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Добірка наукової літератури з теми "ANCA vasculitis"

Автор: Grafiati
Опубліковано: 5 квітня 2025

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Статті в журналах з теми "ANCA vasculitis"

1

Majumdar, Avirup, Virendra Atam, Saurabh Pandey, Prashant Singh, and Himanshu Chauhan. "Digital infarct and mononeuritis in a middle aged female: always suspect Antineutrophil cytoplasmic antibodies associated vasculitis." International Journal of Advances in Medicine 7, no. 4 (March 21, 2020): 707. http://dx.doi.org/10.18203/2349-3933.ijam20201127.

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Анотація:
Vasculitis is a process caused by inflammation of blood vessel walls and results in a variety of disorders. Small-vessel vasculitis (vasculitis involving arteries, venules and capillaries) should be suspected in any patient who presents with a multisystem disease that is not caused by an infectious or malignant process. Testing for Antineutrophil cytoplasmic antibody (ANCA) is the basis of classification of small vessel vasculitis into ANCA associated and non - ANCA associated vasculitis. Apart from cutaneous manifestations like palpable purpura and vasculitic urticaria, digital gangrene in a patient with evidence of mononeuritis multiplex is highly suggestive of ANCA associated vasculitis (AAV). Clinically most of these vasculitides have overlapping clinical presentations and similar treatment. Early diagnosis and rapid initiation of treatment of AAV is recommended rather than ordering for definitive tests (e.g. histopathology or angiograms) since delay in treatment can result in serious end organ damage (pulmonary or renal).
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2

Radwan, Yasser, Sarah Berini, Floranne Ernste, and Ashima Makol. "Proteinase 3 (PR3)-antineutrophil cytoplasmic antibody (ANCA)-associated vasculitic neuropathy in diffuse cutaneous systemic sclerosis: a rare duo." BMJ Case Reports 12, no. 11 (November 2019): e232987. http://dx.doi.org/10.1136/bcr-2019-232987.

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Анотація:
Systemic sclerosis (SSc) is characterised by non-inflammatory vasculopathy, autoimmunity and widespread fibrosis. While the presence of antineutrophil cytoplasmic antibodies (ANCAs) has been reported in SSc, their association with ANCA-associated vasculitis is exceedingly rare. Myeloperoxidase ANCA is more common than proteinase-3 ANCA, and glomerulonephritis is the most common clinical presentation of ANCA-associated vasculitis in SSc. ANCAs have been associated with the adverse disease outcomes in SSc, including higher mortality per recent reports. A 65-year-old man with diffuse cutaneous SSc for 6 years presented with new-onset peripheral neuropathy. Workup revealed a positive proteinase-3 and cytoplasmic ANCA, and histopathology confirmed an inflammatory vasculitic neuropathy. The patient was successfully treated with rituximab. Our case highlights the importance of checking ANCA in SSc at baseline, given the risk of disease-related complications, even years later. Tissue biopsy is often warranted for confirmation of vasculitis and prompt treatment can optimise long-term outcomes.
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3

Csernok, Elena. "The Diagnostic and Clinical Utility of Autoantibodies in Systemic Vasculitis." Antibodies 8, no. 2 (May 1, 2019): 31. http://dx.doi.org/10.3390/antib8020031.

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Анотація:
Considerable progress has been made in understanding the role of autoantibodies in systemic vasculitides (SV), and consequently testing for anti-neutrophil cytoplasmic antibodies (ANCA), anti-glomerular basement membrane antibodies (anti-GBM), and anti-C1q antibodies is helpful and necessary in the diagnosis, prognosis, and monitoring of small-vessel vasculitis. ANCA-directed proteinase 3 (PR3-) or myeloperoxidase (MPO-) are sensitive and specific serologic markers for ANCA-associated vasculitides (AAV), anti-GBM antibodies are highly specific for the patients with anti-GBM antibody disease (formerly Goodpasture’s syndrome), and autoantibodies to C1q are characteristic of hypocomlementemic urticarial vasculitis syndrome (HUVS; anti-C1q vasculitis). The results of a current EUVAS study have led to changes in the established strategy for the ANCA testing in small-vessel vasculitis. The revised 2017 international consensus recommendations for ANCA detection support the primary use PR3- and MPO-ANCA immunoassays without the categorical need for additional indirect immunofluorescence (IIF). Interestingly, the presence of PR3- and MPO-ANCA have led to the differentiation of distinct disease phenotype of AAV: PR3-ANCA-associated vasculitis (PR3-AAV), MPO-ANCA-associated vasculitis (MPO-AAV), and ANCA-negative vasculitis. Further studies on the role of these autoantibodies are required to better categorize and manage appropriately the patients with small-vessel vasculitis and to develop more targeted therapy.
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4

Arnold, S., J. Mahrhold, A. Kerstein-Staehle, E. Csernok, B. Hellmich, N. Venhoff, J. Thiel, et al. "POS0829 SPECTRUM OF ANCA-SPECIFICITIES IN EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS IN A RETROSPECTIVE MULTICENTER STUDY." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 705–6. http://dx.doi.org/10.1136/annrheumdis-2022-eular.3083.

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Анотація:
BackgroundAnti-neutrophil cytoplasmic autoantibodies specific for myeloperoxidase (MPO-ANCA) are found in 10-70% of the patients with eosinophilic granulomatosis with polyangiitis (EGPA) depending on disease activity, methodological aspects and cohort examined [1-3]. Recently, a higher prevalence of anti-pentraxin 3 (PTX3)-ANCA has been reported in EGPA compared to granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) [4].ObjectivesTo investigate the spectrum of ANCA specificities in a multicenter cohort of patients with EGPA and identify novel ANCA antigens.MethodsWe conducted a retrospective analysis of 73 patients with EGPA treated between 2015 and 2020 in 3 tertiary referral centers. In addition to in-house ANCA testing with indirect immunofluorescence (IFT) on fixed human granulocytes and antigen-specific enzyme-linked immunosorbent assays (ELISA), ANCA specificities were determined using a cell-based assay (CBA; Euroimmun, Lübeck, Germany). Diagnosis was based on Chapel Hill consensus conference definitions, ACR- and MIRRA-criteria for EGPA. Patient characteristics and clinical manifestations were evaluated and compared based on ANCA status. Fisher`s exact test was employed for comparison of patient groups.ResultsANCA findings are summarized in Table 1. MPO- and proteinase 3 (PR3)-ANCA positive patients (13.7%) had a higher prevalence of peripheral neuropathy (70% vs. 44.4%, p = 0.0003) and glomerulonephritis (20% vs. 14.3%, not significant). MPO- and PR3-ANCA-negative patients (86.3%) had a higher prevalence of heart (10% vs. 46%, p <0.0001), central nervous system (CNS) (0% vs. 14.3%, p <0.0001) and gastrointestinal (10% vs. 22.2%, p = 0.0327) involvement. PTX3-ANCA were associated with a higher prevalence of ear-nose-throat (ENT) (100% vs. 85.3%, p <0.0001), lung (100% vs. 89.7%, p = 0.0015), gastrointestinal involvement (60% vs. 17.6%, p <0.0001) and peripheral neuropathy (100% vs. 48.5%, p <0.0001). Kidney (0% vs. 16.2%, p <0.0001) and CNS involvement (0% vs. 13.2%, p = 0.0002) occurred less frequently in PTX3-ANCA positive patients. The 2 olfactomedin 4 (OLM4)-ANCA positive patients presented with ENT, lung and kidney involvement, and polyneuropathy, respectively.Table 1.ANCA in EGPA cohort (n = 73). BPI = bactericidal permeability-increasing protein.IFT / ELISANo. of patients (%)P-ANCA11 (15.1)C-ANCA5 (6.8)MPO-ANCA8 (10.9)PR3-ANCA2 (2.7)BPI-ANCA1 (1.4)PTX3-ANCA5 (6.8)OLM4-ANCA2 (2.7)ConclusionWe report on the detection of PTX3-, BPI- and OLM4-ANCA in addition to MPO- and PR3-ANCA in EGPA. OLM4-ANCA has been reported in 2 patients with non-vasculitic inflammatory symptoms previously [5]. Herein, detection of OLM4-ANCA in EGPA is reported for the first time. Our study shows that the presence of ANCA with various specificities other than MPO and PR3 contribute to a higher prevalence of ANCA in EGPA. Moreover, clinical manifestations differ between ANCA-negative EGPA and ANCA-positive EGPA, and between patients with different ANCA-specificities.References[1]Schönermarck U, et al. Prevalence and spectrum of rheumatic diseases associated with proteinase 3-antineutrophil cytoplasmic antibodies (ANCA) and myeloperoxidase-ANCA. Rheumatology 2001;40:178-84.[2]Bremer P, et al. Getting rid of MPO-ANCA: a matter of disease subtype. Rheumatology 2013:752-4.[3]Comarmond C, et al. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss): clinical characteristics and long-term followup of the 383 patients enrolled in the French Vasculitis Study Group cohort. Arthritis Rheum 2013;65:270-81.[4]Padoan R, et al. IgG anti-Pentraxin 3 antibodies are a novel biomarker of ANCA-associated vasculitis and better identify patients with eosinophilic granulomatosis with polyangiitis. J Autoimmun 2021;124:102725.[5]Amirbeagi F, et al. Olfactomedin-4 autoantibodies give unusual c-ANCA staining patterns with reactivity to a subpopulation of neutrophils. J Leukoc Biol 2015;97:181-9.Disclosure of InterestsNone declared
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5

Saha, Biplab, Aditi Saha, Fernanda Cordeiro-Rudnisky, Boris Shkolnik, and Scott Beegle. "Destructive Upper Airway Disease from Eosinophilic Granulomatosis with Polyangiitis (EGPA): The Very First Case." Case Reports in Rheumatology 2019 (May 23, 2019): 1–4. http://dx.doi.org/10.1155/2019/6173869.

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Анотація:
Eosinophilic granulomatosis with polyangiitis (EGPA) is a multisystem vasculitic disorder that predominantly affects medium- and small-sized blood vessels. EGPA belongs to a group of vasculitides known as anti-neutrophil cytoplasmic antibody- (ANCA-) associated vasculitis (AAV). Upper airway involvement is seen in all ANCA-associated vasculitides, but destructive upper airway disease has never been reported in patients with EGPA. We report the first case of erosive chondritis and saddle nose deformity in a 50-year-old patient suffering from EGPA.
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6

Segelmark, Mårten. "Serological testing in small vessel vasculitis." Rheumatology 59, Supplement_3 (April 29, 2020): iii51—iii54. http://dx.doi.org/10.1093/rheumatology/kez633.

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Анотація:
Abstract Serological analysis has a central role in the diagnostic work-up of patients with suspected small vessel vasculitis, both for establishing a specific diagnosis and for the monitoring of response to therapy. Autoantibodies can be detected in all forms of primary small vessel vasculitis as well as in the most common forms of secondary vasculitis. For primary vasculitis the most important serological test is for ANCA. ANCA can be found in 75–95% of patients with pauci-immune small vessel vasculitis leading to this subgroup of vasculitides being named ANCA associated vasculitis. ANCA levels often follow this disease course, but the value of serial ANCA testing is controversial. Other important autoantibodies in primary small vessel vasculitis are anti-glomerular basement membrane antibodies, anti-C1q, anti-galactose deficient IgA and cryoglobulins. A wide variety of systemic inflammatory diseases and infections can be complicated by small vessel vasculitis and detected by serological testing. Important examples are SLE, rheumatoid arthritis, Hepatitis C and HIV.
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7

Preto, Clara, Armandina Silva, Sandra Alves, Margarida Guedes, Paula Matos, Conceição Mota, Paula Rocha, and Paula C. Fernandes. "The Diagnosing Challenge of a Positive ANCA Vasculitis in the Paediatric Age." Case Reports in Pediatrics 2017 (2017): 1–5. http://dx.doi.org/10.1155/2017/2962794.

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Анотація:
ANCA-positive systemic vasculitides, rare in paediatric age, present multiorganic involvement. A female teenager presented with a history of subglottic stenosis diagnosed at the age of 12. From the investigation carried out, we highlight hematoproteinuria and negative ANCAs. At 15 years old, she was admitted for gastrointestinal symptoms and respiratory distress. She presented poor peripheral perfusion, pulmonary haemorrhage, respiratory failure, and severe renal insufficiency. She was started mechanical ventilation and emergency haemodialysis. The immunological study revealed ANCA MPO positive. A presumptive diagnosis of ANCA-positive vasculitis was made, and she was started corticotherapy, cyclophosphamide, and plasmapheresis. A renal biopsy, performed later, showed crescentic glomerulonephritis with chronicity signs. Positive ANCA vasculitis may progress slowly or suddenly. The diagnosis was confirmed by a biopsy; however, we can make a presumptive diagnosis based on clinical findings and in a positive ANCA test in order to start an early treatment and decrease the associated morbimortality.
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8

Palmucci, Stefano, Corrado Inì, Salvatore Cosentino, Luigi Fanzone, Stefano Di Pietro, Alessia Di Mari, Federica Galioto, et al. "Pulmonary Vasculitides: A Radiological Review Emphasizing Parenchymal HRCT Features." Diagnostics 11, no. 12 (December 9, 2021): 2318. http://dx.doi.org/10.3390/diagnostics11122318.

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Анотація:
Vasculitides represent a heterogeneous group of immune-mediated disorders, characterized by a systemic inflammatory destructive process of the blood vessels resulting either in ischemia or hemorrhage. The organ involved and vessel size influence the pattern of presentation of the pathology. The lung is commonly involved in systemic vasculitides, with heterogeneous clinical, radiological, and histopathological presentations. Primary vasculitides most commonly associated with lung parenchymal involvement include small-vessel antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitides, such as granulomatosis with polyangiitis (GPA), eosinophilic granulomatosis with polyangiitis (EGPA), and microscopic polyangiitis (MPA). Several studies have reported cases of interstitial lung diseases (ILDs) associated with systemic vasculitis, particularly those positive for ANCA associated vasculitis/vasculitidis: AAV. We have selected from our case series different radiological features of pulmonary vasculitis (i.e., solitary or multiple nodules, cavitary lesions, nodules with centrilobular or peribronchial distribution, airspace consolidations, “crazy paving” appearance, interstitial disease), including cases with interstitial lung alterations. Therefore, the aim of this review is to describe the typical clinical manifestations of vasculitides and their main radiologic features (especially AAV).
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9

Alba, Marco, J. Jennette, and Ronald Falk. "Pathogenesis of ANCA-Associated Pulmonary Vasculitis." Seminars in Respiratory and Critical Care Medicine 39, no. 04 (August 2018): 413–24. http://dx.doi.org/10.1055/s-0038-1673386.

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AbstractAntineutrophil cytoplasmic antibodies (ANCAs) are autoantibodies specific for antigens located in the cytoplasmic granules of neutrophils and lysosomes of monocytes. ANCAs are associated with a spectrum of necrotizing vasculitis that includes granulomatosis with polyangiitis, microscopic polyangiitis, and eosinophilic granulomatosis with polyangiitis. Pulmonary vasculitis and related extravascular inflammation and fibrosis are frequent components of ANCA vasculitis. In this review, we detail the factors that have been associated with the origin of the ANCA autoimmune response and summarize the most relevant clinical observations, in vitro evidence, and animal studies strongly indicating the pathogenic potential of ANCA. In addition, we describe the putative sequence of pathogenic mechanisms driven by ANCA-induced activation of neutrophils that result in small vessel necrotizing vasculitis and extravascular granulomatous necrotizing inflammation.
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10

Yoneva, Tzvetelina, Yana Zdravkova, Georgi Kotov, Rasho Rashkov, and Ivan Sheytanov. "Structure of the vasculitides observed in the Clinic of Rheumatology." Revmatologiia (Bulgaria) 28, no. 3 (November 16, 2020): 7–24. http://dx.doi.org/10.35465/28.3.2020.pp7-24.

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Анотація:
Systemic vasculitides are a heterogenic group of disorders characterized by destructive inflammation and fibrinoid necrosis of the vascular wall, vessel occlusion and tissue ischemia. Vasculitides presenting with necrosis are included in neither of the contemporary classifications, even though this type of vascular pathology is the one with the most dramatic manifestations in rheumatology. There have been no analyses of the nosological association, clinical features and therapeutic management of the vasculitides with necrosis in the pertinent literature. The aim of the present study was to analyze vasculitides in the Bulgarian population in terms of their nosological association; to examine the portion that ANCA-associated vasculitides represent out of all vasculitic syndromes on the one hand, and to make an analysis of the vasculitides with necrosis according to their nosological association on the other. In the present study, we included 388 patients with vasculitis, 251 of whom were female and 137 male. We conducted a prospective and retrospective analysis which covered the patients with vasculitis who were admitted to the Clinic of Rheumatology over the period 2009-2018. ANCA-associated vasculitides were the most often diagnosed vasculitides in the Clinic of Rheumatology. Vasculitic manifestations over the course of connective tissue diseases (most often systemic lupus erythematosus and systemic sclerosis) were the second most common group. Life-threatening cases of vasculitis with necrosis were mainly the result of flares of different connective tissue diseases. The major necrotizing vasculitides (Wegener’s granulomatosis and microscopic polyangiitis) were responsible for 12.6% of the cases of vasculitis with necrosis. In order to establish the correct diagnosis and start the suitable treatment, it is of vital importance to recognize the different vasculitic syndromes and their wide differential diagnosis. Most of them respond well to the currently available therapeutic options, especially if the correct diagnosis has been established early.
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Більше джерел

Дисертації з теми "ANCA vasculitis"

1

Stassen, Patrica Maria. "ANCA-associated vasculitis triggers and treatment /." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2008. http://irs.ub.rug.nl/ppn/.

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2

Chowdhury, Saifuddin M. Zahed. "Antineutrophil cytoplasmic antibodies and systemic vasculitis." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327199.

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3

Berti, Alvise. "Autoreactive B Cells in ANCA-Associated Vasculitis." Doctoral thesis, Università degli studi di Trento, 2021. http://hdl.handle.net/11572/325394.

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Анотація:
Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a group of B-cell driven, autoimmune systemic vasculitides characterized by a relapsing course and the presence of ANCA autoantibodies which are instrumental in their pathogenesis. We aimed to investigate autoreactive proteinase 3 (PR3+) B cells involved in the development of human AAV. We previously developed a customized flow-cytometry method to identify autoreactive B cells among cryopreserved peripheral blood mononuclear cells (PBMC), using labeled PR3, one of the main AAV autoantigens, as a ligand. We therefore used multicolor flow cytometry in combination with bioinformatics and functional in vitro studies on 1) baseline samples of PBMC from 154 well-characterized participants of the RAVE trial (NCT00104299) with severely active PR3-ANCA+ AAV (PR3-AAV) and myeloperoxidase (MPO)-AAV, and 27 healthy controls (HC); 2) samples of matched bone marrow (BM) and peripheral blood from 8 non-vasculitis patients; and 3) 148 longitudinal samples from 23 PR3-AAV patients of the RAVE trial. Clinical data and outcomes from the trial and medical records were correlated with PR3+ B cells (total and subsets). In brief, we identified and phenotypically characterized autoreactive B cells in AAV and healthy controls, reporting their perturbations among the different B cell subsets, and their functional ability to produce PR3-ANCA autoantibodies in vivo and in vitro. We reported their maturation through central and peripheral tolerance checkpoints from BM to peripheral blood, leading to an accumulation of atypical autoreactive PR3+ memory B cells in PR3-AAV patients but not in MPO-AAV and HC. We also described the longitudinal association between autoreactive plasmablast redetection after anti-B cell 13 targeted therapy with the main disease outcome, relapse. Overall, our findings suggest the presence of defective central antigen-independent and peripheral antigen-dependent checkpoints in patients in PR3-AAV, elucidating the selection process of autoreactive B cells, and their association with disease relapse.
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4

McClean, Andrew. "Why are patients with ANCA-associated vasculitis fatigued?" Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6487/.

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Objective: To assess the severity and predictors of fatigue in ANCA-associated vasculitis (AAV), and the contribution of peripheral and central mechanisms. Methods: Fatigue, anxiety/depression, sleep quality and pain were measured in 152 patients with AAV, 68 patients with CKD, andTl healthy conffols. Muscle mass, strength and endurance, cardio-respiratory fitness, perception of exertion, high-sensitivity C-reactive protein (hsCRP), and dehydroepiandrosterone (DHEA) were measured in 48 patients with AAV and 4l healthy controls. Results: Fatigue in AAV was more severe than in CKD 1p:g.gl3) or controls (p<0.001), and correlated with anxiety/depression, sleep quality and pain (all p<0.001). There was no difference in muscle mass (p:0.979) or strength (p=0.315) between AAV and conhols, but muscle endurance time was shorter in AAV (p=0.006), with greater muscle reserve (p=0.038) indicating central activation failure. Perception of exertion (p=0.006) and cardio-respiratory fitness (p:0.029) were worse in AAV than controls. Only perception of exertion independently predicted AAV fatigue (p:0.01). Sleep disturbance predicted altered perception of exertion (p:0.017). hsCRP was higher (p0.01 1) and DHEAS levels were lower (p<0.001) in AAV than controls, but neither predicted fatigue. Conclusion: Fatigue in AAV is more severe than in CKD or health, is due to central mechanisms, and may be amenable to intervention.
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5

Trivedi, Sapna. "A genetic association study in ANCA associated vasculitis." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607655.

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6

Brown, Nina. "Improving outcomes for patients with ANCA associated vasculitis." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/improving-outcomes-for-patients-with-anca-associated-vasculitis(41ab7c31-2b89-4626-a6a9-4b19b99e4d7b).html.

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Анотація:
Background: ANCA Associated Vasculitis (AAV) is a relatively rare autoimmune condition with the potential to cause life-threatening organ inflammation and failure. Due to the relative rarity, and the heterogenous way in which the disease may present, delay to diagnosis is common. Although initial immunosuppressive treatment is usually effective at controlling disease, morbidity associated with treatment is high and disease relapses frequent, necessitating further immunosuppression exposure. Aims and Objectives: This body of work therefore seeks to address 2 of the main challenges faced by the AAV population; 1) identifying factors that may contribute to a delay to diagnosis and disease recognition 2) reducing morbidity associated with the disease and the treatment. Methods: Patient pathways, knowledge and uptake of protective therapy were explored through a national patient report study. Patient care guidelines to assist with morbidity prevention were informed through Delphi consensus methodology and comprehensive literature review. The development of software to support implementation of a rigorous systematic approach to the assessment of the vasculitis patients was achieved through collaboration with information technology, business development and system architecture and design experts. Results: Patient presentation including symptoms, initial mis-diagnosis and eventual diagnosis appear to influence time to diagnosis. There is substantial delay from symptom onset to diagnosis demonstrating the need for increased awareness and education. Equally patient awareness of treatment related morbidity is low with variable uptake of protective therapy. A Delphi study has produced consensus on which guidelines can be based to address some of these inadequacies. A software programme: "Vasculitis Care Optimisation Tool (VasCOT)", has been designed to support implementation of these guidelines. Discussion: The various approaches used in this body of work have so far allowed evaluation of areas where patient care needs to be improved. This in part will be addressed through the publication of national vasculitis care guidelines, informed by this work and the ongoing development of VasCOT.
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Smith, Rona Marie. "Biological therapy in the treatment of ANCA associated vasculitis." Thesis, University of Cambridge, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709472.

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8

Henderson, Scott Russell. "Dissecting mechanisms of granuloma formation in ANCA-associated vasculitis." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10042084/.

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Анотація:
Anti-neutrophil cytoplasm antibodies (ANCA) are associated with a severe form of small vessel systemic vasculitis, in which they target two specific auto-antigens, proteinase-3 (PR3) and myeloperoxidase (MPO) found within neutrophils and monocytes. Granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) are the main clinical syndromes, both characterized by kidney and lung disease, but granulomatous inflammation is almost exclusively found in GPA, and unlike other manifestations, remains difficult to treat. In GPA patients, PR3 is the predominant ANCA auto-antigen and neutrophil membrane PR3 expression is increased. There has been limited understanding of why granulomata are restricted to this patient subgroup. I have investigated the role of PR3 in driving giant cell and granuloma formation by generating a novel in vitro model. Using extensive tissue culture and microscopy techniques I have been able to demonstrate that PR3 induces both giant cell and granuloma formation in GPA patients’ cells. Giant cells are the precursors to granulomata and I have demonstrated that in GPA patients, monocytes firstly fuse with the persistence of PR3 and then later recruit lymphocytes to form an organized granuloma-like structure. I have developed a unique method of quantifying granuloma formation and I have been able to show that GPA patients show a statistically significant greater rate of PBMC aggregation both spontaneously and in the presence of PR3 compared to MPA patients and healthy controls. I have explored the potential mechanisms of granuloma formation in this patient subgroup. Specifically, IL-6 may be important in driving granuloma formation in GPA patients and supports the notion of PR3-mediated process. PR3 cleaves protease-activated receptor 2 (PAR2) and I have shown that the presence of a PAR2 agonist further augments cell fusion. These findings support the role of PR3-mediated monocyte activation and fusion with additional T cell aggregation. In summary, I have developed a novel system to test giant cell and granuloma formation in GPA patients, a potential platform to evaluate new therapeutic treatments.
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9

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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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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Книги з теми "ANCA vasculitis"

1

Říhová, Zuzana. ANCA-associated renal vasculitis. Prague: Charles University in Prague, Karolinum Press, 2009.

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2

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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4

L, Gross Wolfgang, International Workshop on ANCA, (4th : 1992 : Lübeck, Germany), and International Colloquium on Wegener's Granulomatosis and Vasculitic Disorders, (2nd : 1992 : Lübeck, Germany), eds. ANCA-associated vasculitides: Immunological and clinical aspects. New York: Plenum Press, 1993.

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5

Radford, David John. Investigation of neutrophil signalling pathways activated by autoantibodies (ANCA) from patients with systemic vasculitis. Birmingham: University of Birmingham, 1998.

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6

Tse, Wai Yee. Neutrophil Fc[gamma] receptor polymorphisms and pathogenetic mechanisms of neutrophil activation in anti-neutrophil cytoplasm (ANCA)-associated vasculitis. Birmingham: University of Birmingham, 1999.

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7

Gross, Wolfgang L., ed. ANCA-Associated Vasculitides. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4757-9182-2.

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8

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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9

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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Sudhir, Rajini. Pulmonary vasculitis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0140.

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Pulmonary vasculitis comprises a heterogeneous group of disorders characterized by an inflammatory process damaging the vessel wall, leading to ischaemia and tissue necrosis. Wegener’s granulomatosis, Churg–Strauss syndrome, and microscopic polyangiitis are primary, small-vessel, necrotizing vasculitides linked by an overlapping clinicopathological picture and are referred to collectively as ANCA-associated systemic vasculitis. The European Vasculitis Study Group proposed a clinical staging system based on disease activity, to guide treatment.
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Частини книг з теми "ANCA vasculitis"

1

Bonatti, Francesco, Alessia Adorni, Antonio Percesepe, Augusto Vaglio, and Davide Martorana. "ANCA-Associated Vasculitis." In Genetics of Rare Autoimmune Diseases, 111–28. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03934-9_6.

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Stone, John H., Shoichi Ozaki, Karina Keogh, Ulrich Specks, Carol A. Langford, Niels Rasmussen, Cees G. M. Kallenberg, and Ingeborg M. Bajema. "ANCA-Associated Vasculitis." In A Clinician's Pearls and Myths in Rheumatology, 245–67. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84800-934-9_24.

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3

Marzano, Angelo Valerio, Giovanni Genovese, Francesca Ingegnoli, and Roberto Caporali. "ANCA-Associated Vasculitis." In Diseases of the Oral Mucosa, 273–85. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-82804-2_27.

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4

Balemans, Wendy, Wim Van Hul, Marian Valko, Jan Moncol, Lee A. Denson, Maria Mela, Ulrich Thalheimer, et al. "Vasculitis, ANCA-mediated." In Encyclopedia of Molecular Mechanisms of Disease, 2172–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_3407.

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5

Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "ANCA-associated Vasculitis." In Encyclopedia of Molecular Mechanisms of Disease, 81. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7143.

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6

Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "ANCA-mediated Vasculitis." In Encyclopedia of Molecular Mechanisms of Disease, 81. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9031.

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7

Nachman, Patrick H., and Shannon L. Murphy. "ANCA-Associated Vasculitis, Adult." In Glomerulonephritis, 333–48. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_17.

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8

Gibson, Keisha, and Dorey Glenn. "ANCA-Associated Vasculitis, Pediatric." In Glomerulonephritis, 349–57. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_18.

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Nachman, Patrick H., and Shannon L. Murphy. "ANCA-Associated Vasculitis, Adult." In Glomerulonephritis, 1–17. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-27334-1_17-1.

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Nachman, Patrick H., and Shannon L. Murphy. "ANCA-Associated Vasculitis, Adult." In Glomerulonephritis, 1–17. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-27334-1_17-2.

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Тези доповідей конференцій з теми "ANCA vasculitis"

1

Kim, SM, J. Kim, SW Kang, S.-C. Shim, and S.-J. Yoo. "AB0593 Anca-associated vasculitis with both MPO-ANCA and PR3-ANCA shares characteristics of ANCA-associated vasculitis with single ANCA." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.6476.

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2

Clark, J., S. Hogan, V. Derebail, Y. Hu, A. Froment, and A. G. Henderson. "Spirometry in ANCA Vasculitis." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a3305.

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3

Mohamed, A. O., S. M. D. Chaudhary, P. K. Valestra, and B. Sharma. "ANCA Vasculitis Presenting with Hemoptysis." 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.a6622.

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Barboza, Flavio, Heloisa Maria Lopes Scarinci, Evelyn Angrevski Rodrigues, Talles Henrique Pichinelli Maffei, Ygor Augusto Silva Lima, Lucas do Carmo de Carvalho, Thalyne Aparecida Leite de Lima, et al. "Neurosyphilis mimicking ANCA associated vasculitis." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.16855.

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Nunes Assis Daameche, Luciana, Carlos Eduardo Lins, Tayane Oliveira Pires, Helga Moura Kherle, Dunya Bouchour Basílio, Gustavo de Paiva Costa, Jamille Nascimento Carneiro, et al. "LEPROSY MIMICKING ANCA-ASSOCIATED VASCULITIS." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.17554.

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Ayrosa, R. S., J. P. C. Serra, M. O. C. Ximenes, A. P. T. Pereira, E. P. Oliveira, J. N. A. Junior, E. C. T. Nascimento, C. S. V. Barbas, and A. N. Costa. "Lung Phaeohyphomycosis Mimicking ANCA-Associated Vasculitis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6890.

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Chizinga, M., B. Alzghoul, H. Venigandla, and D. C. Gomez Manjarres. "An Unusual Presentation of ANCA-Associated Vasculitis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4557.

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RIO, ANA PAULA TOLEDO DEL, JESSICA OLIVEIRA FRADE, STEPHANIE OSPINA PRIETO, BRUNO KOSA LINO DUARTE, MANOEL BARROS BERTOLO, MARGARETH CASTRO OZELO, and ZORAIDA SACHETTO. "ENDOTHELIAL PROGENITOR CELLS IN ANCA-ASSOCIATED VASCULITIS." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-419.

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Lee, J., S. Kim, and S. Balamuthusamy. "ANCA Vasculitis Presenting With Diffuse Alveolar Hemorrhage." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a5337.

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10

Perim, Gabriela Camilotti, Carolina Tiemi Tonholo Ikedo, Rodrigo Lorenzetti Serrano, Edgard Torres dos Reis Neto, Alexandre Wagner Silva de Souza, Bruna Romagna Peterle, Lígia Magalhães Biló, et al. "OVERLAP OF IGA-ASSOCIATED VASCULITIS AND PR3-ASSOCIATED ANCA VASCULITIS CASE REPORT." In XL Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2023. http://dx.doi.org/10.47660/cbr.2023.2039.

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Звіти організацій з теми "ANCA vasculitis"

1

Kalinova, Desislava, Valentina Reshkova, Tzvetelina Velikova, Ekaterina Ivanova-Todorova, Dobroslav Kyurkchiev, and Rasho Rashkov. Markers of Endothelial Inflammation and Repair in a Group of Patients with ANCA-associated Vasculitis. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, December 2021. http://dx.doi.org/10.7546/crabs.2021.12.14.

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2

He, Xing, Weiwei Yuan, Yahui Yang, Jiaqi Ji, and Xixi Chen. Risk Factors for Poor Prognosis in ANCA-associated Vasculitis with Interstitial Lung Disease: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2024. http://dx.doi.org/10.37766/inplasy2024.10.0007.

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Zhu, Qing, Bilin Chen, Xi Xie, Jinwei Chen, and Fen Li. A meta-analysis and study about relationship between sex and 1-year mortality in adult patients with ANCA - associated vasculitis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0071.

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Tsai, Meng-Ko, and Miao-Yi Chen. Risk of Severe Infection in Patients with ANCA-Associated Vasculitis Treated with Rituximab: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2023. http://dx.doi.org/10.37766/inplasy2023.5.0037.

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