Vasculitis is a family of rare diseases defined by inflammation in blood vessels. These conditions, if not quickly recognized and properly treated, can cause serious and life-threatening damage to multiple organ systems. The goal of the Vasculitis Translational Research Program (VTRP) is to discover factors that cause vasculitis and to develop novel ways for physicians to diagnose and monitor these diseases more effectively.
Tremendous progress over the last few decades has transformed vasculitis from frequently fatal into a chronic, manageable illness. However, treatment with potentially toxic medications, including steroids and other medications that suppress the immune system, is generally required to induce remission. Although most patients with vasculitis achieve remission with treatment, the majority of patients experience one or more recurrences of the disease. Disease relapse can result in additional permanent organ damage and can be fatal. At present, we have a very crude understanding of what causes vasculitis. There are very few tests available that reliably help a doctor predict which patients will experience a relapsing disease course. The identification of factors that cause vasculitis and the discovery of biomarkers that can predict clinical outcomes and guide patient-specific therapeutic decisions is the major focus of the program.
The VTRP was established in 2013 to evaluate patients with known vasculitis or with clinical suspicion of vasculitis. Diseases of interest include Takayasu's arteritis (TAK), relapsing polychondritis (RP), giant cell arteritis (GCA), granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), eosinophilic granulomatosis with polyangiitis (EGPA), and polyarteritis nodosa (PAN) among other types of vasculitis.
Current projects include the study of:
- Vascular Imaging in Large-Vessel Vasculitis
- Genomic Classification of Vasculitis
- Detailed clinical characterization of Relapsing Polychondritis and Takayasu's Arteritis
- Neutrophil Biology in Small and Medium-Vessel Vasculitis
Dr. Grayson is board-certified in Internal Medicine and Rheumatology. He completed his undergraduate degree from Brown University in 1999, his medical degree from the Medical University of South Carolina in 2004, and a Masters in Science from Boston University in 2008. He served as a Chief Resident in Internal Medicine at Boston Medical Center and completed an additional two-year vasculitis fellowship within the Vasculitis Clinical Research Consortium.
Currently, a Tenure-Track Investigator at the NIAMS, Dr. Grayson’s research focuses on clinical and translational research across many forms of systemic vasculitis. Specifically, his work has focused on biomarker discovery/development, the use of advanced molecular imaging, molecular classification of disease, clinical trials, and genetics/genomics of vasculitis. His group has clinically defined the use of advanced molecular imaging as a surrogate marker of vascular inflammation in large-vessel vasculitis. His group has conducted some of the only translational work related to relapsing polychondritis, including the identification of somatic mutations in UBA1 as a driver of disease in a subset of these patients. Translational work from the group has also defined novel pathways of neutrophil-mediated inflammation in monogenic vasculitis and drug-induced vasculitis and has identified novel biomarkers of disease activity in many forms of vasculitis that suggest novel therapeutic targets.
Dr. Grayson has a strong commitment to mentoring young investigators in rare disease research. He serves as the Associate Program Director for the NIAMS Rheumatology Fellowship Program, and he is the recipient of numerous Teaching Awards. He is actively involved in leadership roles within the American College of Rheumatology and was a recipient of the American College of Rheumatology’s Distinguished Fellow Award in 2011. He has served on the editorial board for Arthritis & Rheumatology and the Journal of Rheumatology. He currently serves on the Board of Directors for the Vasculitis Foundation and is a Steering Committee member on the Vasculitis Clinical Research Consortium.
- Beck DB, Ferrada MA, Sikora KA, Ombrello AK, Collins JC, Pei W, Balanda N, Ross DL, Ospina Cardona D, Wu Z, Patel B, Manthiram K, Groarke EM, Gutierrez-Rodrigues F, Hoffmann P, Rosenzweig S, Nakabo S, Dillon LW, Hourigan CS, Tsai WL, Gupta S, Carmona-Rivera C, Asmar AJ, Xu L, Oda H, Goodspeed W, Barron KS, Nehrebecky M, Jones A, Laird RS, Deuitch N, Rowczenio D, Rominger E, Wells KV, Lee CR, Wang W, Trick M, Mullikin J, Wigerblad G, Brooks S, Dell'Orso S, Deng Z, Chae JJ, Dulau-Florea A, Malicdan MCV, Novacic D, Colbert RA, Kaplan MJ, Gadina M, Savic S, Lachmann HJ, Abu-Asab M, Solomon BD, Retterer K, Gahl WA, Burgess SM, Aksentijevich I, Young NS, Calvo KR, Werner A, Kastner DL, Grayson PC. Somatic Mutations in UBA1 and Severe Adult-Onset Autoinflammatory Disease. N Engl J Med. 2020.
- Grayson PC, Alehashemi S, Bagheri AA, Civelek AC, Cupps TR, Kaplan MJ, Malayeri AA, Merkel PA, Novakovich E, Bluemke DA, Ahlman MA. 18 F-Fluorodeoxyglucose-Positron Emission Tomography As an Imaging Biomarker in a Prospective, Longitudinal Cohort of Patients With Large Vessel Vasculitis. Arthritis Rheumatol. 2018;70(3):439-449.
- Carmona-Rivera C, Purmalek MM, Moore E, Waldman M, Walter PJ, Garraffo HM, Phillips KA, Preston KL, Graf J, Kaplan MJ, Grayson PC. A role for muscarinic receptors in neutrophil extracellular trap formation and levamisole-induced autoimmunity. JCI Insight. 2017;2(3):e89780.
- Carmona-Rivera C, Khaznadar SS, Shwin KW, Irizarry-Caro JA, O'Neil LJ, Liu Y, Jacobson KA, Ombrello AK, Stone DL, Tsai WL, Kastner DL, Aksentijevich I, Kaplan MJ, Grayson PC. Deficiency of adenosine deaminase 2 triggers adenosine-mediated NETosis and TNF production in patients with DADA2. Blood. 2019;134(4):395-406.
- Ferrada M, Rimland CA, Quinn K, Sikora K, Kim J, Allen C, Sirajuddin A, Goodspeed W, Chen M, Grayson PC. Defining Clinical Subgroups in Relapsing Polychondritis: A Prospective Observational Cohort Study. Arthritis Rheumatol. 2020.
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This page was last updated on Friday, November 13, 2020