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76 results on '"Monach, P. A."'

1. A study of implementation factors for a novel approach to clinical trials: constructs for consideration in the coordination of direct-to-patient online-based medical research

Author

Cronholm, Peter F., Applequist, Janelle, Krischer, Jeffrey, Fontenot, Ebony, Davis, Trocon, Burroughs, Cristina, McAlear, Carol A., Borchin, Renée, Kullman, Joyce, Carette, Simon, Khalidi, Nader, Koening, Curry, Langford, Carol A., Monach, Paul, Moreland, Larry, Pagnoux, Christian, Specks, Ulrich, Sreih, Antoine G., Ytterberg, Steven R., and Merkel, Peter A.

Published
2024
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2. The Association Between Age at Diagnosis and Disease Characteristics and Damage in Patients With ANCA-Associated Vasculitis.

Author

Corbridge, Thomas, Khalidi, Nader, Koening, Curry, Langford, Carol, McAlear, Carol, Monach, Paul, Moreland, Larry, Pagnoux, Christian, Rhee, Rennie, Seo, Philip, Silver, Jared, Specks, Ulrich, Warrington, Kenneth, Wechsler, Michael, Merkel, Peter, Bloom, Jessica, Pickett-Nairn, Kaci, Silveira, Lori, Fuhlbrigge, Robert, Cuthbertson, David, and Akuthota, Praveen

Subjects
Child, Middle Aged, Young Adult, Humans, Female, Aged, Male, Antibodies, Antineutrophil Cytoplasmic, Prospective Studies, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, Granulomatosis with Polyangiitis, Microscopic Polyangiitis, Hemorrhage, Churg-Strauss Syndrome
Abstract

OBJECTIVE: This study examined the relationship between age at diagnosis and disease characteristics and damage in patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). METHODS: Analysis of a prospective longitudinal cohort of patients with granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic GPA (EGPA) in the Vasculitis Clinical Research Consortium (2013-2021). Disease cohorts were divided by age at diagnosis (years): children (65). Data included demographics, ANCA type, clinical characteristics, Vasculitis Damage Index (VDI) scores, ANCA Vasculitis Index of Damage (AVID) scores, and novel disease-specific and non-disease-specific damage scores built from VDI and AVID items. RESULTS: Analysis included data from 1020 patients with GPA/MPA and 357 with EGPA. Female predominance in GPA/MPA decreased with age at diagnosis. AAV in childhood was more often GPA and proteinase 3-ANCA positive. Children with GPA/MPA experienced more subglottic stenosis and alveolar hemorrhage; children and young adults with EGPA experienced more alveolar hemorrhage, need for intubation, and gastrointestinal involvement. Older adults (GPA/MPA) had more neurologic manifestations. After adjusting for disease duration, medications, tobacco, and ANCA, all damage scores increased with age at diagnosis for GPA/MPA (P

Published
2023

3. Hypothyroidism in vasculitis.

Author

Kermani, Tanaz, Cuthbertson, David, Carette, Simon, Khalidi, Nader, Koening, Curry, Langford, Carol, McAlear, Carol, Monach, Paul, Moreland, Larry, Pagnoux, Christian, Seo, Philip, Specks, Ulrich, Sreih, Antoine, Warrington, Kenneth, and Merkel, Peter

Subjects
GCA, Takayasu’s arteritis, antineutrophil cytoplasmic antibody, eosinophilic granulomatosis with polyangiitis, granulomatosis with polyangiitis, hypothyroidism, microscopic polyangiitis, polyarteritis nodosa, vasculitis, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, Antibodies, Antineutrophil Cytoplasmic, Churg-Strauss Syndrome, Female, Granulomatosis with Polyangiitis, Humans, Hypothyroidism, Longitudinal Studies, Male, Microscopic Polyangiitis, Middle Aged, Prospective Studies
Abstract

OBJECTIVE: To study the prevalence, risk and clinical associations of hypothyroidism among several forms of vasculitis. METHODS: Patients with GCA, Takayasus arteritis (TAK), PAN and the three forms of ANCA-associated vasculitis [AAV; granulomatosis with polyangiitis (GPA), microscopic polyangiitis and eosinophilic granulomatosis with polyangiitis (EGPA)] enrolled in a prospective, multicentre, longitudinal study were included. RESULTS: The study included data on 2085 patients [63% female, 90% White] with a mean age of 54.6 years (s.d. 17.2). Diagnoses were GCA (20%), TAK (11%), PAN (5%), GPA (42%), microscopic polyangiitis (8%) and EGPA (14%). Hypothyroidism was present in 217 patients (10%) (83% female), with a mean age 59.8 years (s.d. 14.5). Age- and sex-adjusted risk of hypothyroidism was GCA, odds ratio (OR) 0.61 (95% CI 0.41, 0.90); TAK, OR 0.57 (95% CI 0.31, 1.03); PAN, OR 0.59 (95% CI 0.25, 1.38); GPA, OR 1.51 (95% CI 1.12, 2.05); microscopic polyangiitis, OR 1.81 (95% CI 1.18, 2.80) and EGPA, OR 0.82 (95% CI 0.52, 1.30). Among patients with AAV, age- and sex-adjusted risk of hypothyroidism was higher with positive MPO-ANCA [OR 1.89 (95% CI 1.39, 2.76)]. The clinical manifestations of vasculitis were similar in patients with and without hypothyroidism, except transient ischaemic attacks, which were more frequently observed in patients with GCA and hypothyroidism (12% vs 2%; P = 0.001). CONCLUSIONS: Differences in the risk of hypothyroidism among vasculitides may be due to genetic susceptibilities or immune responses. This study confirms an association of hypothyroidism with MPO-ANCA.

Published
2022

4. Renal Recovery for Patients with ANCA-Associated Vasculitis and Low eGFR in the ADVOCATE Trial of Avacopan

Author

Peh, C. Au, Chakera, A., Cooper, B., Kurtkoti, J., Langguth, D., Levidiotis, V., Luxton, G., Mount, P., Mudge, D., Noble, E., Phoon, R., Ranganathan, D., Ritchie, A., Ryan, J., Suranyi, M., Rosenkranz, A., Lhotta, K., Kronbichler, A., Demoulin, N., Bovy, C., Hellemans, R., Hougardy, J., Sprangers, B., Wissing, K., Pagnoux, C., Barbour, S., Brachemi, S., Cournoyer, S., Girard, L., Laurin, L., Liang, P., Philibert, D., Walsh, M., Tesar, V., Becvar, R., Horak, P., Rychlik, I., Szpirt, W., Dieperink, H., Gregersen, J., Ivarsen, P., Krarup, E., Lyngsoe, C., Rigothier, C., Augusto, J., Belot, A., Chauveau, D., Cornec, D., Jourde-Chiche, N., Ficheux, M., Karras, A., Klein, A., Maurier, F., Mesbah, R., Moranne, O., Neel, A., Quemeneur, T., Saadoun, D., Terrier, B., Zaoui, P., Schaier, M., Benck, U., Bergner, R., Busch, M., Floege, J., Grundmann, F., Haller, H., Haubitz, M., Hellmich, B., Henes, J., Hohenstein, B., Hugo, C., Iking-Konert, C., Arndt, F., Kubacki, T., Kotter, I., Lamprecht, P., Lindner, T., Halbritter, J., Mehling, H., Schönermarck, U., Venhoff, N., Vielhauer, V., Witzke, O., Szombati, I., Szucs, G., Garibotto, G., Alberici, F., Brunetta, E., Dagna, L., De Vita, S., Emmi, G., Gabrielli, A., Manenti, L., Pieruzzi, F., Roccatello, D., Salvarani, C., Dobashi, H., Atsumi, T., Fujimoto, S., Hagino, N., Ihata, A., Kaname, S., Kaneko, Y., Katagiri, A., Katayama, M., Kirino, Y., Kitagawa, K., Komatsuda, A., Kono, H., Kurasawa, T., Matsumura, R., Mimura, T., Morinobu, A., Murakawa, Y., Naniwa, T., Nanki, T., Ogawa, N., Oshima, H., Sada, K., Sugiyama, E., Takeuchi, T., Taki, H., Tamura, N., Tsukamoto, T., Yamagata, K., Yamamura, M., van Daele, P., Rutgers, A., Teng, Y., Walker, R., Chua, I., Collins, M., Rabindranath, K., de Zoysa, J., Svensson, M., Grevbo, B., Kalstad, S., Little, M., Clarkson, M., Molloy, E., Pamplona, I. Agraz, Anton, J., Lucia, V. Barrio, Ciggaran, S., Cid, M. Cinta, Encarnacion, M. Diaz, Oliveras, X. Fulladosa, Soler, M. Jose, Rusinol, H. Marco, Praga, M., Porras, L. Quintana, Segarra, A., Bruchfeld, A., Segelmark, M., Soveri, I., Thomaidi, E., Westman, K., Neumann, T., Burnier, M., Daikeler, T., Dudler, J., Hauser, T., Seeger, H., Vogt, B., Jayne, D., Burton, J., Al Jayyousi, R., Amin, T., Andrews, J., Baines, L., Brogan, P., Dasgupta, B., Doulton, T., Flossmann, O., Griffin, S., Harper, J., Harper, L., Kidder, D., Klocke, R., Lanyon, P., Luqmani, R., McLaren, J., Makanjuola, D., McCann, L., Nandagudi, A., Selvan, S., O'Riordan, E., Patel, M., Patel, R., Pusey, C., Rajakariar, R., Robson, J., Robson, M., Salama, A., Smyth, L., Sznajd, J., Taylor, J., Merkel, P., Sreih, A., Belilos, E., Bomback, A., Carlin, J., Chen Lin, Y. Chang, Derebail, V., Dragoi, S., Dua, A., Forbess, L., Geetha, D., Gipson, P., Gohh, R., Greenwood, G.T., Hugenberg, S., Jimenez, R., Kaskas, M., Kermani, T., Kivitz, A., Koening, C., Langford, C., Marder, G., Mohamed, A., Monach, P., Neyra, N., Niemer, G., Niles, J., Obi, R., Owens, C., Parks, D., Podoll, A., Rovin, B., Sam, R., Shergy, W., Silva, A., Specks, U., Spiera, R., Springer, J., Striebich, C., Swarup, A., Thakar, S., Tiliakos, A., Tsai, Y., Waguespack, D., Wasko, M. Chester, Cortazar, Frank B., Niles, John L., Jayne, David R.W., Merkel, Peter A., Bruchfeld, Annette, Yue, Huibin, Schall, Thomas J., and Bekker, Pirow

Published
2023
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5. Arterial lesions in giant cell arteritis: A longitudinal study.

Author

Kermani, Tanaz, Diab, Sehriban, Sreih, Antoine, Cuthbertson, David, Borchin, Renée, Carette, Simon, Forbess, Lindsy, Koening, Curry, McAlear, Carol, Monach, Paul, Moreland, Larry, Pagnoux, Christian, Seo, Philip, Spiera, Robert, Warrington, Kenneth, Ytterberg, Steven, Langford, Carol, Merkel, Peter, and Khalidi, Nader

Subjects
Aortic aneurysm, Computed tomography angiography, Disease activity, Giant cell arteritis, Large-artery stenosis, Magnetic resonance angiography, Aged, Aorta, Thoracic, Axillary Artery, Computed Tomography Angiography, Female, Giant Cell Arteritis, Humans, Longitudinal Studies, Magnetic Resonance Angiography, Male, Middle Aged, Subclavian Artery
Abstract

OBJECTIVES: To evaluate large-vessel (LV) abnormalities on serial imaging in patients with giant cell arteritis (GCA) and discern predictors of new lesions. METHODS: Clinical and imaging data from patients with GCA (including subjects diagnosed by LV imaging) enrolled in a prospective, multicenter, longitudinal study and/or a randomized clinical trial were included. New arterial lesions were defined as a lesion in a previously unaffected artery. RESULTS: The study included 187 patients with GCA, 146 (78%) female, mean (±SD) age at diagnosis 68.5 ± 8.5 years; 39% diagnosed by LV imaging. At least one arterial lesion was present in 123 (66%) on the first study. The most frequently affected arteries were subclavian (42%), axillary (32%), and thoracic aorta (20%). In 106 patients (57%) with serial imaging, new arterial lesions were noted in 41 patients (39%), all of whom had a baseline abnormality, over a mean (±SD) follow-up of 4.39 (2.22) years. New abnormalities were observed in 33% patients by year 2; clinical features of active disease were present at only 50% of these cases. There were no differences in age, sex, temporal artery biopsy positivity, or disease activity in patients with or without new lesions. CONCLUSIONS: In this cohort of patients with GCA, LV abnormalities on first imaging were common. Development of new arterial lesions occurred in patients with arterial abnormalities at first imaging, often in the absence of symptoms of active disease. Arterial imaging should be considered in all patients with GCA at diagnosis and serial imaging at least in patients with baseline abnormalities.

Published
2019

6. Evaluation of damage in giant cell arteritis.

Author

Kermani, Tanaz, Sreih, Antoine, Cuthbertson, David, Carette, Simon, Hoffman, Gary, Khalidi, Nader, Koening, Curry, Langford, Carol, McAlear, Carol, Monach, Paul, Moreland, Larry, Pagnoux, Christian, Seo, Philip, Warrington, Kenneth, Ytterberg, Steven, and Merkel, Peter

Subjects
damage, giant cell arteritis, large-artery manifestations, large-vessel vasculitis, vasculitis, Aged, Eye Diseases, Female, Follow-Up Studies, Giant Cell Arteritis, Humans, Intermittent Claudication, Longitudinal Studies, Male, Middle Aged, Odds Ratio, Prospective Studies, Recurrence, Risk Factors, Severity of Illness Index, Time Factors
Abstract

OBJECTIVES: To evaluate damage and variables associated with damage in GCA. METHODS: Patients with GCA enrolled in a prospective, multicentre, longitudinal study were included. Per-protocol assessments were made with the Vasculitis Damage Index and the Large-Vessel Vasculitis Index of Damage. RESULTS: The study included 204 patients: 156 women (76%), mean age at diagnosis 71.3 years (s.d. 8.3), mean follow-up of 3.5 years (s.d. 1.9). One or more damage item was present in 54% at baseline and 79% at the last follow-up on the Vasculitis Damage Index, and 60% at baseline and 82% at the last follow-up on the Large-Vessel Vasculitis Index of Damage. The most frequently observed damage items were large-artery complications (29% cohort) and ocular (22%). Among 117 patients with new damage, most new items were ocular (63 patients), cardiac/vascular (48) and musculoskeletal (34). Of these, treatment-associated items were frequently observed, including cataracts (46 patients), osteoporosis (22) and weight gain (22). Disease-associated new damage included ischaemic optic neuropathy (3 patients), limb claudication (13), arterial occlusions (10) and damage requiring vascular intervention (10). In univariate analysis, the risk of damage increased 22% for every additional year of disease duration [odds ratio (OR) 1.22 (95% CI 1.04, 1.45)]. In 94 patients enrolled within ⩽90 days of diagnosis of GCA, the risk of new damage at the last follow-up decreased 30% for each additional relapse [OR 0.70 (95% CI 0.51, 0.97)]. CONCLUSIONS: Large-artery complications and ocular manifestations are the most commonly occurring items of damage in GCA. Most new damage is associated with treatment. These findings emphasize the cumulative burden of disease in GCA.

Published
2018

7. Neutrophil activation in patients with anti-neutrophil cytoplasmic autoantibody-associated vasculitis and large-vessel vasculitis

Author

Michailidou, Despina, Duvvuri, Bhargavi, Kuley, Runa, Cuthbertson, David, Grayson, Peter C., Khalidi, Nader A., Koening, Curry L., Langford, Carol A., McAlear, Carol A., Moreland, Larry W., Pagnoux, Christian, Seo, Philip, Specks, Ulrich, Sreih, Antoine G., Warrington, Kenneth J., Mustelin, Tomas, Monach, Paul A., Merkel, Peter A., and Lood, Christian

Published
2022
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9. POS1428 GIANT CELL ARTERITIS SIGNS AND SYMPTOMS LEXICON: AN INTERNATIONAL EXPERT CONSENSUS

Author

Soowamber, M., primary, Bond, M., additional, Touma, Z., additional, Ramiro, S., additional, Langford, C., additional, Sanchez-Alvarez, C., additional, Abril, A., additional, Aydin, S., additional, Buttgereit, F., additional, Camellino, D., additional, Cid, M. C., additional, Grayson, P., additional, Hellmich, B., additional, Kermani, T., additional, Khalidi, N., additional, Lichliter, W., additional, Mackie, S., additional, Matteson, E., additional, Maz, M., additional, Merkel, P. A., additional, Monach, P. A., additional, Neill, L., additional, Ponte, C., additional, Salvarani, C., additional, Schmidt, W. A., additional, Villiger, P., additional, Warrington, K. J., additional, Whitlock, M., additional, and Dejaco, C., additional

Published
2024
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11. The Birmingham Vasculitis Activity Score as a Measure of Disease Activity in Patients with Giant Cell Arteritis.

Author

Kermani, Tanaz, Cuthbertson, David, Carette, Simon, Hoffman, Gary, Khalidi, Nader, Koening, Curry, Langford, Carol, McKinnon-Maksimowicz, Kathleen, McAlear, Carol, Monach, Paul, Seo, Philip, Warrington, Kenneth, Ytterberg, Steven, Merkel, Peter, and Matteson, Eric

Subjects
BIRMINGHAM VASCULITIS ACTIVITY SCORE, COHORT STUDY, DISEASE ACTIVITY, GIANT CELL ARTERITIS, Aged, Aged, 80 and over, Female, Giant Cell Arteritis, Humans, Longitudinal Studies, Male, Middle Aged, Prospective Studies, Severity of Illness Index, Symptom Assessment
Abstract

OBJECTIVE: To evaluate the performance of the Birmingham Vasculitis Activity Score (BVAS) in the assessment of disease activity in giant cell arteritis (GCA). METHODS: Patients with GCA enrolled in a prospective, multicenter, longitudinal study with symptoms of active vasculitis during any visit were included. Spearmans rank correlation was used to explore the association of the BVAS with other measures of disease activity. RESULTS: During a mean (SD) followup of 2.3 (1.6) years, symptoms of active GCA were present in 236 visits in 136 subjects (100 female, 74%). Median (range) BVAS1 (new/worse symptoms) was 1 (0-10) and median (range) BVAS2 (persistent symptoms) was 0 (0-5). Median (range) physicians global assessment (PGA) was 4 (0-9) for disease activity in the past 28 days and 2 (0-9) for activity on the day of the visit. Important ischemic manifestations of active vasculitis not recorded by the BVAS included tongue/jaw claudication (27%), upper extremity claudication (15%), lower extremity claudication (5%), carotidynia (7%), and ischemic retinopathy (5%). During 25 visits (11%) with active disease, all symptoms of active vasculitis were placed in the Other category yet still resulted in a BVAS1 and BVAS2 of 0. BVAS1 moderately correlated with PGA for the past 28 days (Spearmans correlation 0.50) and physician-rated disease activity for the past 28 days (Spearmans correlation 0.46). CONCLUSION: The BVAS has limited utility in GCA. Patients with active GCA can have a BVAS of 0. Many important ischemic symptoms attributable to active vasculitis are not included in the composite score.

Published
2016

12. Renal Recovery for Patients with ANCA-Associated Vasculitis and Low eGFR in the ADVOCATE Trial of Avacopan

Author

Cortazar, F, Niles, J, Jayne, D, Merkel, P, Bruchfeld, A, Yue, H, Schall, T, Bekker, P, Peh, C, Chakera, A, Cooper, B, Kurtkoti, J, Langguth, D, Levidiotis, V, Luxton, G, Mount, P, Mudge, D, Noble, E, Phoon, R, Ranganathan, D, Ritchie, A, Ryan, J, Suranyi, M, Rosenkranz, A, Lhotta, K, Kronbichler, A, Demoulin, N, Bovy, C, Hellemans, R, Hougardy, J, Sprangers, B, Wissing, K, Pagnoux, C, Barbour, S, Brachemi, S, Cournoyer, S, Girard, L, Laurin, L, Liang, P, Philibert, D, Walsh, M, Tesar, V, Becvar, R, Horak, P, Rychlik, I, Szpirt, W, Dieperink, H, Gregersen, J, Ivarsen, P, Krarup, E, Lyngsoe, C, Rigothier, C, Augusto, J, Belot, A, Chauveau, D, Cornec, D, Jourde-Chiche, N, Ficheux, M, Karras, A, Klein, A, Maurier, F, Mesbah, R, Moranne, O, Neel, A, Quemeneur, T, Saadoun, D, Terrier, B, Zaoui, P, Schaier, M, Benck, U, Bergner, R, Busch, M, Floege, J, Grundmann, F, Haller, H, Haubitz, M, Hellmich, B, Henes, J, Hohenstein, B, Hugo, C, Iking-Konert, C, Arndt, F, Kubacki, T, Kotter, I, Lamprecht, P, Lindner, T, Halbritter, J, Mehling, H, Schonermarck, U, Venhoff, N, Vielhauer, V, Witzke, O, Szombati, I, Szucs, G, Garibotto, G, Alberici, F, Brunetta, E, Dagna, L, De Vita, S, Emmi, G, Gabrielli, A, Manenti, L, Pieruzzi, F, Roccatello, D, Salvarani, C, Dobashi, H, Atsumi, T, Fujimoto, S, Hagino, N, Ihata, A, Kaname, S, Kaneko, Y, Katagiri, A, Katayama, M, Kirino, Y, Kitagawa, K, Komatsuda, A, Kono, H, Kurasawa, T, Matsumura, R, Mimura, T, Morinobu, A, Murakawa, Y, Naniwa, T, Nanki, T, Ogawa, N, Oshima, H, Sada, K, Sugiyama, E, Takeuchi, T, Taki, H, Tamura, N, Tsukamoto, T, Yamagata, K, Yamamura, M, van Daele, P, Rutgers, A, Teng, Y, Walker, R, Chua, I, Collins, M, Rabindranath, K, de Zoysa, J, Svensson, M, Grevbo, B, Kalstad, S, Little, M, Clarkson, M, Molloy, E, Pamplona, I, Anton, J, Lucia, V, Ciggaran, S, Cid, M, Encarnacion, M, Oliveras, X, Soler, M, Rusinol, H, Praga, M, Porras, L, Segarra, A, Segelmark, M, Soveri, I, Thomaidi, E, Westman, K, Neumann, T, Burnier, M, Daikeler, T, Dudler, J, Hauser, T, Seeger, H, Vogt, B, Burton, J, Al Jayyousi, R, Amin, T, Andrews, J, Baines, L, Brogan, P, Dasgupta, B, Doulton, T, Flossmann, O, Griffin, S, Harper, J, Harper, L, Kidder, D, Klocke, R, Lanyon, P, Luqmani, R, Mclaren, J, Makanjuola, D, Mccann, L, Nandagudi, A, Selvan, S, O'Riordan, E, Patel, M, Patel, R, Pusey, C, Rajakariar, R, Robson, J, Robson, M, Salama, A, Smyth, L, Sznajd, J, Taylor, J, Sreih, A, Belilos, E, Bomback, A, Carlin, J, Chen Lin, Y, Derebail, V, Dragoi, S, Dua, A, Forbess, L, Geetha, D, Gipson, P, Gohh, R, Greenwood, G, Hugenberg, S, Jimenez, R, Kaskas, M, Kermani, T, Kivitz, A, Koening, C, Langford, C, Marder, G, Mohamed, A, Monach, P, Neyra, N, Niemer, G, Obi, R, Owens, C, Parks, D, Podoll, A, Rovin, B, Sam, R, Shergy, W, Silva, A, Specks, U, Spiera, R, Springer, J, Striebich, C, Swarup, A, Thakar, S, Tiliakos, A, Tsai, Y, Waguespack, D, Wasko, M, Cortazar F. B., Niles J. L., Jayne D. R. W., Merkel P. A., Bruchfeld A., Yue H., Schall T. J., Bekker P., Peh C. A., Chakera A., Cooper B., Kurtkoti J., Langguth D., Levidiotis V., Luxton G., Mount P., Mudge D., Noble E., Phoon R., Ranganathan D., Ritchie A., Ryan J., Suranyi M., Rosenkranz A., Lhotta K., Kronbichler A., Demoulin N., Bovy C., Hellemans R., Hougardy J., Sprangers B., Wissing K., Pagnoux C., Barbour S., Brachemi S., Cournoyer S., Girard L., Laurin L., Liang P., Philibert D., Walsh M., Tesar V., Becvar R., Horak P., Rychlik I., Szpirt W., Dieperink H., Gregersen J., Ivarsen P., Krarup E., Lyngsoe C., Rigothier C., Augusto J., Belot A., Chauveau D., Cornec D., Jourde-Chiche N., Ficheux M., Karras A., Klein A., Maurier F., Mesbah R., Moranne O., Neel A., Quemeneur T., Saadoun D., Terrier B., Zaoui P., Schaier M., Benck U., Bergner R., Busch M., Floege J., Grundmann F., Haller H., Haubitz M., Hellmich B., Henes J., Hohenstein B., Hugo C., Iking-Konert C., Arndt F., Kubacki T., Kotter I., Lamprecht P., Lindner T., Halbritter J., Mehling H., Schonermarck U., Venhoff N., Vielhauer V., Witzke O., Szombati I., Szucs G., Garibotto G., Alberici F., Brunetta E., Dagna L., De Vita S., Emmi G., Gabrielli A., Manenti L., Pieruzzi F., Roccatello D., Salvarani C., Dobashi H., Atsumi T., Fujimoto S., Hagino N., Ihata A., Kaname S., Kaneko Y., Katagiri A., Katayama M., Kirino Y., Kitagawa K., Komatsuda A., Kono H., Kurasawa T., Matsumura R., Mimura T., Morinobu A., Murakawa Y., Naniwa T., Nanki T., Ogawa N., Oshima H., Sada K., Sugiyama E., Takeuchi T., Taki H., Tamura N., Tsukamoto T., Yamagata K., Yamamura M., van Daele P., Rutgers A., Teng Y., Walker R., Chua I., Collins M., Rabindranath K., de Zoysa J., Svensson M., Grevbo B., Kalstad S., Little M., Clarkson M., Molloy E., Pamplona I. A., Anton J., Lucia V. B., Ciggaran S., Cid M. C., Encarnacion M. D., Oliveras X. F., Soler M. J., Rusinol H. M., Praga M., Porras L. Q., Segarra A., Segelmark M., Soveri I., Thomaidi E., Westman K., Neumann T., Burnier M., Daikeler T., Dudler J., Hauser T., Seeger H., Vogt B., Jayne D., Burton J., Al Jayyousi R., Amin T., Andrews J., Baines L., Brogan P., Dasgupta B., Doulton T., Flossmann O., Griffin S., Harper J., Harper L., Kidder D., Klocke R., Lanyon P., Luqmani R., McLaren J., Makanjuola D., McCann L., Nandagudi A., Selvan S., O'Riordan E., Patel M., Patel R., Pusey C., Rajakariar R., Robson J., Robson M., Salama A., Smyth L., Sznajd J., Taylor J., Merkel P., Sreih A., Belilos E., Bomback A., Carlin J., Chen Lin Y. C., Derebail V., Dragoi S., Dua A., Forbess L., Geetha D., Gipson P., Gohh R., Greenwood G. T., Hugenberg S., Jimenez R., Kaskas M., Kermani T., Kivitz A., Koening C., Langford C., Marder G., Mohamed A., Monach P., Neyra N., Niemer G., Niles J., Obi R., Owens C., Parks D., Podoll A., Rovin B., Sam R., Shergy W., Silva A., Specks U., Spiera R., Springer J., Striebich C., Swarup A., Thakar S., Tiliakos A., Tsai Y., Waguespack D., Wasko M. C., Cortazar, F, Niles, J, Jayne, D, Merkel, P, Bruchfeld, A, Yue, H, Schall, T, Bekker, P, Peh, C, Chakera, A, Cooper, B, Kurtkoti, J, Langguth, D, Levidiotis, V, Luxton, G, Mount, P, Mudge, D, Noble, E, Phoon, R, Ranganathan, D, Ritchie, A, Ryan, J, Suranyi, M, Rosenkranz, A, Lhotta, K, Kronbichler, A, Demoulin, N, Bovy, C, Hellemans, R, Hougardy, J, Sprangers, B, Wissing, K, Pagnoux, C, Barbour, S, Brachemi, S, Cournoyer, S, Girard, L, Laurin, L, Liang, P, Philibert, D, Walsh, M, Tesar, V, Becvar, R, Horak, P, Rychlik, I, Szpirt, W, Dieperink, H, Gregersen, J, Ivarsen, P, Krarup, E, Lyngsoe, C, Rigothier, C, Augusto, J, Belot, A, Chauveau, D, Cornec, D, Jourde-Chiche, N, Ficheux, M, Karras, A, Klein, A, Maurier, F, Mesbah, R, Moranne, O, Neel, A, Quemeneur, T, Saadoun, D, Terrier, B, Zaoui, P, Schaier, M, Benck, U, Bergner, R, Busch, M, Floege, J, Grundmann, F, Haller, H, Haubitz, M, Hellmich, B, Henes, J, Hohenstein, B, Hugo, C, Iking-Konert, C, Arndt, F, Kubacki, T, Kotter, I, Lamprecht, P, Lindner, T, Halbritter, J, Mehling, H, Schonermarck, U, Venhoff, N, Vielhauer, V, Witzke, O, Szombati, I, Szucs, G, Garibotto, G, Alberici, F, Brunetta, E, Dagna, L, De Vita, S, Emmi, G, Gabrielli, A, Manenti, L, Pieruzzi, F, Roccatello, D, Salvarani, C, Dobashi, H, Atsumi, T, Fujimoto, S, Hagino, N, Ihata, A, Kaname, S, Kaneko, Y, Katagiri, A, Katayama, M, Kirino, Y, Kitagawa, K, Komatsuda, A, Kono, H, Kurasawa, T, Matsumura, R, Mimura, T, Morinobu, A, Murakawa, Y, Naniwa, T, Nanki, T, Ogawa, N, Oshima, H, Sada, K, Sugiyama, E, Takeuchi, T, Taki, H, Tamura, N, Tsukamoto, T, Yamagata, K, Yamamura, M, van Daele, P, Rutgers, A, Teng, Y, Walker, R, Chua, I, Collins, M, Rabindranath, K, de Zoysa, J, Svensson, M, Grevbo, B, Kalstad, S, Little, M, Clarkson, M, Molloy, E, Pamplona, I, Anton, J, Lucia, V, Ciggaran, S, Cid, M, Encarnacion, M, Oliveras, X, Soler, M, Rusinol, H, Praga, M, Porras, L, Segarra, A, Segelmark, M, Soveri, I, Thomaidi, E, Westman, K, Neumann, T, Burnier, M, Daikeler, T, Dudler, J, Hauser, T, Seeger, H, Vogt, B, Burton, J, Al Jayyousi, R, Amin, T, Andrews, J, Baines, L, Brogan, P, Dasgupta, B, Doulton, T, Flossmann, O, Griffin, S, Harper, J, Harper, L, Kidder, D, Klocke, R, Lanyon, P, Luqmani, R, Mclaren, J, Makanjuola, D, Mccann, L, Nandagudi, A, Selvan, S, O'Riordan, E, Patel, M, Patel, R, Pusey, C, Rajakariar, R, Robson, J, Robson, M, Salama, A, Smyth, L, Sznajd, J, Taylor, J, Sreih, A, Belilos, E, Bomback, A, Carlin, J, Chen Lin, Y, Derebail, V, Dragoi, S, Dua, A, Forbess, L, Geetha, D, Gipson, P, Gohh, R, Greenwood, G, Hugenberg, S, Jimenez, R, Kaskas, M, Kermani, T, Kivitz, A, Koening, C, Langford, C, Marder, G, Mohamed, A, Monach, P, Neyra, N, Niemer, G, Obi, R, Owens, C, Parks, D, Podoll, A, Rovin, B, Sam, R, Shergy, W, Silva, A, Specks, U, Spiera, R, Springer, J, Striebich, C, Swarup, A, Thakar, S, Tiliakos, A, Tsai, Y, Waguespack, D, Wasko, M, Cortazar F. B., Niles J. L., Jayne D. R. W., Merkel P. A., Bruchfeld A., Yue H., Schall T. J., Bekker P., Peh C. A., Chakera A., Cooper B., Kurtkoti J., Langguth D., Levidiotis V., Luxton G., Mount P., Mudge D., Noble E., Phoon R., Ranganathan D., Ritchie A., Ryan J., Suranyi M., Rosenkranz A., Lhotta K., Kronbichler A., Demoulin N., Bovy C., Hellemans R., Hougardy J., Sprangers B., Wissing K., Pagnoux C., Barbour S., Brachemi S., Cournoyer S., Girard L., Laurin L., Liang P., Philibert D., Walsh M., Tesar V., Becvar R., Horak P., Rychlik I., Szpirt W., Dieperink H., Gregersen J., Ivarsen P., Krarup E., Lyngsoe C., Rigothier C., Augusto J., Belot A., Chauveau D., Cornec D., Jourde-Chiche N., Ficheux M., Karras A., Klein A., Maurier F., Mesbah R., Moranne O., Neel A., Quemeneur T., Saadoun D., Terrier B., Zaoui P., Schaier M., Benck U., Bergner R., Busch M., Floege J., Grundmann F., Haller H., Haubitz M., Hellmich B., Henes J., Hohenstein B., Hugo C., Iking-Konert C., Arndt F., Kubacki T., Kotter I., Lamprecht P., Lindner T., Halbritter J., Mehling H., Schonermarck U., Venhoff N., Vielhauer V., Witzke O., Szombati I., Szucs G., Garibotto G., Alberici F., Brunetta E., Dagna L., De Vita S., Emmi G., Gabrielli A., Manenti L., Pieruzzi F., Roccatello D., Salvarani C., Dobashi H., Atsumi T., Fujimoto S., Hagino N., Ihata A., Kaname S., Kaneko Y., Katagiri A., Katayama M., Kirino Y., Kitagawa K., Komatsuda A., Kono H., Kurasawa T., Matsumura R., Mimura T., Morinobu A., Murakawa Y., Naniwa T., Nanki T., Ogawa N., Oshima H., Sada K., Sugiyama E., Takeuchi T., Taki H., Tamura N., Tsukamoto T., Yamagata K., Yamamura M., van Daele P., Rutgers A., Teng Y., Walker R., Chua I., Collins M., Rabindranath K., de Zoysa J., Svensson M., Grevbo B., Kalstad S., Little M., Clarkson M., Molloy E., Pamplona I. A., Anton J., Lucia V. B., Ciggaran S., Cid M. C., Encarnacion M. D., Oliveras X. F., Soler M. J., Rusinol H. M., Praga M., Porras L. Q., Segarra A., Segelmark M., Soveri I., Thomaidi E., Westman K., Neumann T., Burnier M., Daikeler T., Dudler J., Hauser T., Seeger H., Vogt B., Jayne D., Burton J., Al Jayyousi R., Amin T., Andrews J., Baines L., Brogan P., Dasgupta B., Doulton T., Flossmann O., Griffin S., Harper J., Harper L., Kidder D., Klocke R., Lanyon P., Luqmani R., McLaren J., Makanjuola D., McCann L., Nandagudi A., Selvan S., O'Riordan E., Patel M., Patel R., Pusey C., Rajakariar R., Robson J., Robson M., Salama A., Smyth L., Sznajd J., Taylor J., Merkel P., Sreih A., Belilos E., Bomback A., Carlin J., Chen Lin Y. C., Derebail V., Dragoi S., Dua A., Forbess L., Geetha D., Gipson P., Gohh R., Greenwood G. T., Hugenberg S., Jimenez R., Kaskas M., Kermani T., Kivitz A., Koening C., Langford C., Marder G., Mohamed A., Monach P., Neyra N., Niemer G., Niles J., Obi R., Owens C., Parks D., Podoll A., Rovin B., Sam R., Shergy W., Silva A., Specks U., Spiera R., Springer J., Striebich C., Swarup A., Thakar S., Tiliakos A., Tsai Y., Waguespack D., and Wasko M. C.

Abstract

Introduction: In the 330-patient ADVOCATE trial of avacopan for the treatment of antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis, in which 81% of patients had renal involvement, estimated glomerular filtration rate (eGFR) increased on average 7.3 ml/min per 1.73 m2 in the avacopan group and 4.1 ml/min per 1.73 m2 in the prednisone group (P = 0.029) at week 52. This new analysis examines the results in the patient subgroup with severe renal insufficiency at enrollment into the trial, i.e., eGFR ≤20 ml/min per 1.73 m2. Methods: eGFR was determined at baseline and over the course of the trial. Changes in eGFR were compared between the 2 treatment groups. Results: In ADVOCATE, 27 of 166 patients (16%) in the avacopan group and 23 of 164 patients (14%) in the prednisone group had a baseline eGFR ≤20 ml/min per 1.73 m2. At week 52, eGFR increased on average 16.1 and 7.7 ml/min per 1.73 m2 in the avacopan and prednisone groups, respectively (P = 0.003). The last eGFR value measured during the 52-week treatment period was ≥2-fold higher than baseline in 41% of patients in the avacopan group compared to 13% in the prednisone group (P = 0.030). More patients in the avacopan group versus prednisone group had increases in eGFR above 20, 30, and 45 ml/min per 1.73 m2, respectively. Serious adverse events occurred in 13 of 27 patients (48%) in the avacopan group and 16 of 23 patients (70%) in the prednisone group. Conclusion: Among patients with baseline eGFR ≤20 ml/min per 1.73 m2 in the ADVOCATE trial, eGFR improved more in the avacopan group than in the prednisone group.

Published
2023

13. Renal Recovery for Patients with ANCA-Associated Vasculitis and Low eGFR in the ADVOCATE Trial of Avacopan

Author

Cortazar, Frank B., primary, Niles, John L., additional, Jayne, David R.W., additional, Merkel, Peter A., additional, Bruchfeld, Annette, additional, Yue, Huibin, additional, Schall, Thomas J., additional, Bekker, Pirow, additional, Peh, C. Au, additional, Chakera, A., additional, Cooper, B., additional, Kurtkoti, J., additional, Langguth, D., additional, Levidiotis, V., additional, Luxton, G., additional, Mount, P., additional, Mudge, D., additional, Noble, E., additional, Phoon, R., additional, Ranganathan, D., additional, Ritchie, A., additional, Ryan, J., additional, Suranyi, M., additional, Rosenkranz, A., additional, Lhotta, K., additional, Kronbichler, A., additional, Demoulin, N., additional, Bovy, C., additional, Hellemans, R., additional, Hougardy, J., additional, Sprangers, B., additional, Wissing, K., additional, Pagnoux, C., additional, Barbour, S., additional, Brachemi, S., additional, Cournoyer, S., additional, Girard, L., additional, Laurin, L., additional, Liang, P., additional, Philibert, D., additional, Walsh, M., additional, Tesar, V., additional, Becvar, R., additional, Horak, P., additional, Rychlik, I., additional, Szpirt, W., additional, Dieperink, H., additional, Gregersen, J., additional, Ivarsen, P., additional, Krarup, E., additional, Lyngsoe, C., additional, Rigothier, C., additional, Augusto, J., additional, Belot, A., additional, Chauveau, D., additional, Cornec, D., additional, Jourde-Chiche, N., additional, Ficheux, M., additional, Karras, A., additional, Klein, A., additional, Maurier, F., additional, Mesbah, R., additional, Moranne, O., additional, Neel, A., additional, Quemeneur, T., additional, Saadoun, D., additional, Terrier, B., additional, Zaoui, P., additional, Schaier, M., additional, Benck, U., additional, Bergner, R., additional, Busch, M., additional, Floege, J., additional, Grundmann, F., additional, Haller, H., additional, Haubitz, M., additional, Hellmich, B., additional, Henes, J., additional, Hohenstein, B., additional, Hugo, C., additional, Iking-Konert, C., additional, Arndt, F., additional, Kubacki, T., additional, Kotter, I., additional, Lamprecht, P., additional, Lindner, T., additional, Halbritter, J., additional, Mehling, H., additional, Schönermarck, U., additional, Venhoff, N., additional, Vielhauer, V., additional, Witzke, O., additional, Szombati, I., additional, Szucs, G., additional, Garibotto, G., additional, Alberici, F., additional, Brunetta, E., additional, Dagna, L., additional, De Vita, S., additional, Emmi, G., additional, Gabrielli, A., additional, Manenti, L., additional, Pieruzzi, F., additional, Roccatello, D., additional, Salvarani, C., additional, Dobashi, H., additional, Atsumi, T., additional, Fujimoto, S., additional, Hagino, N., additional, Ihata, A., additional, Kaname, S., additional, Kaneko, Y., additional, Katagiri, A., additional, Katayama, M., additional, Kirino, Y., additional, Kitagawa, K., additional, Komatsuda, A., additional, Kono, H., additional, Kurasawa, T., additional, Matsumura, R., additional, Mimura, T., additional, Morinobu, A., additional, Murakawa, Y., additional, Naniwa, T., additional, Nanki, T., additional, Ogawa, N., additional, Oshima, H., additional, Sada, K., additional, Sugiyama, E., additional, Takeuchi, T., additional, Taki, H., additional, Tamura, N., additional, Tsukamoto, T., additional, Yamagata, K., additional, Yamamura, M., additional, van Daele, P., additional, Rutgers, A., additional, Teng, Y., additional, Walker, R., additional, Chua, I., additional, Collins, M., additional, Rabindranath, K., additional, de Zoysa, J., additional, Svensson, M., additional, Grevbo, B., additional, Kalstad, S., additional, Little, M., additional, Clarkson, M., additional, Molloy, E., additional, Pamplona, I. Agraz, additional, Anton, J., additional, Lucia, V. Barrio, additional, Ciggaran, S., additional, Cid, M. Cinta, additional, Encarnacion, M. Diaz, additional, Oliveras, X. Fulladosa, additional, Soler, M. Jose, additional, Rusinol, H. Marco, additional, Praga, M., additional, Porras, L. Quintana, additional, Segarra, A., additional, Bruchfeld, A., additional, Segelmark, M., additional, Soveri, I., additional, Thomaidi, E., additional, Westman, K., additional, Neumann, T., additional, Burnier, M., additional, Daikeler, T., additional, Dudler, J., additional, Hauser, T., additional, Seeger, H., additional, Vogt, B., additional, Jayne, D., additional, Burton, J., additional, Al Jayyousi, R., additional, Amin, T., additional, Andrews, J., additional, Baines, L., additional, Brogan, P., additional, Dasgupta, B., additional, Doulton, T., additional, Flossmann, O., additional, Griffin, S., additional, Harper, J., additional, Harper, L., additional, Kidder, D., additional, Klocke, R., additional, Lanyon, P., additional, Luqmani, R., additional, McLaren, J., additional, Makanjuola, D., additional, McCann, L., additional, Nandagudi, A., additional, Selvan, S., additional, O'Riordan, E., additional, Patel, M., additional, Patel, R., additional, Pusey, C., additional, Rajakariar, R., additional, Robson, J., additional, Robson, M., additional, Salama, A., additional, Smyth, L., additional, Sznajd, J., additional, Taylor, J., additional, Merkel, P., additional, Sreih, A., additional, Belilos, E., additional, Bomback, A., additional, Carlin, J., additional, Chen Lin, Y. Chang, additional, Derebail, V., additional, Dragoi, S., additional, Dua, A., additional, Forbess, L., additional, Geetha, D., additional, Gipson, P., additional, Gohh, R., additional, Greenwood, G.T., additional, Hugenberg, S., additional, Jimenez, R., additional, Kaskas, M., additional, Kermani, T., additional, Kivitz, A., additional, Koening, C., additional, Langford, C., additional, Marder, G., additional, Mohamed, A., additional, Monach, P., additional, Neyra, N., additional, Niemer, G., additional, Niles, J., additional, Obi, R., additional, Owens, C., additional, Parks, D., additional, Podoll, A., additional, Rovin, B., additional, Sam, R., additional, Shergy, W., additional, Silva, A., additional, Specks, U., additional, Spiera, R., additional, Springer, J., additional, Striebich, C., additional, Swarup, A., additional, Thakar, S., additional, Tiliakos, A., additional, Tsai, Y., additional, Waguespack, D., additional, and Wasko, M. Chester, additional

Published
2023
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15. Association between age at disease onset of anti-neutrophil cytoplasmic antibody-associated vasculitis and clinical presentation and short-term outcomes

Author

Monti, S., Craven, A., Klersy, C., Montecucco, C., Caporali, R., Watts, R., Merkel, P. A., Luqmani, R., Achilleos, K., Adler, M., Alba, M. A., Albert, D. A., Alibaz-Oner, F., Allcoat, P., Amano, K., Amarasuriya, M., Amudala, N. A., Andrews, J., Archer, A. M., Arimura, Y., Atukorala, I., Azevedo, E., Bajad, S., Baldwin, C., Barra, L. J., Baslund, B., Basu, N., Baykal, M., Berger, C., Berglin, E., Besada, E., Bhardwaj, M., Bischof, A., Blockmans, D., Blood, J., Draibe, J. B., Brand, S., Brandao, M., Bruce, I. N., Butler, A., Calabrese, L. H., Ferrer, D. C., Carette, S., Carmona, D., Ceunen, H., Chakravarty, K., Chapman, P. T., Chocova, Z., Chung, S. A., Ci, W., Cid, M. C., Clark, T. M., Clarkson, M. R., De Jesus Contreras-Rodriguez, F., Conway, R., Cooke, K., Viros, X. C., Cordeiro, A., Costa, A., Culfear, K., Daikeler, T., Danda, D., Das, S. K., Dasgupta, B., De Castro, A. M., Dehghan, N., Devassy, R., Dhindsa, N., Diamantopoulos, A. P., Direskeneli, H., Dobashi, H., Juan, D., Durrani, M., Edelsten, C., Eifert, J., Elhayek, S., Elsideeg, S., Endo, T., Erden, A., Erer, B., Eriksson, P., Erturk, Z., Espigol-Frigole, G., Felicetti, M., Ferraro, A., Ferro, J. M., Fifi-Mah, A., Flores-Suarez, L. F., Flossmann, O., Flynn, D., Fonseca, J. E., Foot, J., Foote, M., Forbess, L., Fujimoto, S., Fukuoka, K., Furtado, C., Furuta, S., Gaffo, A. L., Gallagher, P., Gao, N., Gatenby, P., Gendi, N., Geraldes, R., Gerits, A., Gioffredi, A., Gomples, L., Goncalves, M. J., Gondo, P., Graham, A., Grainger, R., Gray, D. T., Grayson, P. C., Griffiths, L., Guo, Y., Gupta, R., Gylling, M., Hajj-Ali, R. A., Hammam, N., Harigai, M., Hartley, L., Haslett, J., Hassan, A., Hatemi, G., Hellmich, B., Henckaerts, L., Henes, J. C., Hepburn, J., Herd, V., Hess, C., Hill, C., Hinojosa-Azaola, A., Hirahashi, J., Hirano, F., Hocevar, A., Holle, J., Hollinger, N., Homma, S., Howard, T., Hoyles, R. K., Hruskova, Z., Hutcheon, G., Ignacak, M., Igney-Oertel, A., Ikeda, K., Ikegaya, N., Jagadeesh, S., Jaquith, J., Jayne, D. R. W., Jewell, T., Jones, C., Joshi, A., Kalyoncu, U., Kamall, S., Kamath, S., Lai, K. S., Kaname, S., Kanchinadham, S., Karadag, O., Karube, M., Kaszuba, M., Kaur, R., Kawakami, T., Kawashima, S., Khalidi, N., Khan, A., Kikuchi, M., Kilic, L., Kimura, M., King, M. J., Klapa, S., Klocke, R., Kobayashi, T., Kobayashi, S., Komagata, Y., Kronbichler, A., Kuczia, P., Kumar, M. S., Kurosawa, M., Lamprecht, P., Langford, C. A., Lanyon, P., Laversuch, C., Lee, S. J., Leoni, S., Li, J., Liang, K., Liang, P., Liao, H., Lee, L. A., Luqmani, R. A., Lyle, A., Macdonald, M., Mackie, S. L., Madden, L., Magliano, M., Makino, H., Makol, A., Malaiya, R., Malaviya, A., Manthri, R., Maritati, F., Da Silva, A. M., Mason, J. C., Matara, C., Matsui, K., Matteson, E. L., Mcbride, D., Mccullough, K., Mcgeoch, L., Mclaren, J., Mcmillian, C., Mendiratta, N., Menon, A., Merinopoulos, D., Merkel, P., Messier, S., Micheletti, R. G., Mills, K., Milman, N., Minoda, M., Minz, R. W., Mock, C., Mohammad, A. J., Moiseev, S., Moitinho, M., Molloy, E., Monach, P. A., Montgomery, M., Moosig, F., Moradizadeh, M., Morgan, M., Morgan, A. W., Morgan, A. -M., Muir, A., Mukhtyar, C., Muller, A., Muratore, F., Muso, E., Nada, R., Nakajima, H., Nakajima, T., Nakano, H., Nandagudi, A., Neumann, T., Y. F., Ng, K. H., Ng, Nogueira, E. L., Nolkha, N., Nordstrom, D., Novikov, P., Nugaliyadde, A., O'Donnell, J. L., O'Donoghue, J., O'Neill, L., O'Riordan, E., Oatley, M., Okubo, K., Oliva, E., Oshikawa, H., Ota, Y., Padoan, R., Pagnoux, C., Pan, L., Panaritis, K., Park, J. K., Patel, S., Patil, P., Pazzola, G., Peall, A., Pearce, F., Pehlevan, S., Pereira, L., Pettersson, T., Pineau, C. A., Pirila, L., Poglodek, B., Ponte, C., Prieto-Gonzalez, S., Priya, S. R., Purewal, B., Purschke, S., Putaala, J., Quickert, S., Quincey, V., Raghuvanshi, S., Rajasekhar, L., Ranganathan, D., Rathi, M., Rees, D., Rees, F., Renken, U., Restuccia, G., Rhee, R. L., Rice, B., Robins, D., Robson, J., Rodrigues, M., Romao, V. C., Rotar, C., Ruediger, C., Rutgers, A., A. C., Sa, Saavedra, M. J., Sada, K. -E., Sahbudin, I., Salvarani, C., Sandhu, N., Santos, E., Sato, Y., Schafer, V. S., Schiavon, F., Schmidt, W. A., Segelmark, M., Shahin, A., Sharma, A., Shotton, J., Silva, C., Singer, O. G., Sivasuthan, G., Smolen, S., Solanich-Moreno, X., Boixader, L. S., Song, Y. W., Springer, J., Sreih, A. G., Srivastava, R., Stamp, L. K., Stevens, R., Strbian, D., Sugino, K., Sunderkotter, C., Suppiah, R., Suzuki, K., Szekanecz, Z., Sznajd, J., Taimen, K., Tak, P. P., Takeuchi, T., Takizawa, N., Tames, L., Tan, B. E., Tanaka, M., Tang, M. W., Tatlisumak, T., Tesar, V., Thomas, A., Tian, X., Tokunaga, K., Tombetti, E., Tomsic, M., Toz, B., Tsukamoto, T., Uchida, S., Unal, A. U., Urban, M. L., Usui, J., Vaglio, A., Venkatachalam, S., Vermaak, E., Viswanath, V., Wada, T., Wagh, S., Wallace, D. J., Walters, G., Walz, B., Wan, J., Wang, T., Wang, G., Warrington, K. J., Watts, R. A., Wawrzycka-Adamczyk, K., Weeratunga, P., Weisman, M. H., Wickramasinghe, S., Williams, M., Wojcik, K., Woodruff, L., Xenitidis, T., Yamada, H., Yamagata, K., Yee, C. -S., Yoon, M., Yoshida, K., Yoshifuji, H., Ytterberg, S. R., Yumura, W., Zayed, H., Zeng, X., Zhao, M. -H., Zugaj, A., Zuk, J., İç Hastalıkları, Clinical Haematology, and Translational Immunology Groningen (TRIGR)

Subjects
Male, Outcome, Antineutrophil Cytoplasmic, 030232 urology & nephrology, 0302 clinical medicine, Risk Factors, 80 and over, Pharmacology (medical), Age of Onset, Young adult, Aged, 80 and over, education.field_of_study, age, anti-neutrophil cytoplasmic antibody-associated vasculitis, outcome, Adolescent, Adult, Aged, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, Antibodies, Antineutrophil Cytoplasmic, Female, Humans, Middle Aged, Morbidity, Prognosis, Retrospective Studies, Risk Assessment, Survival Rate, United Kingdom, Young Adult, Vasculitis, Systemic vasculitis, medicine.medical_specialty, Population, anti-neutrophil cytoplasmic antibody–associated vasculitis, Antibodies, 03 medical and health sciences, Rheumatology, Internal medicine, medicine, education, Anti-neutrophil cytoplasmic antibody–associated vasculitis, Survival rate, Anti-neutrophil cytoplasmic antibody, 030203 arthritis & rheumatology, business.industry, Retrospective cohort study, medicine.disease, Age of onset, business
Abstract

Objectives ANCA-associated vasculitis (AAV) can affect all age groups. We aimed to show that differences in disease presentation and 6 month outcome between younger- and older-onset patients are still incompletely understood. Methods We included patients enrolled in the Diagnostic and Classification Criteria for Primary Systemic Vasculitis (DCVAS) study between October 2010 and January 2017 with a diagnosis of AAV. We divided the population according to age at diagnosis: Results A total of 1338 patients with AAV were included: 66% had disease onset at Conclusion Within 6 months of diagnosis of AAV, patients >65 years of age display a different pattern of organ involvement and an increased risk of significant damage and mortality compared with younger patients.

Published
2021
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17. POS0244 ASSOCIATION OF PROTEINASE 3 GENE (PRTN3) Val119Ile POLYMORPHISM (SNP rs351111) WITH RISK OF RELAPSE AMONG HOMOZYGOUS PATIENTS WITH PR3 ANCA-ASSOCIATED VASCULITIS

Author

Casal Moura, M., primary, Deng, Z., additional, Brooks, S., additional, Tew, W., additional, Hummel, A., additional, Fervenza, F., additional, Kallenberg, C., additional, Langford, C., additional, Merkel, P. A., additional, Monach, P. A., additional, Seo, P., additional, Spiera, R., additional, St. Clair, W., additional, Stone, J. H., additional, Prunotto, M., additional, Grayson, P., additional, and Specks, U., additional

Published
2022
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18. Investigating Interactions Between MUC5B and Other Genetic Risk Variants with Cigarette Smoking and Race on the Risk of Rheumatoid Arthritis-Associated Interstitial Lung Disease

Author

Wheeler, A., primary, Poole, J.A., additional, Baker, J., additional, Ascherman, D., additional, Kerr, G., additional, Reimold, A., additional, Kunkel, G., additional, Wysham, K., additional, Singh, N., additional, Lazaro, D., additional, Monach, P., additional, Bridges, L., additional, Mikuls, T., additional, and England, B., additional

Published
2022
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21. Avacopan for the Treatment of ANCA-Associated Vasculitis

Author

Jayne, David R W, Merkel, Peter A, Schall, Thomas J, Bekker, Pirow, ADVOCATE Study Group:, C Au Peh, Chakera, A, Cooper, B, Kurtkoti, J, Langguth, D, Levidiotis, V, Luxton, G, Mount, P, Mudge, D, Noble, E, Phoon, R, Ranganathan, D, Ritchie, A, Ryan, J, Suranyi, M, Rosenkranz, A, Lhotta, K, Kronbichler, A, Demoulin, N, Bovy, C, Hellemans, R, Hougardy, J, Sprangers, B, Wissing, K, Pagnoux, C, Barbour, S, Brachemi, S, Cournoyer, S, Girard, L, Laurin, L, Liang, P, Philibert, D, Walsh, M, Tesar, V, Becvar, R, Horak, P, Rychlik, I, Szpirt, W, Dieperink, H, Gregersen, J, Ivarsen, P, Krarup, E, Lyngsoe, C, Rigothier, C, Augusto, J, Belot, A, Chauveau, D, Cornec, D, Jourde-Chiche, N, Ficheux, M, Karras, A, Klein, A, Maurier, F, Mesbah, R, Moranne, O, Neel, A, Quemeneur, T, Saadoun, D, Terrier, B, Zaoui, P, Schaier, M, Benck, U, Bergner, R, Busch, M, Floege, J, Grundmann, F, Haller, H, Haubitz, M, Hellmich, B, Henes, J, Hohenstein, B, Hugo, C, Iking-Konert, C, Arndt, F, Kubacki, T, Kotter, I, Lamprecht, P, Lindner, T, Halbritter, J, Mehling, H, Schönermarck, U, Venhoff, N, Vielhauer, V, Witzke, O, Szombati, I, Szucs, G, Garibotto, G, Alberici, F, Brunetta, E, Dagna, L, S De Vita, Emmi, G, Gabrielli, A, Manenti, L, Pieruzzi, F, Roccatello, D, Salvarani, C, Dobashi, H, Atsumi, T, Fujimoto, S, Hagino, N, Ihata, A, Kaname, S, Kaneko, Y, Katagiri, A, Katayama, M, Kirino, Y, Kitagawa, K, Komatsuda, A, Kono, H, Kurasawa, T, Matsumura, R, Mimura, T, Morinobu, A, Murakawa, Y, Naniwa, T, Nanki, T, Ogawa, N, Oshima, H, Sada, K, Sugiyama, E, Takeuchi, T, Taki, H, Tamura, N, Tsukamoto, T, Yamagata, K, Yamamura, M, P van Daele, Rutgers, A, Teng, Y, Walker, R, Chua, I, Collins, M, Rabindranath, K, J de Zoysa, Svensson, M, Grevbo, B, Kalstad, S, Little, M, Clarkson, M, Molloy, E, I Agraz Pamplona, Anton, J, V Barrio Lucia, Ciggaran, S, M Cinta Cid, M Diaz Encarnacion, X Fulladosa Oliveras, M Soler, J, H Rusinol, M, Praga, M, L Quintana Porras, Segarra, A, Bruchfeld, A, Segelmark, M, Soveri, I, Thomaidi, E, Westman, K, Neumann, T, Burnier, M, Daikeler, T, Dudler, J, Hauser, T, Seeger, H, Vogt, B, Jayne, D, Burton, J, R Al Jayyousi, Amin, T, Andrews, J, Baines, L, Brogan, P, Dasgupta, B, Doulton, T, Flossmann, O, Griffin, S, Harper, J, Harper, L, Kidder, D, Klocke, R, Lanyon, P, Luqmani, R, Mclaren, J, Makanjuola, D, Mccann, L, Nandagudi, A, Selvan, S, O'Riordan, E, Patel, M, Patel, R, Pusey, C, Rajakariar, R, Robson, J, Robson, M, Salama, A, Smyth, L, Sznajd, J, Taylor, J, Merkel, P, Sreih, A, Belilos, E, Bomback, A, Carlin, J, Y Chang Chen Lin, Derebail, V, Dragoi, S, Dua, A, Forbess, L, Geetha, D, Gipson, P, Gohh, R, T Greenwood, G, Hugenberg, S, Jimenez, R, Kaskas, M, Kermani, T, Kivitz, A, Koening, C, Langford, C, Marder, G, Mohamed, A, Monach, P, Neyra, N, Niemer, G, Niles, J, Obi, R, Owens, C, Parks, D, Podoll, A, Rovin, B, Sam, R, Shergy, W, Silva, A, Specks, U, Spiera, R, Springer, J, Striebich, C, Swarup, A, Thakar, S, Tiliakos, A, Tsai, Y, Waguespack, D, M Chester Wasko, Internal Medicine, Immunology, Jayne, D, Merkel, P, Schall, T, Bekker, P, Pieruzzi, F, Jayne, David RW [0000-0002-1712-0637], Apollo - University of Cambridge Repository, and Translational Immunology Groningen (TRIGR)

Subjects
Male, Receptor, Anaphylatoxin C5a/antagonists & inhibitors, Anaphylatoxin C5a, Anaphylatoxin C5a/antagonists & inhibitors, Nipecotic Acids, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculiti, Administration, Oral, Azathioprine, Kaplan-Meier Estimate, 030204 cardiovascular system & hematology, urologic and male genital diseases, Gastroenterology, C5a receptor, Cyclophosphamide/administration & dosage, Rituximab/administration & dosage, Immunosuppressive Agent, renal vasculitis, Prednisone/administration & dosage, 0302 clinical medicine, Glucocorticoid, immune system diseases, Prednisone, Recurrence, Medicine, 030212 general & internal medicine, skin and connective tissue diseases, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/drug therapy, Aniline Compounds, Remission Induction, General Medicine, Aniline Compound, Middle Aged, Administration, Combination, Rituximab, Drug Therapy, Combination, Female, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, Cyclophosphamide, Double-Blind Method, Glucocorticoids, Humans, Immunosuppressive Agents, Receptor, Anaphylatoxin C5a, Vasculitis, Receptor, medicine.drug, Human, Azathioprine/administration & dosage, Oral, medicine.medical_specialty, Nipecotic Acid, ANCA-Associated Vasculitis, 03 medical and health sciences, Drug Therapy, Internal medicine, Aniline Compounds/adverse effects, cardiovascular diseases, Immunosuppressive Agents/administration & dosage, Anti-neutrophil cytoplasmic antibody, business.industry, Glucocorticoids/administration & dosage, medicine.disease, Nipecotic Acids/adverse effects, respiratory tract diseases, business
Abstract

BACKGROUND: The C5a receptor inhibitor avacopan is being studied for the treatment of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis.METHODS: In this randomized, controlled trial, we assigned patients with ANCA-associated vasculitis in a 1:1 ratio to receive oral avacopan at a dose of 30 mg twice daily or oral prednisone on a tapering schedule. All the patients received either cyclophosphamide (followed by azathioprine) or rituximab. The first primary end point was remission, defined as a Birmingham Vasculitis Activity Score (BVAS) of 0 (on a scale from 0 to 63, with higher scores indicating greater disease activity) at week 26 and no glucocorticoid use in the previous 4 weeks. The second primary end point was sustained remission, defined as remission at both weeks 26 and 52. Both end points were tested for noninferiority (by a margin of 20 percentage points) and for superiority.RESULTS: A total of 331 patients underwent randomization; 166 were assigned to receive avacopan, and 165 were assigned to receive prednisone. The mean BVAS at baseline was 16 in both groups. Remission at week 26 (the first primary end point) was observed in 120 of 166 patients (72.3%) receiving avacopan and in 115 of 164 patients (70.1%) receiving prednisone (estimated common difference, 3.4 percentage points; 95% confidence interval [CI], -6.0 to 12.8; PCONCLUSIONS: In this trial involving patients with ANCA-associated vasculitis, avacopan was noninferior but not superior to prednisone taper with respect to remission at week 26 and was superior to prednisone taper with respect to sustained remission at week 52. All the patients received cyclophosphamide or rituximab. The safety and clinical effects of avacopan beyond 52 weeks were not addressed in the trial. (Funded by ChemoCentryx; ADVOCATE ClinicalTrials.gov number, NCT02994927.).

Published
2021

22. The effects of plasma exchange and glucocorticoids on early kidney function among patients with ANCA-associated vasculitis in the PEXIVAS trial

Author

Odler, Balazs, Riedl, Regina, Geetha, Duvuru, Szpirt, Wladimir M., Hawley, Carmel, Uchida, Lisa, Wallace, Zachary S., Walters, Giles, Muso, Eri, Tesar, Vladimir, Pusey, Charles D., Little, Mark A., Merkel, Peter A., Walsh, Michael, Jayne, David R.W., Kronbichler, Andreas, Paizis, Kathy, Walters, Giles, Jardine, Meg, Milton, Caroline, Ibraham, Abu, Siva, Brian, Desmond, Michael, Perkovic, Vlado, Kurtkoti, Jadadeesh, Vilayur, Eswari, Cass, Alan, Summers, Shaun, Brown, Fiona, Ryan, Jessica, Kerr, Peter, Noble, Euan, Luxton, Grant, Mudge, David W., Hawley, Carmel, Johnson, David W., Peh, Chen Au, Faull, Randall J., Ranganathan, Dwarakanathan, Jeffs, Lisa, Nicholls, Kathy, Hughes, Peter, Cooper, Bruce, Boudville, Neil, Ford, Sharon, Langham, Robyn, Reidlinger, Donna, AliciaMorrish, Badve, Sunil V., Pascoe, Elaine, Paul-Brent, Peta-Anne, Robison, Laura, Valks, Andrea, Blockmans, Daniel, Henckaerts, Liesbet, Sprangers, Ben, Suri, Rita, Brachemi, Soumeya, Clark, William, Garg, Amit, Carette, Simon, Pagnoux, Christian, Reich, Heather, Barth, David, Walsh, Michael, Khalidi, Nader, Cox, Gerry, Mazzetti, Andrea, Robins, Diane, Wald, Ron, Perl, Jeffrey, Pavenski, Katerina, Dacouris, Niki, Levin, Adeera, Copland, Michael, Fairhead, Todd, Pannu, Neesh, Qarni, Muhammad Uwais, Habib, Syed, Girard, Louis, Manns, Braden, Tesar, Vladimir, Hruskova, Zdenka, Chocova, Zdenka, Povlsen, Johan, Gregersen, Jon, Ivarsen, Per, Birn, Henrik, Krarup, Elizabeth, Pedersen, Erling B., Thomsen, Ingrid, Bech, Jesper Nørgaard, Szpirt, Wladmir, Egfjord, Martin, Mesbah, Rafik, Bataille, Pierre, Rey, Isabelle, Chantrel, François, Vanhille, Philipe, Quémeneur, Thomas, Carron, Pierre-Louis, Zaoui, Philippe, de Moreuil, Claire, Gosselin, Morgane, Delluc, Aurélien, Hanrotel-Saliou, Catherine, Le Jeune, Mathilde, Ficheux, Maxence, Aniort, Julien, Lavigne, Christian, Augusto, Jean Francois, Chauveau, Dominique, Guitard, Joëlle, Huart, Antoine, Ribes, David, Gatault, Philippe, Becmeur, Camille, Muller, Sandrine, Betz, Valérie, Klein, Alexandre, Blaison, Gilles, Seror, Raphaele, Francois, Hélène, Mariette, Xavier, Aubrun, Aurore, Coustet, Baptiste, Palazzo, Elisabeth, Ottaviani, Sébastien, Goulenok, Tiphaine, Daugas, Eric, Dieudé, Philipe, Papo, Thomas, Lebas, Céline, Lionet, Arnaud, Guillevin, Loïc, Mouthon, Luc, Puéchal, Xavier, Jourde-Chiche, Noémie, Ruivard, Marc, Karras, Alexandre, Limal, Nicolas, Kofman, Thomas, Le Quellec, Alain, Maurier, François, Gibelin, Aude, Parrot, Antoine, Bachmeyer, Claude, Gombert, Bruno, Nouvier, Mathilde, Lega, Jean-Christophe, Fain, Olivier, Andrès, Emmanuel, Cottet, Rachel, Gregorini, Gina, Jeannin, Guido, Possenti, Stefano, Buzio, Carlo, Vaglio, Augusto, Oliva, Elena, Makino, Hirofumi, Muso, Eri, Endo, Tomomi, Kakita, Hiroko, Suzuki, Hiroyuki, Handa, Takaya, Kang, Youngna, Ariyasu, Yuki, Tsukamoto, Tatsuo, Endo, Shuichiro, Miyata, Hitomi, Yamada, Hiroyuki, Ito-Ihara, Toshiko, Uchida, Shunya, Kono, Hajime, Fujigaki, Yoshihide, Kikuchi, Hirotoshi, Nanki, Toshihiro, Kato, Hideki, Okamoto, Akiko, Asako, Kurumi, Suzuki, Kazuo, Hamano, Yoshitomo, Yamagata, Kunihiro, Usui, Joichi, Fujimoto, Shouichi, Sato, Yuji, Kikuchi, Masao, Flores-Suárez, Luis Felipe, Sánchez-Guerrero, Sergio A., Collins, Michael, Schollum, John, de Zoysa, Janak, Quincy, Vicki, Sizeland, Peter, Aasarod, Knut, Solbu, Marit, Bruun, Trude Jannecke, Koldingsnes, Wenche, Wludarczyk, Anna, Nowak, Ilona, Gorka, Jacek, Sznajd, Jan, Padjas, Agnieszka, Jankowski, Milosz, Widawska, Agnieszka, Szczeklik, Wojciech, Ballarin, Jose, Bruchfeld, Annette, Efvergren, Mats, Eriksson, Per, Westman, Kerstin, Selga, Daina, Heijl, Caroline, Ohlsson, Sophie, Segelmark, Marten, Basu, Neil, Kidder, Dana, Fluck, Nicholas, Jayne, David R.W., Smith, Rona, Wilcocks, Lisa, McClure, Mark, Jones, Rachel, Trivedi, Sapna, Gopaluni, Seerapani, Brettell, Elizabeth, Crump, Paul, Feilbach, Annika, Hewitt, Catherine, Hilken, Nick, Howman, Andrew, Hughes, Terry, Ives, Natalie, Jarrett, Hugh, Mehta, Samir, Record, Rebecca, Ryan, Gemma, Sidile, Chaka, Wheatley, Keith, Sheerin, Brown, Alison, Baines, Laura Anne, Lordan, Jim, Pusey, Charles, Tanna, Anisha, McAdoo, Stephen, Levy, Jeremy, Griffith, Megan, Klebe, Bernhard, Doulton, Timothy, Warwick, Graham, Burton, James, Barratt, Jonathon, Topham, Peter, Baines, Richard, Brunskill, Nigel, Al-Jayyousi, Reem, Hamilton, Patrick, Patel, Mumtaz, Mitra, Sandip, Brown, Nina, Sharples, Edward, Luqmani, Raashid, Harper, Lorraine, Rhodes, Benjamin, Chanouzas, Dimitrios, Morgan, Matthew, Hewins, Peter, Floßmann, Oliver, Bhandary, Nitin, Foxton, Julie, Jones, Linda, King, Jenny, Smyth, Lucy, D’Souza, Richard, Haigh, Richard, Hough, Maxine, Smyth, Lucy, Haigh, Richard, Hough, Maxine, Salama, Alan, Burns, Aine, Little, Mark, Dhaun, Neeraj, Dhaygude, Ajay, Basnayake, Kolitha, Iggo, Neil, Jones, Daniel, Oliveira, David, MacPhee, Iain A.M., Dunn, Emma, Lewington, Andrew J.P., Fan, Stanley Linsun, Rajakariar, Ravindra, Yaqoob, Magdi, Short, Andrew, Geddes, Colin, Mackinnon, Bruce, Jardine, Alan G., Monach, Paul, Merkel, Peter A., Amudala, Naomi, Quillen, Karen, Weisman, Michael, Wallace, Daniel, Forbess, Lindsy, Venuturupalli, Swamy, Langford, Carol, Hajj-Ali, Rula, Koo, Anna, Hoffman, Gary, Specks, Ulrich, Keogh, Karina, Ytterberg, Steven, Winters, Jeff, Warrington, Kenneth, Cartin-Ceba, Rodrigo, Peikert, Tobias, Fervenza, Fernando, Baqir, Misbah, Nachman, Patrick, Detwiler, Randy, Mottl, Amy, Derebail, Vimal, McGregor, JulieAnne, Merkel, Peter A., Sreih, Antoine, Rhee, Rennie, McAlear, Carol, Aqui, Nicole, Moreland, Larry, Kiss, Joseph, Liang, Kimberly, Mohan, Niveditha, Balogun, Rasheed, Li, Tingting, and Brasington, Richard

Abstract

Therapeutic plasma exchange (PLEX) is an adjunctive treatment for patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis and kidney involvement. Little is known about the effect of PLEX on early changes in kidney function. This post-hocanalysis of the PEXIVAS trial investigated the effects of PLEX on changes in kidney function within 12 months. PEXIVAS was a randomized controlled trial recruiting 691 patients with ANCA-associated glomerulonephritis, of whom 349 underwent PLEX and 342 received no-PLEX. The primary outcomes of this post hocstudy of PEXIVAS were change in estimated glomerular filtration rate (eGFR) from baseline and recovery of kidney function (defined as eGFR increase of 15ml/min/1.73m2or more). Baseline eGFR was 21.7 ± 20.3 and 20.6 ± 18.7 ml/min/1.73m2in the PLEX and no-PLEX groups, respectively. Mean improvements in eGFR at weeks two, four, and eight after initiation of therapy were greater for the PLEX vs. the no-PLEX groups. The greatest significant difference in recovery of kidney function in the PLEX compared to the no-PLEX groups was at week four (relative risk (RR): 1.41; 95% confidence interval:1.09-1.82). Increased eGFR or recovery of kidney function at week four were significantly associated with lower risk for end-stage kidney disease at week 52 (RR: 0.96: 0.95-0.97, and RR: 0.29: 0.16-0.52; respectively). Neither changes in eGFR nor recovery of kidney function differed by reduced- compared to standard-dose glucocorticoid group. Overall, our study indicates that PLEX improves early kidney function in patients with ANCA-associated glomerulonephritis.

Published
2025
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23. The association of TNF inhibitor use with incident cardiovascular events in radiographic axial spondyloarthritis.

Author

Liew, Jean W., Treu, Timothy, Park, Yojin, Ferguson, Jacqueline M., Rosser, Morgan A., Ho, Yuk-Lam, Gagnon, David R., Stovall, Rachael, Monach, Paul, Heckbert, Susan R., Gensler, Lianne S., Liao, Katherine P., and Dubreuil, Maureen

Abstract

Whether tumor necrosis factor inhibitor (TNFi) use is cardioprotective among individuals with radiographic axial spondyloarthritis (r-axSpA), who have heightened cardiovascular (CV) risk, is unclear. We tested the association of TNFi use with incident CV outcomes in r-axSpA. We identified a r-axSpA cohort within a Veterans Affairs database between 2002 and 2019 using novel phenotyping methods and secondarily using ICD codes. TNFi use was assessed as a time-varying exposure using pharmacy dispense records. The primary outcome was incident CV disease identified using ICD codes for coronary artery disease, myocardial infarction or stroke. We fit Cox models with inverse probability weights to estimate the risk of each outcome with TNFi use versus non-use. Analyses were performed in the overall cohort, and separately in two periods (2002–2010, 2011–2019) to account for secular trends. Using phenotyping we identified 26,928 individuals with an r-axSpA diagnosis (mean age 63.4 years, 94 % male); at baseline 3633 were TNFi users and 23,295 were non-users. During follow-up of a mean 3.3 ± 4.2 years, 674 (18.6 %) TNFi users had incident CVD versus 11,838 (50.8 %) non-users. In adjusted analyses, TNFi use versus non-use was associated with lower risk of incident CVD (HR 0.34, 95 % CI 0.29–0.40) in the cohort overall, and in the two time periods separately. In this r-axSpA cohort identified using phenotyping methods, TNFi use versus non-use had a lower risk of incident CVD. These findings provide reassurance regarding the CV safety of TNFi agents for r-axSpA treatment. Replication of these results in other cohorts is needed. [ABSTRACT FROM AUTHOR]

Published
2024
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25. THU0318 PATTERNS OF CLINICAL PRESENTATION IN TAKAYASU’S ARTERITIS

Author

Quinn, K. A., primary, Gribbons, K. B., additional, Carette, S., additional, Cuthbertson, D., additional, Khalidi, N., additional, Koening, C., additional, Langford, C., additional, Mcalear, C., additional, Monach, P., additional, Moreland, L., additional, Pagnoux, C., additional, Seo, P., additional, Sreih, A., additional, Warrington, K. J., additional, Ytterberg, S. R., additional, Novakovich, E., additional, Merkel, P. A., additional, and Grayson, P., additional

Published
2020
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26. THU0040 PROTEINASE 3-REACTIVE B CELL RECONSTITUTION AFTER TREATMENT WITH RITUXIMAB FOR ANCA-ASSOCIATED VASCULITIS

Author

Berti, A., primary, Hillion, S., additional, Hummel, A., additional, Carmona, E., additional, Peikert, T., additional, Langford, C., additional, Merkel, P. A., additional, Monach, P., additional, Seo, P., additional, Spiera, R., additional, St Clair, E. W., additional, Fervenza, F., additional, Harris, K., additional, Stone, J. H., additional, Pers, J. O., additional, Specks, U., additional, and Cornec, D., additional

Published
2020
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27. THU0310 CASE–CONTROL SEROPREVALENCE STUDY ON THE ASSOCIATION BETWEEN BARTONELLA INFECTION AND ANTI-NEUTROPHIL CYTOPLASMIC ANTIBODY-ASSOCIATED VASCULITIS

Author

Mahr, A., primary, Edouard, S., additional, Cornec, D., additional, Gonzalez-Chiappe, S., additional, Goronzy, J., additional, Guilpain, P., additional, Langford, C., additional, Lévy, P. Y., additional, Merkel, P. A., additional, Monach, P., additional, St Clair, E. W., additional, Seo, P., additional, Spiera, R., additional, Weyand, C., additional, Stone, J. H., additional, Rauolt, D., additional, and Specks, U., additional

Published
2020
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28. The COVID-19 hospitalization metric in the pre- and postvaccination eras as a measure of pandemic severity: A retrospective, nationwide cohort study

Author

Fillmore, Nathanael R., La, Jennifer, Zheng, Chunlei, Doron, Shira, Do, Nhan V., Monach, Paul A., and Branch-Elliman, Westyn

Abstract

AbstractBackground:Coronavirus disease 2019 (COVID-19) hospitalization definitions do not include a disease severity assessment. Thus, we sought to identify a simple and objective mechanism for identifying hospitalized severe cases and to measure the impact of vaccination on trends.Methods:All admissions to a Veterans’ Affairs (VA) hospital, where routine inpatient screening is recommended, between March 1, 2020, and November 22, 2021, with laboratory-confirmed severe acute respiratory coronavirus virus 2 (SARS-CoV-2) were included. Moderate-to-severe COVID-19 was defined as any oxygen supplementation or any oxygen saturation (SpO2) <94% between 1 day before and 2 weeks after the positive SARS-CoV-2 test. Admissions with moderate-to-severe disease were divided by the total number of admissions, and the proportion of admissions with moderate-to-severe COVID-19 was modelled using a penalized spline in a Poisson regression and stratified by vaccination status. Dexamethasone receipt and its correlation with moderate-to-severe cases was also assessed.Results:Among 67,025 admissions with SARS-CoV-2, the proportion with hypoxemia or supplemental oxygen fell from 64% prior to vaccine availability to 56% by November 2021, driven in part by lower rates in vaccinated patients (vaccinated, 52% versus unvaccinated, 58%). The proportion of cases of moderate-to-severe disease identified using SpO2levels and oxygen supplementation was highly correlated with dexamethasone receipt (correlation coefficient, 0.95), and increased after July 1, 2021, concurrent with δ (delta) variant predominance.Conclusions:A simple and objective definition of COVID-19 hospitalizations using SpO2levels and oxygen supplementation can be used to track pandemic severity. This metric could be used to identify risk factors for severe breakthrough infections, to guide clinical treatment algorithms, and to detect trends in changes in vaccine effectiveness over time and against new variants.

Published
2022
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29. Expression profiling of constitutive mast cells reveals a unique identity within the immune system

Author

Dwyer, D, Barrett, N, Austen, K, Kim, E, Brenner, M, Shaw, L, Yu, B, Goldrath, A, Mostafavi, S, Regev, A, Rhoades, A, Moodley, D, Yoshida, H, Mathis, D, Benoist, C, Nabekura, T, Lam, V, Lanier, L, Brown, B, Merad, M, Cremasco, V, Turley, S, Monach, P, Dustin, M, Li, Y, Shinton, S, Hardy, R, Shay, T, Qi, Y, Sylvia, K, Kang, J, Fairfax, K, Randolph, G, Robinette, M, Fuchs, A, and Colonna, M

Subjects
Male, 0301 basic medicine, Immunology, chemical and pharmacologic phenomena, Spleen, Cell Separation, Basophil, Immunoglobulin E, Article, Mice, 03 medical and health sciences, Immune system, medicine, Animals, Immunology and Allergy, Mast Cells, Interleukin 5, Cells, Cultured, Connective Tissue Cells, Blood Cells, biology, Gene Expression Profiling, Degranulation, Flow Cytometry, Basophils, Cell biology, Mice, Inbred C57BL, Interleukin 33, Gene expression profiling, 030104 developmental biology, medicine.anatomical_structure, Tissue Array Analysis, biology.protein
Abstract

Mast cells are evolutionarily ancient sentinel cells. Like basophils, mast cells express the high-affinity receptor for immunoglobulin E (IgE) and have been linked to host defense and diverse immune-system-mediated diseases. To better characterize the function of these cells, we assessed the transcriptional profiles of mast cells isolated from peripheral connective tissues and basophils isolated from spleen and blood. We found that mast cells were transcriptionally distinct, clustering independently from all other profiled cells, and that mast cells demonstrated considerably greater heterogeneity across tissues than previously appreciated. We observed minimal homology between mast cells and basophils, which shared more overlap with other circulating granulocytes than with mast cells. The derivation of mast-cell and basophil transcriptional signatures underscores their differential capacities to detect environmental signals and influence the inflammatory milieu.

Published
2016
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32. Patterns of clinical presentation in Takayasu's arteritis.

Author

Quinn, Kaitlin A., Gribbons, K. Bates, Carette, Simon, Cuthbertson, David, Khalidi, Nader A., Koening, Curry L., Langford, Carol A., McAlear, Carol A., Monach, Paul A., Moreland, Larry W., Pagnoux, Christian, Seo, Philip, Sreih, Antoine G., Warrington, Kenneth J., Ytterberg, Steven R., Novakovich, Elaine, Merkel, Peter A., and Grayson, Peter C.

Abstract

Takayasu's arteritis (TAK) is a clinically heterogenous disease. Patterns of clinical presentation in TAK at diagnosis have not been well described, and a "triphasic pattern" of constitutional symptoms evolving into vascular inflammation and fibrosis has been reported but never systematically evaluated. Patients with TAK were prospectively recruited from the National Institutes of Health (NIH) and the Vasculitis Clinical Research Consortium (VCRC). Based on clinical presentation at diagnosis, patients were divided into five categories: (1) constitutional symptoms alone, (2) carotidynia, (3) other vascular-associated symptoms, (4) major ischemic event, or (5) asymptomatic. Associated clinical characteristics were evaluated in each category. Preceding symptoms were also assessed to determine the presence of a triphasic disease pattern. A total of 275 patients with TAK were included (VCRC=208; NIH=67). Similar heterogeneity of clinical presentation was identified in each cohort: constitutional symptoms (8%), carotidynia (13-15%), other vascular symptoms (43-47%), major ischemic event (28-30%), and asymptomatic (2-6%). An increased relative proportion of males was seen in patients who presented with constitutional symptoms or were asymptomatic at diagnosis (p <0.01). Patients who presented with constitutional symptoms and major ischemic events were youngest at diagnosis. Patients in the asymptomatic group were oldest at diagnosis and often were not treated (p <0.01). Relapse was most frequent in patients who presented with carotidynia (p <0.01). A minority of patients (19%) who presented with a major ischemic event reported a triphasic pattern of disease. There are diverse clinical presentations at diagnosis in TAK. Patients do not necessarily progress sequentially through phases of disease. [ABSTRACT FROM AUTHOR]

Published
2020
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33. Evaluation of Potential Serum Biomarkers of Disease Activity in Diverse Forms of Vasculitis.

Author

Rodriguez-Pla, Alicia, Warner, Roscoe L, Cuthbertson, David, Carette, Simon, Khalidi, Nader A, Koening, Curry L, Langford, Carol A, McAlear, Carol A, Moreland, Larry W, Pagnoux, Christian, Seo, Philip, Specks, Ulrich, Sreih, Antoine G, Ytterberg, Steven R, Johnson, Kent J, Merkel, Peter A, Monach, Paul A, for the Vasculitis Clinical Research Consortium, and Vasculitis Clinical Research Consortium

Published
2020
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34. Long‐Term Safety of Rituximab in Granulomatosis With Polyangiitis and in Microscopic Polyangiitis

Author

Merkel, Peter A., Niles, John L., Mertz, Lester E., Lehane, Patricia B., Pordeli, Pooneh, Erblang, Félix, Allen, Nancy, Block, Joel A., Cartin‐Ceba, Rodrigo, Koening, Curry, Langford, Carol, Monach, Paul, Moreland, Larry W., Nachman, Patrick, and Wallace, Daniel

Abstract

The present study was undertaken to conduct a phase IV, open‐label, prospective study to characterize the long‐term safety of rituximab in a 4‐year observational registry of adult patients with granulomatosis with polyangiitis (GPA) or microscopic polyangiitis (MPA) within the US. Patients initiating treatment with rituximab were evaluated every 6 months for up to 4 years. Outcomes included the incidence of serious adverse events (SAEs), infusion‐related reactions (IRRs), and SAEs of specific interest, including serious infections, serious cardiac events, serious vascular events, and malignancies. Overall, 97 patients (72 with GPA and 25 with MPA) received rituximab through a median of 8 (range 1–28) infusions and were followed up for a median of 3.94 years (range 0.05–4.32 years). The estimated incidence rates (95% confidence interval [95% CI]) of serious infections, serious cardiac events, and serious vascular events were 7.11 (4.55–10.58), 5.03 (2.93–8.06), and 2.37 (1.02–4.67) per 100 patient‐years (PYs), respectively. No IRRs or SAEs occurred within 24 hours of an infusion of rituximab. None of the 9 deaths reported (crude mortality rate 2.67 [95% CI 1.22–5.06] per 100 PYs) were considered to be related to use of rituximab. The safety profile of long‐term treatment with rituximab in patients with GPA or MPA was consistent with that of rituximab administered for shorter durations and with rituximab’s known safety profile in other autoimmune diseases for which it has received regulatory approval. These findings provide clinicians with long‐term, practice‐level safety data for rituximab in the treatment of GPA or MPA.

Published
2021
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35. IgA antibodies to myeloperoxidase in patients with eosinophilic granulomatosis with polyangiitis (Churg-Strauss)

Author

Oommen, E., Hummel, A., Allmannsberger, L., Cuthbertson, D., Carette, S., Pagnoux, C., Hoffman, G. S., Jenne, D. E., Khalidi, N. A., Koening, C. L., Langford, C. A., Mcalear, C. A., Larry Moreland, Seo, P., Sreih, A., Ytterberg, S. R., Merkel, P. A., Specks, U., and Monach, P. A.

Subjects
Adult, Aged, 80 and over, Male, Canada, Adolescent, Remission Induction, Enzyme-Linked Immunosorbent Assay, Churg-Strauss Syndrome, Middle Aged, Article, United States, Antibodies, Antineutrophil Cytoplasmic, Immunoglobulin A, Young Adult, Treatment Outcome, Predictive Value of Tests, Case-Control Studies, Immunoglobulin G, Humans, Female, Biomarkers, Immunosuppressive Agents, Aged, Peroxidase
Abstract

OBJECTIVES: To determine the prevalence of anti-myeloperoxidase (MPO) antibodies of IgA (IgA anti-MPO) isotype in patients with eosinophilic granulomatosis with polyangiitis (EGPA), and the association of the IgA antibodies with IgG anti-MPO and with disease activity. METHODS: Serum samples from patients with EGPA followed in a multi-center longitudinal cohort were tested by ELISA for the presence of IgA anti-MPO and IgG anti-MPO antibodies. Sera from 87 healthy controls were used to define a positive test. Sera from 168 patients with EGPA (298 samples) were tested. Frequencies of positive testing for IgA anti-MPO were compared between patients with active EGPA, patients in remission, and controls. RESULTS: IgA anti-MPO was detected in 10 of 168 (6%) patients with EGPA (11 of 298 serum samples) compared to 1 of 87 (1%) healthy controls (p=0.10). All 11 samples testing positive for IgA anti-MPO also tested positive for IgG anti-MPO. Ninety samples tested positive for IgG anti-MPO but negative for IgA. Samples taken during active EGPA were positive for IgA anti-MPO in 6/72 cases (8%), compared to 5/226 (2%) during remission (p=0.03). Among samples taken during moderate or high disease activity, 5/41 were positive (12%, p=0.01 compared to remission). CONCLUSIONS: Although IgA anti-MPO antibodies are detectable in some patients with EGPA and may be detectable more frequently during active disease, their presence seems unlikely to provide information beyond what is obtained from conventional IgG anti-MPO.

Published
2017

36. Assessment of disease activity in large-vessel vasculitis: Results of an international delphi exercise

Author

Aydin, S. Z., Direskeneli, H., Merkel, P. A., Toloza, S., Blockmans, D., Sato, E. I., De Souza, A. W. S., Cabral, D., Carette, S., Famorca, L., Khalidi, N., Milman, N., Yacyshyn, E., Tesar, V., Baslund, B., Faurschou, M., Guillevin, L., Puechal, X., Aries, P., Hellmich, B., Herlyn, K., Holle, J., Lamprecht, P., Moosig, F., Neumann, T., Zwerina, J., Tomasson, G., Bambery, P., Jois, R., Rajasekhar, L., Sharma, A., Sivakumar, R., Molloy, E., Hashkes, P., Catapano, F., Cimino, L., De Fanti, A., Pipitone, N., Salvarani, C., Vaglio, A., Kobayashi, S., Suzuki, K., Flores-Suarez, L. F., Hinojosa-Azaola, A., Brouwer, E., Rutgers, A., Stegeman, C., Suppiah, R., Hollan, I., Arguis, P., Cid, M. C., Daikeler, T., Alibaz-Oner, F., Hamuryudan, V., Hatemi, G., Hazirolan, T., Inanc, M., Kalayci, M. B., Kamali, S., Kansu, T., Karaaslan, Y., Karadag, O., Keser, G., Onat, A. M., Ozbalkan, Z., Ozen, S., Ozer, H. T. E., Pamuk, O. N., Yilmaz, S. G., Basu, N., Casian, A., Chakravarty, K., D'Cruz, D., Edelsten, C., Harper, L., Jayne, D., Levy, J., Mason, J., Robson, J., Scott, D., Stanford, M., Watts, R., Albert, D., Amudala, N., Beckman, J., Chacko, B., Chung, S., Fessler, B., Giardino, A., Grayson, P., Hunder, G., Langford, C., Lerman, M., Liang, K., Litt, H., Mason, T., Matteson, E., Mikdashi, J., Mohler, E., Monach, P., Rice, B., Sreih, A., Stone, J., Tsapatsaris, N., Villa-Forte, A., Warrington, K., Yazici, Y., Ytterberg, S., Çukurova Üniversitesi, Aydin, S.Z., Direskeneli, H., Merkel, P.A., Toloza, S., Blockmans, D., Sato, E.I., De Souza, A.W.S., and Yeditepe Üniversitesi

Subjects
Vasculitis, medicine.medical_specialty, Delphi Technique, Immunology, Delphi method, Outcomes, Severity of Illness Index, Article, Disease activity, 03 medical and health sciences, 0302 clinical medicine, Rheumatology, Large vessel vasculitis, Severity of illness, medicine, Large vessel, Humans, Immunology and Allergy, 030212 general & internal medicine, computer.programming_language, Giant cell arteritis, 030203 arthritis & rheumatology, Takayasu arteritis, business.industry, medicine.disease, Clinical trial, Physical therapy, business, computer, Delphi
Abstract

PubMedID: 28864648 Objective. To arrive at consensus for candidate outcomes for disease activity assessment in largevessel vasculitis (LVV) in clinical trials. Methods.A Delphi survey including 99 items was circulated among international experts for 3 rounds. Results. Fifty-seven items were accepted for both giant cell arteritis and Takayasu arteritis. Sixty-seven percent of experts voted to have a common approach for both diseases with additional disease-specific items such as weight loss, scalp tenderness/necrosis, morning stiffness, dizziness, visual symptoms, and imaging. Conclusion. This study highlights similarities and differences in experts' perspectives for assessing clinical activity in LVV and may guide a consensus-driven core set of validated outcomes. Copyright © 2017. All rights reserved. National Institute of Arthritis and Musculoskeletal and Skin Diseases: U01 AR51874 04, U54 AR057319 National Center for Research Resources: U54 RR019497 Sponsored by the Vasculitis Clinical Research Consortium, which has received support from the US National Institute of Arthritis and Musculoskeletal and Skin Diseases (U54 AR057319 and U01 AR51874 04), the National Center for Research Resources (U54 RR019497), and the Office of Rare Diseases Research. Additional support for the work of the OMERACT Vasculitis Working Group was received through a Patient-Centered Outcomes Research Institute Pilot Project Grant. S.Z. Aydin, MD, Associate Professor, Division of Rheumatology, The Ottawa Hospital Research Institute, University of Ottawa; H. Direskeneli, MD, Professor of Rheumatology, Division of Rheumatology, Marmara University Faculty of Medicine; P.A. Merkel, MD, MPH, Professor of Medicine and Epidemiology, Division of Rheumatology, and Department of Biostatistics, Epidemiology, and Informatics, University of Pennsylvania. Address correspondence to Dr. P.A. Merkel, Section of Rheumatology, University of Pennsylvania, White Building, 5th Floor Penn, 3400 Spruce St., Philadelphia, Pennsylvania 19104, USA. E-mail: pmerkel@upenn.edu Accepted for publication June 3, 2017.

Published
2017

37. OP0320 Determinants of rituximab pharmacokinetics and clinical outcomes in patients with anca-associated vasculitis

Author

Cornec, D, primary, Kabat, B, additional, Mills, J, additional, Cheu, M, additional, Hummel, A, additional, Schroeder, D, additional, Cascino, M, additional, Brunetta, P, additional, Murray, D, additional, Snyder, M, additional, Fervenza, F, additional, Hoffman, G, additional, Kallenberg, C, additional, Langford, C, additional, Merkel, P, additional, Monach, P, additional, Seo, P, additional, Spiera, R, additional, Clair, WSt, additional, Ytterberg, S, additional, Stone, J, additional, Barnidge, D, additional, and Specks, U, additional

Published
2017
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38. Patterns of Arterial Disease in Takayasu Arteritis and Giant Cell Arteritis

Author

Gribbons, K. Bates, Ponte, Cristina, Carette, Simon, Craven, Anthea, Cuthbertson, David, Hoffman, Gary S., Khalidi, Nader A., Koening, Curry L., Langford, Carol A., Maksimowicz-McKinnon, Kathleen, McAlear, Carol A., Monach, Paul A., Moreland, Larry W., Pagnoux, Christian, Quinn, Kaitlin A., Robson, Joanna C., Seo, Philip, Sreih, Antoine G., Suppiah, Ravi, Warrington, Kenneth J., Ytterberg, Steven R., Luqmani, Raashid, Watts, Richard, Merkel, Peter A., and Grayson, Peter C.

Abstract

To identify and validate, using computer‐driven methods, patterns of arterial disease in Takayasu arteritis (TAK) and giant cell arteritis (GCA). Patients with TAK or GCA were studied from the Diagnostic and Classification Criteria for Vasculitis (DCVAS) cohort and a combined North American cohort. Case inclusion required evidence of large‐vessel involvement, defined as stenosis, occlusion, or aneurysm by angiography/ultrasonography, or increased 18F‐fluorodeoxyglucose (FDG) uptake by positron emission tomography (PET) in at least 1 of 11 specified arterial territories. K‐means cluster analysis identified groups of patients based on the pattern of arterial involvement. Cluster groups were identified in the DCVAS cohort and independently validated in the North American cohort. A total of 1,068 patients were included (DCVAS cohort: TAK = 461, GCA = 217; North American cohort: TAK = 225, GCA = 165). Six distinct clusters of patients were identified in DCVAS and validated in the North American cohort. Patients with TAK were more likely to have disease in the abdominal vasculature, bilateral disease of the subclavian and carotid arteries, or focal disease limited to the left subclavian artery than GCA (P< 0.01). Patients with GCA were more likely to have diffuse disease, involvement of bilateral axillary/subclavian arteries, or minimal disease without a definable pattern than TAK (P< 0.01). Patients with TAK were more likely to have damage by angiography, and patients with GCA were more likely to have arterial FDG uptake by PET without associated vascular damage. Arterial patterns of disease highlight both shared and divergent vascular patterns between TAK and GCA and should be incorporated into classification criteria for large‐vessel vasculitis.

Published
2020
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39. Feasibility and Construct Validation of the Patient Reported Outcomes Measurement Information System in Systemic Vasculitis.

Author

Tomasson, Gunnar, Farrar, John T., Cuthbertson, David, McAlear, Carol A., Ashdown, Susan, Cronholm, Peter F., Dawson, Jill, Gebhart, Don, Lanier, Georgia, Luqmani, Raashid A., Milman, Nataliya, Peck, Jacqueline, Robson, Joanna C., Shea, Judy A., Carette, Simon, Khalidi, Nader, Koening, Curry L., Langford, Carol A., Monach, Paul A., and Moreland, Larry

Published
2019
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40. A microRNA expression and regulatory element activity atlas of the mouse immune system

Author

Rose, Samuel A., Wroblewska, Aleksandra, Dhainaut, Maxime, Yoshida, Hideyuki, Shaffer, Jonathan M., Bektesevic, Anela, Ben-Zvi, Benjamin, Rhoads, Andrew, Kim, Edy Y., Yu, Bingfei, Lavin, Yonit, Merad, Miriam, Buenrostro, Jason D., Brown, Brian D., Aguilar, Oscar, Allan, Rhys, Arakawa-Hoyt, Janice, Astarita, Jilian, Austen, K. Frank, Barrett, Nora, Baysoy, Alev, Benoist, Christophe, Buechler, Matthew, Buenrostro, Jason, Casanova, Maria Acebes, Choi, Kyunghee, Chowdhary, Kaitavjeet, Colonna, Marco, Crowl, Ty, Deng, Tianda, Desai, Jigar V., Desland, Fiona, Ding, Jiarui, Dominguez, Claudia, Dwyer, Daniel, Frascoli, Michela, Gal-Oz, Shani, Goldrath, Ananda, Grieshaber-Bouyer, Ricardo, Jia, Baosen, Johanson, Tim, Jordan, Stefan, Kang, Joonsoo, Kapoor, Varun, Kenigsberg, Ephraim, Kim, Joel, Kim, Ki wook, Kiner, Evgeny, Kronenberg, Mitchell, Lanier, Lewis, Laplace, Catherine, Lareau, Caleb, Leader, Andrew, Lee, Jisu, Magen, Assaf, Maier, Barbara, Maslova, Alexandra, Mathis, Diane, McFarland, Adelle, Meunier, Etienne, Monach, Paul, Mostafavi, Sara, Muller, Soren, Muus, Christoph, Ner-Gaon, Hadas, Nguyen, Quyhn, Nigrovic, Peter A., Niizuma, Kouta, Novakovsky, German, Nutt, Stephen, Omilusik, Kayla, Ortiz-Lopez, Adriana, Paynich, Mallory, Peng, Vincent, Potempa, Marc, Pradhan, Rachana, Quon, Sara, Ramirez, Ricardo, Ramanan, Deepshika, Randolph, Gwendalyn, Regev, Aviv, Seddu, Kumba, Shay, Tal, Shemesh, Avishai, Shyer, Justin, Smilie, Christopher, Spidale, Nick, Subramanian, Ayshwarya, Sylvia, Katelyn, Tellier, Julie, Turley, Shannon, Vijaykumar, Brinda, Wagers, Amy, Wang, Chendi, Wang, Peter L., Yang, Liang, and Yim, Aldrin

Subjects
Immunology, Immunology and Allergy
Abstract

microRNAs (miRNA) play an important role in immune system development and function, often participating in regulatory networks with the transcription factors that drive their expression. However, many of these relationships remain obscured because regulatory elements controlling miRNA expression in different immune cells remain largely uncharacterized. To address this, we analyzed miRNA expression and open chromatin regions (OCR) from >60 immune cell populations. This enabled us to establish maps of miRNA promoter and enhancer usage across the immune system. Unique miRNA signatures within different populations were associated with local chromatin accessibility changes, revealing putative regulatory elements for differentially expressed miRNAs. These maps suggest many miRNAs utilize multiple promoters to increase abundance, and also identified dominant and divergent miRNA regulatory elements between lineages and during immune cell development, as well as between closely clustered miRNAs. This study provides insight into the miRNA regulatory network of the immune system and is a resource for further discovery., Accepted Manuscript

Published
2021

41. SAT0369 Weight Gain in Anca-Associated Vasculitis Is Independent of Glucocorticoid Dosing

Author

Wallace, Z., primary, Miloslavsky, E., additional, Unizony, S., additional, Lu, L., additional, Specks, U., additional, Hoffman, G., additional, Kallenberg, C., additional, Langford, C., additional, Merkel, P., additional, Monach, P., additional, Seo, P., additional, Spiera, R., additional, Clair, B.St., additional, Choi, H., additional, and Stone, J., additional

Published
2016
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44. Using Mass Spectrometry to Quantify Rituximab and Perform Individualized Immunoglobulin Phenotyping in ANCA-Associated Vasculitis.

Author

Mills, John R., Cornec, Divi, Dasari, Surendra, Ladwig, Paula M., Hummel, Amber M., Cheu, Melissa, Murray, David L., Willrich, Maria A., Snyder, Melissa R., Hoffman, Gary S., Kallenberg, Cees G. M., Langford, Carol A., Merkel, Peter A., Monach, Paul A., Seo, Philip, Spiera, Robert F., St. Clair, E. William, Stone, John H., Specks, Ulrich, and Barnidge, David R.

Published
2016
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46. Effect of Disease Activity, Glucocorticoid Exposure, and Rituximab on Body Composition During Induction Treatment of Antineutrophil Cytoplasmic Antibody–Associated Vasculitis

Author

Wallace, Zachary S., Miloslavsky, Eli M., Cascino, Matthew, Unizony, Sebastian H., Lu, Na, Hoffman, Gary S., Kallenberg, Cees G. M., Langford, Carol A., Merkel, Peter A., Monach, Paul A., Seo, Philip, Spiera, Robert, St.Clair, E. William, Specks, Ulrich, Brunetta, Paul, Choi, Hyon K., and Stone, John H.

Abstract

We investigated the relationships between glucocorticoid use, disease activity, and changes in body mass index (BMI) in patients with antineutrophil cytoplasmic antibody–associated vasculitis (AAV). We analyzed AAV patients enrolled in the Rituximab in AAV trial. Glucocorticoid use, BMI, and disease activity were measured regularly during the trial period. We performed mixed‐effects regressions to examine the associations of time‐dependent cumulative average glucocorticoid use and disease activity with changes in BMI over time, while adjusting for potential confounders. The mean ± SD baseline BMI of the 197 patients enrolled was 28.8 ± 6.3 kg/m2. Patients with newly diagnosed AAV tended to have a lower mean ± SD BMI than those with relapsing disease (28.0 ± 5.7 kg/m2versus 29.6 ± 6.8 kg/m2) and higher disease activity (mean ± SD Birmingham Vasculitis Activity Score for Wegener's Granulomatosis 8.7 ± 3.3 versus 7.4 ± 2.7). The most significant change in BMI occurred during the first 6 months of the trial (mean ± SD increase of 1.1 ± 2.2 kg/m2; P< 0.0001). Disease activity improvement, glucocorticoid exposure, and randomization to rituximab were each independently associated with an increase in BMI (P< 0.001 for all analyses). Our findings suggest that changes in BMI, as well as glucocorticoid exposure, are independently associated with improvements in disease activity in AAV. Rituximab may also have effects on BMI independent of its impact on disease activity.

Published
2017
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47. Vasculitis in patients with inflammatory bowel diseases: A study of 32 patients and systematic review of the literature.

Author

Sy, Alice, Khalidi, Nader, Dehghan, Natasha, Barra, Lillian, Carette, Simon, Cuthbertson, David, Hoffman, Gary S., Koening, Curry L., Langford, Carol A., McAlear, Carol, Moreland, Larry, Monach, Paul A., Seo, Philip, Specks, Ulrich, Sreih, Antoine, Ytterberg, Steven R., Assche, Gert Van, Merkel, Peter A., and Pagnoux, Christian

Abstract

Background Published small case series suggest that inflammatory bowel disease [IBD; Crohn’s disease (CD) or ulcerative colitis (UC)] and vasculitis co-occur more frequently than would be expected by chance. Objectives To describe this association by an analysis of a large cohort of carefully studied patients and through a systematic literature review. Methods Patients with both IBD and vasculitis enrolled in the Vasculitis Clinical Research Consortium (VCRC) Longitudinal Studies, followed in Canadian Vasculitis research network (CanVasc) centers and/or in the University of Toronto’s IBD clinic were included in this case series. A systematic literature review of patients with IBD and vasculitis involved a PubMed search through February 2014. The main characteristics of patients with Takayasu arteritis (TAK) and IBD were compared to those in patients with TAK without IBD followed in the VCRC. Results The study identified 32 patients with IBD and vasculitis: 13 with large-vessel vasculitis [LVV; 12 with TAK, 1 with giant cell arteritis (GCA); 8 with CD, 5 with UC]; 8 with ANCA-associated vasculitis [AAV; 6 granulomatosis with polyangiitis (GPA), 2 with eosinophilic granulomatosis with polyangiitis (EGPA)]; 5 with isolated cutaneous vasculitis; and 6 with other vasculitides. Patients with LVV and AAV were mostly female (18/21). The diagnosis of IBD preceded that of vasculitis in 12/13 patients with LVV and 8/8 patients with AAV. The review of the literature identified 306 patients with IBD and vasculitis: 144 with LVV (133 TAK; 87 with IBD preceding LVV), 19 with AAV [14 GPA, 1 EGPA, 4 microscopic polyangiitis (MPA)], 66 with isolated cutaneous vasculitis, and 77 with other vasculitides. Patients with IBD and TAK were younger and had more frequent headaches, constitutional symptoms, or gastrointestinal symptoms compared to those patients in the VCRC who had TAK without IBD. Conclusions These findings highlight the risk of vasculitis, especially TAK, in patients with IBD (both CD and UC). [ABSTRACT FROM AUTHOR]

Published
2016
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49. Cardiac Involvement in Granulomatosis with Polyangiitis.

Author

McGeoch, Lucy, Carette, Simon, Cuthbertson, David, Hoffman, Gary S., Khalidi, Nader, Koening, Curry L., Langford, Carol A., McAlear, Carol A., Moreland, Larry, Monach, Paul A., Seo, Philip, Specks, Ulrich, Ytterberg, Steven R., Merkel, Peter A., and Pagnoux, Christian

Published
2015
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50. Genetic, social, and environmental risk factors in rheumatoid arthritis-associated interstitial lung disease.

Author

Wheeler, Austin M., Baker, Joshua F., Poole, Jill A., Ascherman, Dana P., Yang, Yangyuna, Kerr, Gail S., Reimold, Andreas, Kunkel, Gary, Cannon, Grant W., Wysham, Katherine D., Singh, Namrata, Lazaro, Deana, Monach, Paul, Bridges, S. Louis, Mikuls, Ted R., and England, Bryant R.

Abstract

MUC5B and TOLLIP single nucleotide polymorphisms (SNPs) and cigarette smoking were associated with rheumatoid arthritis-interstitial lung disease (RA-ILD) in a predominantly Northern European population. We evaluated whether RA-ILD is associated with these genetic variants and HLA-DRB1 shared epitope (SE) alleles in a large RA cohort stratified by race and smoking history. HLA-DRB1 SE alleles and MUC5B rs35705950 and TOLLIP rs5743890 SNPs were genotyped in U.S. veterans with RA. ILD was validated through medical record review. Genetic associations with ILD were assessed in logistic regression models overall and in subgroups defined by race and smoking status, with additive interactions assessed by the relative excess risk of interaction (RERI). Of 2,556 participants (88% male, 77% White), 238 (9.3%) had ILD. The MUC5B variant was associated with ILD (OR 2.25 [95% CI 1.69, 3.02]), whereas TOLLIP and HLA-DRB1 SE were not. The MUC5B variant was less frequent among Black/African American participants (5.8% vs. 22.6%), though its association with RA-ILD was numerically stronger (OR 4.23 [1.65, 10.86]) compared to all other participants (OR 2.32 [1.70, 3.16]). Those with the MUC5B variant and a smoking history had numerically higher odds of ILD (OR 4.18 [2.53, 6.93]) than non-smokers (OR 2.41 [1.16, 5.04]). Additive interactions between MUC5B- race and MUC5B- smoking were not statistically significant. In this large RA cohort, the MUC5B promoter variant was associated with >2-fold higher odds of RA-ILD. While this variant is less common among Black/African American patients, its presence in this population carried >4-fold higher odds of RA-ILD. [ABSTRACT FROM AUTHOR]

Published
2022
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