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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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3
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.
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.
10
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.
11
Watts, Richard A., and Eleana Ntatsaki. Miscellaneous vasculitides. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0137.
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The vasculitides are a group of relatively rare conditions with a broad spectrum of clinical presentations that can cause significant morbidity and mortality. Classification of the vasculitic syndromes is done according to the size of the vessels affected and also the presence of anti-neutrophil cytoplasmic antibodies (ANCA). Vasculitides can be either primary or secondary to an underlying systemic disease, malignancy, or infection. This chapter covers the spectrum of the secondary vasculitides; some of the non-ANCA-associated primary vasculitides and miscellaneous types of vasculitic syndromes. Secondary vasculitis can occur in the background of systemic rheumatic diseases such as rheumatoid arthritis, spondyloarthropathies, or other connective tissue diseases. Vasculitis can also present in relation to precipitants such as drugs (propylthiouracil, hydralazine, leucotriene antagonists) or vaccines. Infection (bacterial, mycobacterial, viral, and fungal) has been associated with vasculitis either as a trigger or as a consequence of iatrogenic immunosuppression. Infection-related vasculitis can affect all types and sizes of vessels. Certain forms of vasculitis such as cryoglobulinaemia are closely associated with viral infections and more specifically with HCV infection. There are forms of vasculitis, which appear to be isolated or localized to a single organ, or site (skin, gastrointestinal, genital, and primary central nervous system vasculitis) that may be histologically similar to systemic syndromes, but have a different prognosis. Other conditions that may mimic vasculitis and miscellaneous conditions such as Cogan's syndrome and relapsing polychondritis are also discussed.
12
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.
13
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) ...
14
Watts, Richard A., and David G. I. Scott. Vasculitis—classification and diagnosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0130.
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The vasculitides are a group of conditions characterized by inflammation and necrosis of blood vessels; they are generally of unknown aetiology. The classification of vasculitides is based on the size of vessel involved and whether there is a known cause (secondary) or not (primary). This approach has stood the test of time. The American College of Rheumatology (ACR) in 1990 produced classification criteria for the major types of vasculitis and in 1994 definitions were promulgated by the Chapel Hill Consensus Conference. These did not include anti-neutrophil cytoplasm antibodies (ANCA) and the ACR scheme did not include microscopic polyangiitis. The definitions have recently been updated to include modern concepts of pathogenesis including ANCA. No validated diagnostic criteria are available for routine clinical practice. The diagnosis of vasculitis requires a high index of suspicion, especially in the systemically unwell patient with multiorgan involvement. The key to diagnosis is a detailed and systematic approach to patient assessment involving all potentially involved organs. In a patient with suspected vasculitis immediate urinalysis is mandatory as the severity of renal involvement at presentation is a major determinant of outcome. Each potentially involved organ should be comprehensively evaluated. Tissue biopsy should be obtained whenever possible, as treatment is potentially toxic using glucocorticoids combined with cytotoxic agents. Biopsy should not, however, delay initiation of treatment. Potential alternative diagnosis should be considered, especially infection and malignancy, and excluded whenever possible.
15
Gross, Wolfgang L. ANCA-Associated Vasculitides: Immunological and Clinical Aspects. Springer London, Limited, 2013.
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16
Swales, Catherine. Inflammatory connective tissue disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.010005.
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♦ Systemic lupus erythematosus (SLE) is the commonest multisystem connective tissue disease♦ All patients with SLE are antinuclear antibody (ANA) positive, but not all ANA-positive patients have SLE♦ Renal lupus carries a high mortality and requires aggressive immunosuppression♦ Dermatomyositis may be associated with malignancy in the elderly♦ The vasculitides are classified according to vessel size and ANCA (antineutrophil cytoplasmic antibody) profile♦ Therapy for vasculitis includes corticosteroids, steroid-sparing agents, and cytotoxics.
17
Foster, Brogan, and Paul A. Brogan. Systemic diseases. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738756.003.0004.
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This chapter covers the full spectrum of systemic diseases in paediatric rheumatology including: the systemic vasculitides (HSP, Kawasaki disease, PAN, ANCA-associated vasculitis, Takayasu arteritis, Behçet's disease, cerebral vasculitis, and many others); juvenile SLE; scleroderma; JDM; overlap syndromes; antiphospholipid syndrome; sarcoid; and paediatric uveitis. In addition, it provides updated descriptions and treatment approaches for autoinflammatory diseases, including recently described diseases such as DADA, SAVI, CANDLE, and many others. Other systemic diseases described in detail include mucopolysaccharidoses and mucolipidoses; musculoskeletal features of chromosomal abnormalities; cystic fibrosis; and inflammatory bowel disease. Treatment guidelines for all these systemic diseases have been fully updated, and aligned with recent evidence-based/consensus European guidance.
18
Rodriguez-Iturbe, Bernardo, and Mark Haas. Glomerulonephritis associated with endocarditis, deep-seated infections, and shunt nephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0079_update_001.
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Endocarditis is a cause of glomerulonephritis. Healthcare interventions (prosthetic valves, indwelling catheters, pacemaker wires) and intravenous drug abuse are presently the most common causes of endocarditis and Staphylococcus aureus is frequently the infecting bacteria. Shunt nephritis is a form of glomerulonephritis associated with infection of ventriculoatrial shunts implanted to relieve hydrocephalus and, typically, are caused by prolonged infections of low-pathogenicity microorganisms. This complication led to the replacement of the technique by ventriculoperitoneal shunts. Deep-seated infections such as chronic abscesses and osteomyelitis can sometimes cause a similar syndrome. In all cases, treatment of the infection is the key strategy. The nature of the glomerulonephritis tends in subacute infection to be a lobular membranoproliferative glomerulonephritis type I pattern associated with low C3 levels. However, an acute post-infectious pattern may also be seen, and a third pattern is focal necrotizing and crescentic glomerulonephritis, which tends to be pauci-immune as seen in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, but usually without positive fluorescence or solid phase assays for ANCA antigens.
19
Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0073_update_001.
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Cyclophosphamide and plasma exchange are the standard of care in rapidly progressive glomerulonephritis or lung haemorrhage caused by antiglomerular basement membrane (anti-GBM) disease, and it is unusual to encounter patients at earlier stages. Steroids are universally used in addition. There is some evidence that plasma exchange may not be a critical part of treatment at an earlier stage. There is no more than anecdotal evidence for other therapies. Slower-onset therapies such as antibodies to B cells are rarely appropriate. If untreated, patients with severe anti-GBM disease will not recover renal function and are at risk of pulmonary haemorrhage. Evidence for the pathogenicity of circulating anti-GBM antibodies provides rationale for removal of circulating antibodies as rapidly as possible, whilst simultaneously inhibiting their synthesis. This was behind the introduction of the combination of plasma exchange with immunosuppressive therapy in mid 1970s, which revolutionized outcomes. Plasmapheresis aims to remove circulating pathogenic antibodies against GBM and possibly other mediators; cyclophosphamide prevents further synthesis of autoantibodies; and steroids act as anti-inflammatory agents to attenuate the glomerular inflammatory response initiated by anti-GBM antibodies. It is clear from experimental models and occasional observations in man that the anti-cell mediated effects of current therapies are important too. Outcomes vary, but in general patient survival is now good, while renal survival remains poor, in many series less than 50% at 1 year. Treatment is toxic and after an early peak in deaths due to pulmonary haemorrhage, secondary infections are the next threat. It may therefore be best not to immunosuppress patients with a very poor renal prognosis who appear to be at low risk of pulmonary haemorrhage. Treatment can usually be curtailed after 3 months without recurrence. ANCA and anti-GBM antibodies occur together in some patients. This is typically an older group which often has features of vasculitis, and the anti-GBM response may often be secondary. Longer treatment as for small vessel vasculitis is usually indicated.
20
Gross, Wolfgang L. ANCA-Associated Vasculitides: Immunological and Clinical Aspects. Springer, 2013.
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21
Lewis, Myles, and Tim Vyse. Genetics of connective tissue diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0042.
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The advent of genome-wide association studies (GWAS) has been an exciting breakthrough in our understanding of the genetic aetiology of autoimmune diseases. Substantial overlap has been found in susceptibility genes across multiple diseases, from connective tissue diseases and rheumatoid arthritis (RA) to inflammatory bowel disease, coeliac disease, and psoriasis. Major technological advances now permit genotyping of millions of single nucleotide polymorphisms (SNPs). Group analysis of SNPs by haplotypes, aided by completion of the Hapmap project, has improved our ability to pinpoint causal genetic variants. International collaboration to pool large-scale cohorts of patients has enabled GWAS in systemic lupus erythematosus (SLE), systemic sclerosis and Behçet's disease, with studies in progress for ANCA-associated vasculitis. These 'hypothesis-free' studies have revealed many novel disease-associated genes. In both SLE and systemic sclerosis, identified genes map to known pathways including antigen presentation (MHC, TNFSF4), autoreactivity of B and T lymphocytes (BLK, BANK1), type I interferon production (STAT4, IRF5) and the NFκB pathway (TNIP1). In SLE alone, additional genes appear to be involved in dysregulated apoptotic cell clearance (ITGAM, TREX1, C1q, C4) and recognition of immune complexes (FCGR2A, FCGR3B). Future developments include whole-genome sequencing to identify rare variants, and efforts to understand functional consequences of susceptibility genes. Putative environmental triggers for connective tissue diseases include infectious agents, especially Epstein-Barr virus; cigarette smoking; occupational exposure to toxins including silica; and low vitamin D, due to its immunomodulatory effects. Despite numerous studies looking at toxin exposure and connective tissue diseases, conclusive evidence is lacking, due to either rarity of exposure or rarity of disease.
22
Immunogenetic Aspects of Anca-Associated Vasculitides (Experimental and Clinical Immunogenetics (Experimental & Clinical Immunogenetics). S Karger Pub, 1998.
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