autoimmune inflammatory diseases, as RA or AAV. This PhD work aimed at studying the variability of PK and cconcentration-response relationship of rituximab using population PK and pharmacokinetic-pharmacodynamic (PK-PD) modeling. This work was done using data from : - 52 RA patients of the rheumatology department of Tours University Hospital, where rituximab concentrations, CD4+ counts (biomarker) and disease activity score in 28 joints (DAS28, clinical response) were measured. - 92 AAV patients included in the RAVE trial (Rituximab for AAV), where rituximab concentrations, antibodies to proteinase 3 (PR3-ANCA), and antibodies to myeloperoxidase (MPO-ANCA) (biomarkers) were measured. In RA patients, rituximab PK was described using a two-compartment model with linear (endogenous) elimination. No target-elimination of rituximab or influence of B-cell count was detected. This may be due to (i) a low amount of target antigen compared to B-cell neoplasia, and/or (ii) insufficiently dense PK data. In AAV patients, nonlinear target-mediated elimination was detected at the beginning of the follow-up. A simplified TMDD model was used, where target was modeled as a latent variable, and irreversible binding to rituximab on its target was assumed. Latent variable may be partly interpreted as the fraction of CD20 (circulating or present at the B-cell membrane) available for rituximab binding. The negligible target-mediated elimination towards the end of the follow-up in RA and AAV may be due to the sustained B-cell depletion after rituximab treatment. Rituximab-induced B cell depletion was shown to alter count and function of other immune cells. However, quantitative relationship between depletion of blood B cells, immune cells, and clinical response in both RA and AAV remain unclear. In addition, this relationship, highly variable among patients, was never quantified using PK-PD modeling. In RA patients, the relationship between rituximab concentrations and CD19+ counts, between CD19+ and CD4+ counts, and between CD4+ counts and DAS28 (clinical activity score in RA) was described using cell lifespan, indirect response and direct Emax models, respectively. This study showed that (i) the amplitude of CD19+ count depletion was not associated with CD4+ decrease or DAS28, and (ii) CD4+ decrease leads to two-fold DAS28 decrease compared to no CD4+ decrease, and (iii) higher rituximab concentrations were related to a better clinical improvement. In AAV patients, the relationship between rituximab concentrations and ANCA levels was described using a semi-mechanistic transit model with negative feedback. This model showed that (i) rituximab-induced decrease of ANCA levels was deep but delayed, and more sustained in patients with MPO-ANCA than in those with PR3-ANCA, and (ii) higher rituximab concentrations were associated with deeper decrease of ANCA levels. Moreover, repeated rituximab courses may improve clinical response to rituximab, and increase the time to disease relapse. Overall, this work was the first to report nonlinear PK of rituximab in autoimmune disease (AAV), and to quantify the complex relationship between rituximab-induced B-cell depletion, CD4+ decrease, and the clinical response
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Tieu, Joanna. "Optimising Management in ANCA-Associated Vasculitis." Thesis, 2021. https://hdl.handle.net/2440/135593.

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From early descriptions of vasculitis to our currently understanding of the vasculitides, there has been continual evolution of the concepts on pathogenesis, classification, management and the impacts on patients. This is a thesis by publication, with an overarching aim of optimising therapy in anti-neutrophil cytoplasm antibody (ANCA)- associated vasculitis (AAV). The first chapter provides an overarching background for the subsequent chapters, providing an historical perspective on disease, disease manifestations including AAV subgroups and some of the impacts of AAV to patients. Chapter 2 provides insights into the impacts of AAV in Australia. Using data-linkage of WA hospitalisation, emergency department and death registry data, mortality including cause of death in patients with AAV and polyarteritis nodosa (PAN) were compared against the general population and controls. Data-linkage of WA hospitalisation and cancer registry data enabled analysis of cancer rates in patients with AAV/PAN compared with the general population. Chapters 3 and 4 examines the use of rituximab in AAV in the United Kingdom. Chapter 3 includes a literature review examining the evidence for use of rituximab in the maintenance of remission in AAV, and the results of a Delphi exercise conducted to develop consensus guidelines on the use of rituximab for the maintenance of remission in AAV. Chapter 4 examines the longer-term outcomes of patients who have develop rituximab associated hypogammaglobulinaemia in a quaternary referral centre. Chapter 5 examines the health-related quality of life (HRQoL) of patients with a relapse of AAV amongst patients in the multi-centre RITAZAREM study. This presents an unpublished manuscript examining the HRQoL of these patients during the induction phase of this study and compares the HRQoL in patients who received two different glucocorticoid regimens for induction of remission. Finally, chapter 6 provides a discussion on the thesis and directions for future research.
Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2022
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Books on the topic "Anti-neutrophil cytoplasm antibody"

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Sinico, Renato Alberto, and Loïc Guillevin, eds. Anti-Neutrophil Cytoplasmic Antibody (ANCA) Associated Vasculitis. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-02239-6.

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Rajp, Amit. The immunogenetics of anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis. Birmingham: University of Birmingham, 2002.

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Guillevin, Loïc, and Renato Alberto Sinico. Anti-Neutrophil Cytoplasmic Antibody Associated Vasculitis. Springer, 2019.

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Gross, Wolfgang L., and Julia U. Holle. Clinical features of ANCA-associated vasculitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0131.

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The primary ANCA-associated vasculitides are granulomatosis with polyangiitis (Wegener's, GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA, Churg-Strauss syndrome, CSS). They predominantly affect small (and medium-sized) vessels and share a variable association with ANCA (anti-neutrophil cytoplasm antibody) directed against neutrophil proteinase 3 (PR3, mainly in GPA) and myeloperoxidase (MPO, mainly in MPA and CSS). Crescentic necrotizing glomerulonephritis and alveolar haemorrhage due to pulmonary capillaritis represent classical (vasculitic) organ manifestations of the ANCA-associated vasculitides (AAV). MPA occurs as a 'pure' small (to medium-size) vessel vasculitis, whereas GPA and CSS are characterized by additional distinct clinical and pathological features. In GPA, granulomatous lesions of the upper and/or lower respiratory tract are a hallmark of the disease. Granulomatous lesions may be large in appearance and occur as space-consuming, infiltrating, and destructive inflammatory masses. GPA is believed to follow a stagewise course with an initial localized form, restricted granulomatous lesions of the upper and/or lower respiratory tract without clinical signs of vasculitis, and a consecutive generalization to systemic vasculitis which may be either non-organ-threatening (early systemic) or organ- and life- threatening (generalized GPA). Rarely, patients arrest in the localized stage and do not progress to systemic disease. In EGPA asthma, hypereosinophilia and eosinophilic organ infiltration (e.g. eosinophilic myocarditis) are typical features of the disease apart from vasculitis. Similarly to GPA, EGPA follows a stagewise course: asthma and eosinophilia may precede full-blown disease for several months or years. Recent cohort studies suggest different phenotypes in EGPA (predominantly vasculitic and MPO-ANCA-positive and predominantly with eosinophilic organ infiltration, usually ANCA-negative). This chapter focuses on the clinical features of the primary AAV and their outcome.
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Foster, Helen, and Paul A. Brogan, eds. Systemic diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199592630.003.0004.

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VasculitisThe classification of paediatric vasculitis 168The epidemiology of paediatric vasculitis 171The investigation of primary systemic vasculitis 172The standard treatment of childhood vasculitis 174Henoch–Schönlein purpura 179Kawasaki disease 183The anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides 188Polyarteritis nodosa (PAN) 192Cutaneous polyarteritis nodosa (cPAN) ...
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Jayne, David. Treatment of ANCA-associated vasculitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0132.

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The goals of treatment in anti-neutrophil cytoplasm antibody (ANCA) vasculitis are to stop vasculitic activity, to prevent vasculitis returning, and to address longer-term comorbidities caused by tissue damage, drug toxicity, and increased cardiovascular and malignancy risk. Cyclophosphamide and high-dose glucocorticoids remain the standard induction therapy with alternative immunosuppressives, such as methotrexate or azathioprine, to prevent relapse. Refractory disease resulting from a failure of induction or remission maintenance therapy requires alternative agents and rituximab has been particularly effective. Replacement of cyclophosphamide by rituximab for remission induction is supported by recent evidence. Additional therapy with intravenous methylprednisolone and plasma exchange is employed in severe presentations with failing vital organ function. Drug toxicity contributes to comorbidity and mortality and has led to newer regimens with reduced cyclophosphamide exposure. Glucocorticoid toxicity remains a major problem, with controversy over the rapidity with which glucocorticoids can be reduced or withdrawn. Disease relapse occurs in 50% and requires early detection at a stage when it will not adversely affect outcomes. Rates of cardiovascular disease and malignancy are higher than in control populations but strategies to reduce their risk, apart from cyclophosphamide-sparing regimens, have not been developed. Thromboembolic events occur in 10% and may be linked to the recently identified autoantibodies to plasminogen and tissue plasminogen activator. Outcomes of vasculitis depend heavily on the level of tissue damage at diagnosis, especially renal dysfunction, but are also influenced by patient age, ANCA subtype, disease extent, and response to therapy. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)is treated along similar principles to granulomatosis with polyangiitis (GPA) and microscopic polyangiitis but the persistence of steroid-dependent asthma in over one-third and differences in pathogenesis has suggested alternative treatment approaches. Chronic morbidity results from tissue damage and is especially common in the upper and lower respiratory tract and kidneys. Tracheobronchial disease is a severe late complication of GPA, while deafness, nasal obstruction, and chronic sinusitis are sequelae of nasal and ear vasculitis. Chronic infection of damaged epithelial surfaces acts as a drive for vasculitic activity and adequate infection control is necessary for stable remission. Chronic kidney disease can stabilize for many years but the risks of endstage renal disease (ESRD) are increased by acute kidney injury at presentation or renal relapse. Renal transplantation is successful, with similar outcomes to other causes of ESRD.
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Tombetti, Enrico, and Justin C. Mason. Pathophysiology of vasculitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0017.

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Vasculitis represents a spectrum of disorders that are often divided on the basis of the predominant vessel size affected into large-, medium- and small-vessel vasculitides. This chapter will focus on the pathogenesis of the anti-neutrophil cytoplasmic antibody (ANCA)-associated medium- and small-vessel vasculitides (AAV), and large-vessel vasculitis, Takayasu arteritis, and giant cell arteritis. Underlying pathogenic mechanisms in vasculitis remain to be fully understood. In particular, the initiating event(s) are not known. A combination of infectious or other environmental triggers on a susceptible genetic background is currently favoured. In addition to the vessel size affected, the mechanisms of vascular injury vary. Moreover, extravascular granulomatosis may play an important role in disease manifestations. The innate and adaptive immune systems contribute to its pathogenesis. Although pathogenic antibodies have not been identified in large-vessel vasculitis, ANCA are directly implicated in small- and medium-vessel AAV. Disease manifestations are varied and diverse and may include arterial stenosis or aneurysms, glomerulonephritis and renal failure, gastro-intestinal, pulmonary, cutaneous, and neurological complications, visual disturbance, deafness, and nasal bridge collapse. Life-threatening cardiovascular disease is also seen, with myocarditis, pericarditis, valvular heart disease, thrombosis, systemic and pulmonary arterial hypertension, and accelerated coronary heart disease all reported. Despite this, the prognosis for patients with vasculitis has improved significantly in recent decades. Further understanding of the pathogenesis of vasculitis will lead to the discovery of further therapeutic targets and novel, safer biologic therapies.
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Book chapters on the topic "Anti-neutrophil cytoplasm antibody"

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Selvakumar, Vijayalakshmi, Thenmozhi Manivel, Ramachandran Chelliah, Kaliyan Barathikannan, Akanksha Tyagi, Xiuqin Chen, Umair Shabbir, et al. "Microorganisms in Pathogenesis and Management of Anti-Neutrophil Cytoplasmic Antibody (ANCA)-Associated Vasculitis." In Role of Microorganisms in Pathogenesis and Management of Autoimmune Diseases, 311–39. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-4800-8_16.

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Boomsma, Maarten M., Coen A. Stegeman, Cees G. M. Kallenberg, and Jan W. Cohen Tervaert. "Prevention of relapsing disease in anti-neutrophil cytoplasmic antibody related necrotizing small-vessel vasculitis: the role for autoantibody guided and anti-bacterial treatment." In Disease-modifying Therapy in Vasculitides, 181–99. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8235-4_10.

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Gross, Wolfgang L., and Julia U. Holle. "Clinical features of ANCA-associated vasculitis." In Oxford Textbook of Rheumatology, 1090–102. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0131_update_001.

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The primary ANCA-associated vasculitides are granulomatosis with polyangiitis (Wegener’s, GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA, Churg-Strauss syndrome, CSS). They predominantly affect small (and medium-sized) vessels and share a variable association with ANCA (anti-neutrophil cytoplasm antibody) directed against neutrophil proteinase 3 (PR3, mainly in GPA) and myeloperoxidase (MPO, mainly in MPA and CSS). Crescentic necrotizing glomerulonephritis and alveolar haemorrhage due to pulmonary capillaritis represent classical (vasculitic) organ manifestations of the ANCA-associated vasculitides (AAV). MPA occurs as a ’pure’ small (to medium-size) vessel vasculitis, whereas GPA and CSS are characterized by additional distinct clinical and pathological features. In GPA, granulomatous lesions of the upper and/or lower respiratory tract are a hallmark of the disease. Granulomatous lesions may be large in appearance and occur as space-consuming, infiltrating, and destructive inflammatory masses. GPA is believed to follow a stagewise course with an initial localized form, restricted granulomatous lesions of the upper and/or lower respiratory tract without clinical signs of vasculitis, and a consecutive generalization to systemic vasculitis which may be either non-organ-threatening (early systemic) or organ- and life- threatening (generalized GPA). Rarely, patients arrest in the localized stage and do not progress to systemic disease. In EGPA asthma, hypereosinophilia and eosinophilic organ infiltration (e.g. eosinophilic myocarditis) are typical features of the disease apart from vasculitis. Similarly to GPA, EGPA follows a stagewise course: asthma and eosinophilia may precede full-blown disease for several months or years. Recent cohort studies suggest different phenotypes in EGPA (predominantly vasculitic and MPO-ANCA-positive and predominantly with eosinophilic organ infiltration, usually ANCA-negative). This chapter focuses on the clinical features of the primary AAV and their outcome.
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4

Chung, Sharon, and Paul A. Monach. "Anti-neutrophil Cytoplasmic Antibody–Associated Vasculitis." In Kelley and Firestein's Textbook of Rheumatology, 1541–58. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-323-31696-5.00089-9.

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Jayne, David. "Treatment of ANCA-associated vasculitis." In Oxford Textbook of Rheumatology, 1103–12. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0132_update_001.

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The goals of treatment in anti-neutrophil cytoplasm antibody (ANCA) vasculitis are to stop vasculitic activity, to prevent vasculitis returning, and to address longer-term comorbidities caused by tissue damage, drug toxicity, and increased cardiovascular and malignancy risk. Cyclophosphamide and high-dose glucocorticoids remain the standard induction therapy with alternative immunosuppressives, such as methotrexate or azathioprine, to prevent relapse. Refractory disease resulting from a failure of induction or remission maintenance therapy requires alternative agents and rituximab has been particularly effective. Replacement of cyclophosphamide by rituximab for remission induction is supported by recent evidence. Additional therapy with intravenous methylprednisolone and plasma exchange is employed in severe presentations with failing vital organ function. Drug toxicity contributes to comorbidity and mortality and has led to newer regimens with reduced cyclophosphamide exposure. Glucocorticoid toxicity remains a major problem, with controversy over the rapidity with which glucocorticoids can be reduced or withdrawn. Disease relapse occurs in 50% and requires early detection at a stage when it will not adversely affect outcomes. Rates of cardiovascular disease and malignancy are higher than in control populations but strategies to reduce their risk, apart from cyclophosphamide-sparing regimens, have not been developed. Thromboembolic events occur in 10% and may be linked to the recently identified autoantibodies to plasminogen and tissue plasminogen activator. Outcomes of vasculitis depend heavily on the level of tissue damage at diagnosis, especially renal dysfunction, but are also influenced by patient age, ANCA subtype, disease extent, and response to therapy. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)is treated along similar principles to granulomatosis with polyangiitis (GPA) and microscopic polyangiitis but the persistence of steroid-dependent asthma in over one-third and differences in pathogenesis has suggested alternative treatment approaches. Chronic morbidity results from tissue damage and is especially common in the upper and lower respiratory tract and kidneys. Tracheobronchial disease is a severe late complication of GPA, while deafness, nasal obstruction, and chronic sinusitis are sequelae of nasal and ear vasculitis. Chronic infection of damaged epithelial surfaces acts as a drive for vasculitic activity and adequate infection control is necessary for stable remission. Chronic kidney disease can stabilize for many years but the risks of endstage renal disease (ESRD) are increased by acute kidney injury at presentation or renal relapse. Renal transplantation is successful, with similar outcomes to other causes of ESRD.
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Vuković Brinar, Ivana, and Matija Matošević. "Complement-Mediated Kidney Disease." In Novel Topics in the Diagnosis, Treatment, and Follow-Up of Nephritis, Nephrotic Syndrome, and Nephrosis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108555.

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From very discovery of the complement cascade, it had an intriguing role in pathophysiology of kidney disease. The hallmark of complement cascade involvement in kidney diseases comprises of immune-complexes deposits in the glomeruli, acting as activation for the classical pathway. However, additional mechanisms of complement activation, namely alternative and lectin pathways are extremely important and prominent in complement-mediated kidney disease. Disease prototype of activation of complement is an atypical hemolytic uremic syndrome with solid activation of complement and C3 glomerulopathy is a hallmark of fluid phase activation of alternative complement pathway. Further research has shown that alternative pathway also plays a role in pathogenesis and progression of other kidney diseases including anti-neutrophil cytoplasmic antibody-associated vasculitis and immune complex-mediated glomerulonephritis as well as IgA nephropathy. A better understanding of complement system’s role in kidney disease has also brought forth novel therapeutic approaches in form of complement cascade inhibitors, revolutionizing the treatment of patients that were faced with unfavorable outcomes. Through this chapter, we bring to you an overview of most prevalent complement-mediated kidney diseases with emphasis on the role of complement in their pathogenesis and the potential for treatment targeting the complement cascade.
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Conference papers on the topic "Anti-neutrophil cytoplasm antibody"

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Chopra, M., and E. Cristan. "Rivaroxaban Induced Anti-Neutrophil Cytoplasmic Antibody (ANCA) Associated Vasculitis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4953.

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2

Fidler, L., S. Kandel, J. H. Fisher, S. Mittoo, and S. Shapera. "Anti-Neutrophil Cytoplasmic Antibody Screening in Idiopathic Interstitial Lung Disease." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3367.

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Mulleman, Denis, Amina Bensalem, David Ternant, Gilles Paintaud, Divi Cornec, and Ulrich Specks. "THU0309 NONLINEAR PHARMACOKINETICS OF RITUXIMAB IN ANTI-NEUTROPHIL CYTOPLASMIC ANTIBODY ASSOCIATED VASCULITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4897.

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4

Nakagawa, Naoko, Yoshinori Tanino, Yayoi Inokoshi, Kazue Saito, Taeko Ishii, Takefumi Nikaido, Atsuro Fukuhara, et al. "Clinical Analysis Of Anti-Neutrophil Cytoplasmic Antibody In Patients With Interstitial Pneumonia." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6006.

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Nakahara, M., H. Yamashita, Y. Takahashi, K. Araki, N. Mino, K. Suga, A. Yashima, and H. Kaneko. "AB0682 Risk factors associated with relapse of anti-neutrophil cytoplasmic antibody-associated vasculitis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5468.

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Kaghazian, M., C. W. Akabusi, K. P. Acosta, K. Kallakuri, and P. Shakouri. "Anti-Neutrophil Cytoplasmic Antibody Associated Vasculitis Secondary to Pfizer-BioNTech COVID-19 Vaccine." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1384.

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Bensalem, Amina, David Ternant, Nicolas Azzopardi, Gilles Paintaud, Valérie Gouilleux-Gruart, Divi Cornec, Ulrich Specks, and Denis Mulleman. "SAT0236 RELATIONSHIP BETWEEN RITUXIMAB CONCENTRATION AND AUTOANTIBODY LEVELS IN ANTI-NEUTROPHIL CYTOPLASMIC ANTIBODY ASSOCIATED VASCULITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7552.

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8

Antovic, A., M. Kostic, F. Mobarrez, A. Nordin, J. Vojinovic, A. Bruchfeld, and I. Gunnarsson. "OP0052 Microparticles as potential biomarkers of disease activity in anti-neutrophil cytoplasmic antibody – associated vasculitis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5465.

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Shah, R., R. Trachtman, B. Coakley, and A. Vicencio. "A Rare Case of Anti-Neutrophil Cytoplasmic Antibody and Anti-Glomerular Basement Membrane Antibody Double Positive Disease in a Preschool-Aged Child." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3264.

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Kobayashi, K., D. Nakagomi, S. Hanai, M. Yamagata, T. Sugiyama, H. Kawashima, M. Hiraguri, et al. "AB0676 Efficacy of rituximab therapy against anti-neutrophil cytoplasmic antibody-related hypertrophic pachymeningitis: a case series." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5345.

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