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

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

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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2

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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3

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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4

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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5

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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6

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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8

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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9

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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10

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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11

HISAYAMA, FUMIKO. "A case of Churg-Strauss syndrome showing anti-neutrophil cytoplasm antibody positivity." Nihon Naika Gakkai Zasshi 84, no. 8 (1995): 1327–28. http://dx.doi.org/10.2169/naika.84.1327.

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12

Koselj-Kajtna, M., M. Koselj, T. Rott, A. Kandus, and A. Bren. "Infectious complications of immunosuppressive treatment for anti-neutrophil cytoplasm antibody-related vasculitis." Transplantation Proceedings 34, no. 7 (November 2002): 3001–2. http://dx.doi.org/10.1016/s0041-1345(02)03514-5.

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13

Jayne, David, Michael Walsh, Peter A. Merkel, Chen Au Peh, Wladimir Szpirt, Xavier Puéchal, Shouichi Fujimoto, et al. "Plasma exchange and glucocorticoids to delay death or end-stage renal disease in anti-neutrophil cytoplasm antibody-associated vasculitis: PEXIVAS non-inferiority factorial RCT." Health Technology Assessment 26, no. 38 (September 2022): 1–60. http://dx.doi.org/10.3310/pnxb5040.

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Background Anti-neutrophil cytoplasm antibody-associated vasculitis is a multisystem, autoimmune disease that causes organ failure and death. Physical removal of pathogenic autoantibodies by plasma exchange is recommended for severe presentations, along with high-dose glucocorticoids, but glucocorticoid toxicity contributes to morbidity and mortality. The lack of a robust evidence base to guide the use of plasma exchange and glucocorticoid dosing contributes to variation in practice and suboptimal outcomes. Objectives We aimed to determine the clinical efficacy of plasma exchange in addition to immunosuppressive therapy and glucocorticoids with respect to death and end-stage renal disease in patients with severe anti-neutrophil cytoplasm antibody-associated vasculitis. We also aimed to determine whether or not a reduced-dose glucocorticoid regimen was non-inferior to a standard-dose regimen with respect to death and end-stage renal disease. Design This was an international, multicentre, open-label, randomised controlled trial. Patients were randomised in a two-by-two factorial design to receive either adjunctive plasma exchange or no plasma exchange, and either a reduced or a standard glucocorticoid dosing regimen. All patients received immunosuppressive induction therapy with cyclophosphamide or rituximab. Setting Ninety-five hospitals in Europe, North America, Australia/New Zealand and Japan participated. Participants Participants were aged ≥ 16 years with a diagnosis of granulomatosis with polyangiitis or microscopic polyangiitis, and either proteinase 3 anti-neutrophil cytoplasm antibody or myeloperoxidase anti-neutrophil cytoplasm antibody positivity, and a glomerular filtration rate of < 50 ml/minute/1.73 m2 or diffuse alveolar haemorrhage attributable to active anti-neutrophil cytoplasm antibody-associated vasculitis. Interventions Participants received seven sessions of plasma exchange within 14 days or no plasma exchange. Oral glucocorticoids commenced with prednisolone 1 mg/kg/day and were reduced over different lengths of time to 5 mg/kg/day, such that cumulative oral glucocorticoid exposure in the first 6 months was 50% lower in patients allocated to the reduced-dose regimen than in those allocated to the standard-dose regimen. All patients received the same glucocorticoid dosing from 6 to 12 months. Subsequent dosing was at the discretion of the treating physician. Primary outcome The primary outcome was a composite of all-cause mortality and end-stage renal disease at a common close-out when the last patient had completed 10 months in the trial. Results The study recruited 704 patients from June 2010 to September 2016. Ninety-nine patients died and 138 developed end-stage renal disease, with the primary end point occurring in 209 out of 704 (29.7%) patients: 100 out of 352 (28%) in the plasma exchange group and 109 out of 352 (31%) in the no plasma exchange group (adjusted hazard ratio 0.86, 95% confidence interval 0.65 to 1.13; p = 0.3). In the per-protocol analysis for the non-inferiority glucocorticoid comparison, the primary end point occurred in 92 out of 330 (28%) patients in the reduced-dose group and 83 out of 325 (26%) patients in the standard-dose group (partial-adjusted risk difference 0.023, 95% confidence interval 0.034 to 0.08; p = 0.5), thus meeting our non-inferiority hypothesis. Serious infections in the first year occurred in 96 out of 353 (27%) patients in the reduced-dose group and in 116 out of 351 (33%) patients in the standard-dose group. The rate of serious infections at 1 year was lower in the reduced-dose group than in the standard-dose group (incidence rate ratio 0.69, 95% confidence interval 0.52 to 0.93; p = 0.016). Conclusions Plasma exchange did not prolong the time to death and/or end-stage renal disease in patients with anti-neutrophil cytoplasm antibody-associated vasculitis with severe renal or pulmonary involvement. A reduced-dose glucocorticoid regimen was non-inferior to a standard-dose regimen and was associated with fewer serious infections. Future work A meta-analysis examining the effects of plasma exchange on kidney outcomes in anti-neutrophil cytoplasm antibody-associated vasculitis is planned. A health-economic analysis of data collected in this study to examine the impact of both plasma exchange and reduced glucocorticoid dosing is planned to address the utility of plasma exchange for reducing early end-stage renal disease rates. Blood and tissue samples collected in the study will be examined to identify predictors of response to plasma exchange in anti-neutrophil cytoplasm in antibody-associated vasculitis. The benefits associated with reduced glucocorticoid dosing will inform future studies of newer therapies to permit further reduction in glucocorticoid exposure. Data from this study will contribute to updated management recommendations for anti-neutrophil cytoplasm antibody-associated vasculitis. Limitations This study had an open-label design which may have permitted observer bias; however, the nature of the end points, end-stage renal disease and death, would have minimised this risk. Despite being, to our knowledge, the largest ever trial in anti-neutrophil cytoplasm antibody-associated vasculitis, there was an insufficient sample size to assess clinically useful benefits on the separate components of the primary end-point: end-stage renal disease and death. Use of a fixed-dose plasma exchange regimen determined by consensus rather than data-driven dose ranging meant that some patients may have been underdosed, thus reducing the therapeutic impact. In particular, no biomarkers have been identified to help determine dosing in a particular patient, although this is one of the goals of the biomarker plan of this study. Trial registration This trial is registered as ISRCTN07757494, EudraCT 2009-013220-24 and Clinicaltrials.gov NCT00987389. Funding This project was funded by the National Institute for Health and Care Research (NIHR) Health Technology Assessment programme and will be published in full in Health Technology Assessment; Vol. 26, No. 38. See the NIHR Journals Library website for further project information.

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14

Pusey, Charles D. "The Continuing Challenge of Anti-Neutrophil Cytoplasm Antibody–Associated Systemic Vasculitis and Glomerulonephritis." Journal of the American Society of Nephrology 17, no. 5 (April 19, 2006): 1221–23. http://dx.doi.org/10.1681/asn.2006030192.

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15

Guerry, M. J. C. J., P. Brogan, I. N. Bruce, D. P. D'Cruz, L. Harper, R. Luqmani, C. D. Pusey, et al. "Recommendations for the use of rituximab in anti-neutrophil cytoplasm antibody-associated vasculitis." Rheumatology 51, no. 4 (May 25, 2011): 634–43. http://dx.doi.org/10.1093/rheumatology/ker150.

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16

SAITO, MINEO. "A case of anti neutrophil cytoplasm antibody positive SLE died with large pneumonorrhagia." Nihon Naika Gakkai Zasshi 82, no. 11 (1993): 1884–86. http://dx.doi.org/10.2169/naika.82.1884.

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17

Pepper, Ruth J., Stephen P. McAdoo, Sarah M. Moran, Dearbhla Kelly, Jennifer Scott, Sally Hamour, Aine Burns, et al. "A novel glucocorticoid-free maintenance regimen for anti-neutrophil cytoplasm antibody–associated vasculitis." Rheumatology 58, no. 2 (January 21, 2019): 373. http://dx.doi.org/10.1093/rheumatology/kez001.

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18

Keogan, MT, VLM Esnault, AJ Green, CM Lockwood, and DL Brown. "Pathogenetic Mechanisms in Vasculitis, I: Anti-Neutrophil Cytoplasm Antibody (ANCA) Stimulates UN-Primed Neutrophils." Clinical Science 80, s24 (March 1, 1991): 33P. http://dx.doi.org/10.1042/cs080033pa.

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19

HAYES, M., and G. CAMBRIDGE. "An IgM class anti-neutrophil cytoplasm antibody inhibits neutrophil adhesion and apoptosis via a Syk dependent signaling cascade." Molecular Immunology 41, no. 4 (June 2004): 457–68. http://dx.doi.org/10.1016/j.molimm.2004.03.031.

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20

Zamoner, Welder, Pâmela Falbo dos Reis, and Vanessa dos Santos Silva. "Crescent IgA Nephropathy and its association with anti-neutrophil cytoplasm antibody: what do we know?" Brazilian Journal of Nephrology 44, no. 1 (March 2022): 1–2. http://dx.doi.org/10.1590/2175-8239-jbn-2022-e001.

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21

SAVIGE, J. A., M. GALLICCHIO, T. GEORGIOU, and D. J. DAVIES. "Diverse target antigens recognized by circulating antibodies in anti-neutrophil cytoplasm antibody-associated renal vasculitides." Clinical & Experimental Immunology 82, no. 2 (June 28, 2008): 238–43. http://dx.doi.org/10.1111/j.1365-2249.1990.tb05433.x.

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22

Lee, Ji Yeon, Ji Min Lee, Tae Han Lee, Hye Jin Jeong, Go Choi, Jin Nyeong Chae, Ji-Min Kim, and Sang-Hyon Kim. "Erratum: Title, Introduction: A Case of Propylthiouracil induced Anti-neutrophil Cytoplasm Antibody Positive Pyoderma Gangrenosum." Journal of Rheumatic Diseases 21, no. 4 (2014): 224. http://dx.doi.org/10.4078/jrd.2014.21.4.224.

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23

Patro, Pallavi, Vikas Agarwal, and Durga Prasanna Misra. "Comment on: A novel glucocorticoid-free maintenance regimen for anti-neutrophil cytoplasm antibody-associated vasculitis." Rheumatology 58, no. 6 (March 16, 2019): 1117–19. http://dx.doi.org/10.1093/rheumatology/kez036.

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24

Croft, Adam P., Stuart W. Smith, Sue Carr, Sajeda Youssouf, Alan D. Salama, Aine Burns, Charles D. Pusey, et al. "Successful outcome of pregnancy in patients with anti-neutrophil cytoplasm antibody–associated small vessel vasculitis." Kidney International 87, no. 4 (April 2015): 807–11. http://dx.doi.org/10.1038/ki.2014.329.

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25

Little, Mark A., Gurjeet Bhangal, C. Lucy Smyth, Marian T. Nakada, H. Terence Cook, Sussan Nourshargh, and Charles D. Pusey. "Therapeutic Effect of Anti–TNF-α Antibodies in an Experimental Model of Anti-Neutrophil Cytoplasm Antibody–Associated Systemic Vasculitis." Journal of the American Society of Nephrology 17, no. 1 (November 23, 2005): 160–69. http://dx.doi.org/10.1681/asn.2005060616.

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26

Tang, Sydney, Kwok-Wah Chan, Tak-Mao Chan, Sing-Leung Lui, and Ignatius K. P. Cheng. "Anti-Glomerular Basement Membrane and Anti-Neutrophil Cytoplasm Antibody-Positive Vasculitis Presenting with Peripheral Neuropathy and Acute Renal Failure." Nephron 79, no. 2 (1998): 225–26. http://dx.doi.org/10.1159/000045033.

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27

Pearce, Fiona A., Anthea Craven, Peter A. Merkel, Raashid A. Luqmani, and Richard A. Watts. "Global ethnic and geographic differences in the clinical presentations of anti-neutrophil cytoplasm antibody–associated vasculitis." Rheumatology 56, no. 11 (August 10, 2017): 1962–69. http://dx.doi.org/10.1093/rheumatology/kex293.

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28

Todd, S. K., R. J. Pepper, J. Draibe, A. Tanna, C. D. Pusey, C. Mauri, and A. D. Salama. "Regulatory B cells are numerically but not functionally deficient in anti-neutrophil cytoplasm antibody-associated vasculitis." Rheumatology 53, no. 9 (April 11, 2014): 1693–703. http://dx.doi.org/10.1093/rheumatology/keu136.

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29

Pepper, Ruth, David Jayne, Mark Little, Charles Pusey, and Alan D. Salama. "Comment on: A novel glucocorticoid-free maintenance regimen for anti-neutrophil cytoplasm antibody–associated vasculitis: reply." Rheumatology 58, no. 4 (January 15, 2019): 738–39. http://dx.doi.org/10.1093/rheumatology/key388.

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30

Salama, Alan, Ruth Pepper, Stephen Mcadoo, and Charles Pusey. "Comment on: A novel glucocorticoid-free maintenance regimen for anti-neutrophil cytoplasm antibody-associated vasculitis: reply." Rheumatology 58, no. 6 (March 16, 2019): 1119. http://dx.doi.org/10.1093/rheumatology/kez038.

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31

Tieu, Joanna, Susan Lester, Warren Raymond, Helen Keen, Catherine L. Hill, and Johannes Nossent. "Cancer in Anti‐Neutrophil Cytoplasm Antibody‐Associated Vasculitis and Polyarteritis Nodosa in Australia: A Population‐Based Study." ACR Open Rheumatology 4, no. 3 (December 7, 2021): 223–30. http://dx.doi.org/10.1002/acr2.11378.

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32

HOLLAND, M., P. HEWINS, M. GOODALL, D. ADU, R. JEFFERIS, and C. O. S. SAVAGE. "Anti-neutrophil cytoplasm antibody IgG subclasses in Wegener's granulomatosis: a possible pathogenic role for the IgG4 subclass." Clinical and Experimental Immunology 138, no. 1 (October 2004): 183–92. http://dx.doi.org/10.1111/j.1365-2249.2004.02566.x.

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33

Walsh, M., A. Chaudhry, and D. Jayne. "Long-term follow-up of relapsing/refractory anti-neutrophil cytoplasm antibody associated vasculitis treated with the lymphocyte depleting antibody alemtuzumab (CAMPATH-1H)." Annals of the Rheumatic Diseases 67, no. 9 (November 30, 2007): 1322–27. http://dx.doi.org/10.1136/ard.2007.081661.

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34

Prendecki, Maria, Tom Cairns, and Charles D. Pusey. "Familial vasculitides: granulomatosis with polyangitis and microscopic polyangitis in two brothers with differing anti-neutrophil cytoplasm antibody specificity." Clinical Kidney Journal 9, no. 3 (April 14, 2016): 429–31. http://dx.doi.org/10.1093/ckj/sfw016.

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35

WILLIAMS, Julie M., Lavanya KAMESH, and Caroline O. S. SAVAGE. "Translating basic science into patient therapy for ANCA-associated small vessel vasculitis." Clinical Science 108, no. 2 (January 21, 2005): 101–12. http://dx.doi.org/10.1042/cs20040232.

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ANCA (anti-neutrophil cytoplasm antibody)-associated small vessel vasculitis is an inflammatory condition associated with the production of autoantibodies to neutrophil cytoplasmic components. The disorder results in destruction of the microvasculature, infiltration of neutrophils into tissues, which is followed later by mononuclear cells, leading to injury and the formation of granulomatous lesions. Initiators for the disease are undetermined but a pro-inflammatory environment is required. Other influencing factors may include environmental triggers, genetic propensity or infectious agents. The primary cellular event in the condition involves the neutrophils, which are likely to be responsible for the majority of tissue injury. Binding of the autoantibody to neutrophils initiates cell activation via a complex intracellular signalling cascade, culminating in the release of pro-inflammatory mediators, proteolytic enzymes and reactive oxygen species. Adhesion of neutrophils to endothelial cells is observed in vitro and more investigations in this area may explain the focussing of the disease to certain vessels/tissues. Current treatment regimens have substantial toxicity. Although newer developments are an improvement there is still a pressing need for more targeted therapies, which could be provided by extrapolating information emerging from basic scientific research.

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36

Walsh, M., and D. Jayne. "Rituximab in the treatment of anti-neutrophil cytoplasm antibody associated vasculitis and systemic lupus erythematosus: past, present and future." Kidney International 72, no. 6 (September 2007): 676–82. http://dx.doi.org/10.1038/sj.ki.5002395.

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37

McAdoo, Stephen P., Nicholas Medjeral-Thomas, Seerapani Gopaluni, Anisha Tanna, Nicholas Mansfield, Jack Galliford, Megan Griffith, et al. "Long-term follow-up of a combined rituximab and cyclophosphamide regimen in renal anti-neutrophil cytoplasm antibody-associated vasculitis." Nephrology Dialysis Transplantation 34, no. 1 (February 14, 2018): 63–73. http://dx.doi.org/10.1093/ndt/gfx378.

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38

McAdoo, Stephen P., Nicholas Medjeral-Thomas, Seerapani Gopaluni, Anisha Tanna, Nicholas Mansfield, Jack Galliford, Megan Griffith, et al. "Long-term follow-up of a combined rituximab and cyclophosphamide regimen in renal anti-neutrophil cytoplasm antibody-associated vasculitis." Nephrology Dialysis Transplantation 33, no. 5 (March 30, 2018): 899. http://dx.doi.org/10.1093/ndt/gfy075.

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39

Pagano, Rosana L., Maria Angela Amorim Dias, Camila S. Dale, and Renata Giorgi. "Neutrophils and the calcium-binding protein MRP-14 mediate carrageenan-induced antinociception in mice." Mediators of Inflammation 11, no. 4 (2002): 203–10. http://dx.doi.org/10.1080/0962935029000050.

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Background: We have previously shown that the calcium-binding protein MRP-14 secreted by neutrophils mediates the antinociceptive response in an acute inflammatory model induced by the intraperitoneal injection of glycogen in mice.Aim: In an attempt to broaden the concept that neutrophils and MRP-14 controls inflammatory pain induced by different type of irritants, in the present study, after demonstrating that carrageenan (Cg) also induces atinociception in mice, we investigated the participation of both neutrophils and MRP-14 in the phenomenon.Methods: Male Swiss mice were injected intraperitoneally with Cg and after different time intervals, the pattern of cell migration of the peritoneal exudate and the nociceptive response of animals submitted to the writhing test were evaluated. The participation of neutrophils and of the MRP-14 on the Cg effect was evaluated by systemic inoculation of monoclonal antibodies anti-granulocyte and anti-MRP-14.Results: Our results demonstrate that the acute neutrophilic peritonitis evoked by Cg induced antinociception 2, 4 and 8 h after inoculation of the irritant. Monoclonal antibodies anti-granulocyte or anti-MRP-14 reverts the antinociceptive response only 2 and 8 h after Cg injection. The antibody anti-MRP-14 partially reverts the antinociception observed after 4 h of Cg injection while the anti-granulocyte antibody enhances this effect. This effect is reverted by simultaneous treatment of the animals with both antibodies. After 4 h of Cg injection in neutrophil-depleted mice a significant expression of the calcium-binding protein MRP-14 was detected in the cytoplasm of peritoneal macrophages. This suggests that the enhancement of the effect observed after treatment with the anti-neutrophil antibody may be due to secretion of MRP-14 by macrophages. It has also been demonstrated that endogenous opioids and glucocorticoids are not involved in the antinociception observed at the 4th hour after Cg injection.Conclusion: These data support the hypothesis that neutrophils and the calcium-binding protein MRP-14 are participants of the endogenous control of inflammatory pain in mice despite the model of acute inflammation used.

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Jin, Shanshan, Danqiong Wang, Jian Luo, Weiwen Zhang, and Meng Wu. "Diffuse alveolar hemorrhage in a patient with anti-neutrophil cytoplasm antibody-associated vasculitis successfully treated with immunoadsorption combined with methylprednisolone." Medicina Clínica 158, no. 3 (February 2022): 133–36. http://dx.doi.org/10.1016/j.medcli.2021.08.004.

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41

Jin, Shanshan, Danqiong Wang, Jian Luo, Weiwen Zhang, and Meng Wu. "Diffuse alveolar hemorrhage in a patient with anti-neutrophil cytoplasm antibody-associated vasculitis successfully treated with immunoadsorption combined with methylprednisolone." Medicina Clínica (English Edition) 158, no. 3 (February 2022): 133–36. http://dx.doi.org/10.1016/j.medcle.2021.08.011.

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42

Tanna, Anisha, Laura Guarino, Frederick W. K. Tam, Beatriz Rodriquez-Cubillo, Jeremy B. Levy, Tom D. Cairns, Megan Griffith, et al. "Long-term outcome of anti-neutrophil cytoplasm antibody-associated glomerulonephritis: evaluation of the international histological classification and other prognostic factors." Nephrology Dialysis Transplantation 30, no. 7 (July 12, 2014): 1185–92. http://dx.doi.org/10.1093/ndt/gfu237.

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43

Brezina, B., and D. Jayne. "Plasma exchange and glucocorticoid dosing in the treatment of anti-neutrophil cytoplasm antibody associated vasculitis: A randomized controlled trial. PEXIVAS." La Presse Médicale 42, no. 4 (April 2013): 772. http://dx.doi.org/10.1016/j.lpm.2013.02.285.

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44

Prendecki, Maria, and Charles D. Pusey. "Recent advances in understanding of the pathogenesis of ANCA-associated vasculitis." F1000Research 7 (July 19, 2018): 1113. http://dx.doi.org/10.12688/f1000research.14626.1.

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Anti-neutrophil cytoplasm antibody (ANCA)-associated vasculitides (AAV) are rare systemic autoimmune diseases characterised by inflammation of small blood vessels. Recent developments have been made in our understanding of the pathogenesis of these diseases, including the pathogenic role of ANCA, neutrophils and monocytes as mediators of injury, dysregulation of the complement system, and the role of T and B cells. Current treatment strategies for AAV are based on broad immunosuppression, which may have significant side effects. Advances in understanding of the pathogenesis of disease have led to the identification of new therapeutic targets which may lead to treatment protocols with less-toxic side effects. The aim of this review is to summarise current information and recent advances in understanding of the pathogenesis of AAV.

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45

Hellmich, B., O. Flossmann, W. L. Gross, P. Bacon, J. Willem Cohen-Tervaert, L. Guillevin, D. Jayne, et al. "EULAR recommendations for conducting clinical studies and/or clinical trials in systemic vasculitis: focus on anti-neutrophil cytoplasm antibody-associated vasculitis." Annals of the Rheumatic Diseases 66, no. 5 (May 1, 2007): 605–17. http://dx.doi.org/10.1136/ard.2006.062711.

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46

Kronbichler, Andreas, and David R. W. Jayne. "Estimating the epidemiology of anti-neutrophil cytoplasm antibody-associated renal vasculitis and the role of histologic chronicity in predicting renal outcomes." Nephrology Dialysis Transplantation 34, no. 9 (January 14, 2019): 1429–32. http://dx.doi.org/10.1093/ndt/gfy402.

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47

Prendecki, Maria, Stephen P. McAdoo, and Charles D. Pusey. "Is There a Role for Plasma Exchange in ANCA-Associated Vasculitis?" Current Treatment Options in Rheumatology 6, no. 4 (September 12, 2020): 313–24. http://dx.doi.org/10.1007/s40674-020-00161-y.

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Abstract Purpose of review This review summarises the evidence for the use of therapeutic plasma exchange (TPE) in anti-neutrophil cytoplasm antibody (ANCA)–associated vasculitis. TPE is an extra-corporeal treatment which efficiently removes IgG and other pathogenic small molecules from the blood. There are several mechanistic reasons why this should be of benefit in AAV including the well-described pathogenicity of ANCA. Recent findings The recently published PEXIVAS trial is the largest study of TPE in AAV to date. It did not show a benefit for adjunctive TPE on a primary end point of ESRD or death. There was no difference in serious adverse events between those treated with TPE and those treated with immunosuppressive drugs alone. Conclusions Based on the results of PEXIVAS, most patients with AAV should not be treated with adjunctive TPE. However, there are subgroups of patients with AAV for whom TPE may still be of benefit, including those with double positivity for anti-GBM antibodies and ANCA.

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Robson, J., H. Doll, R. Suppiah, O. Flossmann, L. Harper, P. Hoglund, D. Jayne, A. Mahr, K. Westman, and R. Luqmani. "Glucocorticoid treatment and damage in the anti-neutrophil cytoplasm antibody-associated vasculitides: long-term data from the European Vasculitis Study Group trials." Rheumatology 54, no. 3 (September 8, 2014): 471–81. http://dx.doi.org/10.1093/rheumatology/keu366.

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Walsh, Michael, Peter A. Merkel, Chen Au Peh, Wladimir Szpirt, Loïc Guillevin, Charles D. Pusey, Janak deZoysa, et al. "Plasma exchange and glucocorticoid dosing in the treatment of anti-neutrophil cytoplasm antibody associated vasculitis (PEXIVAS): protocol for a randomized controlled trial." Trials 14, no. 1 (2013): 73. http://dx.doi.org/10.1186/1745-6215-14-73.

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Plastiras, Sotiris C., and Haralampos M. Moutsopoulos. "Arrhythmias and Conduction Disturbances in Autoimmune Rheumatic Disorders." Arrhythmia & Electrophysiology Review 10, no. 1 (April 12, 2021): 17–25. http://dx.doi.org/10.15420/aer.2020.43.

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Abstract:

Rhythm and conduction disturbances and sudden cardiac death are important manifestations of cardiac involvement in autoimmune rheumatic diseases (ARD), which have a serious impact on morbidity and mortality. While the underlying arrhythmogenic mechanisms are multifactorial, myocardial fibrosis plays a pivotal role. It accounts for a substantial portion of cardiac mortality and may manifest as atrial and ventricular arrhythmias, conduction system abnormalities, biventricular cardiac failure or sudden death. In patients with ARD, myocardial fibrosis is considered to be the hallmark of cardiac involvement as a result of inflammatory process or to coronary artery occlusive disease. Myocardial fibrosis constitutes the pathological substrates for reentrant circuits. The presence of supraventricular extra systoles, tachyarrhythmias, ventricular activity and conduction disturbances are not uncommon in patients with ARDs, more often in systemic lupus erythematosus, systemic sclerosis, rheumatoid arthritis, inflammatory muscle disorders and anti-neutrophil cytoplasm antibody-associated vasculitis. In this review, the type, the relative prevalence and the underlying mechanisms of rhythm and conduction disturbances in the emerging field of cardiorheumatology are provided.

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