Shubhasree Banerjee1,2, Kaitlin A Quinn1,2, K Bates Gribbons1,2, Joel S Rosenblum1,2, Ali Cahid Civelek1,2, Elaine Novakovich1,2, Peter A Merkel1,2, Mark A Ahlman1,2, Peter C Grayson3,4. 1. From the Systemic Autoimmunity Branch, US National Institutes of Health (NIH), National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), Bethesda, Maryland; Division of Rheumatology, Georgetown University, Washington, DC; National Institutes of Health, Clinical Center, Radiology and Imaging Sciences, Bethesda, Maryland; Division of Rheumatology and Department of Biostatistics, Epidemiology, and Informatics, University of Pennsylvania, Philadelphia, Pennsylvania, USA. 2. S. Banerjee, MD, Systemic Autoimmunity Branch, NIH, NIAMS; K.A. Quinn, MD, Systemic Autoimmunity Branch, NIH, NIAMS, and Division of Rheumatology, Georgetown University; K.B. Gribbons, BS, Systemic Autoimmunity Branch, NIH, NIAMS; J.S. Rosenblum, BS, Systemic Autoimmunity Branch, NIH, NIAMS; A.C. Civelek, MD, NIH, Clinical Center, Radiology and Imaging Sciences; E. Novakovich, BSN, Systemic Autoimmunity Branch, NIH, NIAMS; P.A. Merkel, MD, MPH, Division of Rheumatology and Department of Biostatistics, Epidemiology, and Informatics, University of Pennsylvania; M.A. Ahlman, MD, NIH, Clinical Center, Radiology and Imaging Sciences; P.C. Grayson, MD, MSc, Systemic Autoimmunity Branch, NIH, NIAMS. 3. From the Systemic Autoimmunity Branch, US National Institutes of Health (NIH), National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), Bethesda, Maryland; Division of Rheumatology, Georgetown University, Washington, DC; National Institutes of Health, Clinical Center, Radiology and Imaging Sciences, Bethesda, Maryland; Division of Rheumatology and Department of Biostatistics, Epidemiology, and Informatics, University of Pennsylvania, Philadelphia, Pennsylvania, USA. peter.grayson@nih.gov. 4. S. Banerjee, MD, Systemic Autoimmunity Branch, NIH, NIAMS; K.A. Quinn, MD, Systemic Autoimmunity Branch, NIH, NIAMS, and Division of Rheumatology, Georgetown University; K.B. Gribbons, BS, Systemic Autoimmunity Branch, NIH, NIAMS; J.S. Rosenblum, BS, Systemic Autoimmunity Branch, NIH, NIAMS; A.C. Civelek, MD, NIH, Clinical Center, Radiology and Imaging Sciences; E. Novakovich, BSN, Systemic Autoimmunity Branch, NIH, NIAMS; P.A. Merkel, MD, MPH, Division of Rheumatology and Department of Biostatistics, Epidemiology, and Informatics, University of Pennsylvania; M.A. Ahlman, MD, NIH, Clinical Center, Radiology and Imaging Sciences; P.C. Grayson, MD, MSc, Systemic Autoimmunity Branch, NIH, NIAMS. peter.grayson@nih.gov.
Abstract
OBJECTIVE: Disease activity in large-vessel vasculitis (LVV) is traditionally assessed by clinical and serological variables rather than vascular imaging. This study determined the effect of treatment on 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) vascular activity in relation to clinical- and serologic-based assessments. METHODS: Patients with giant cell arteritis (GCA) or Takayasu arteritis (TA) were prospectively evaluated at 6-month intervals in an observational cohort. Treatment changes were made at least 3 months before the followup visit and categorized as increased, decreased, or unchanged. Imaging (FDG-PET qualitative analysis), clinical, and serologic (erythrocyte sedimentation rate, C-reactive protein) assessments were determined at each visit and compared over interval visits. RESULTS: Serial assessments were performed in 52 patients with LVV (GCA = 31; TA = 21) over 156 visits. Increased, decreased, or unchanged therapy was recorded for 36-, 23-, and 32-visit intervals, respectively. When treatment was increased, there was significant reduction in disease activity by imaging, clinical, and inflammatory markers (p ≤ 0.01 for each). When treatment was unchanged, all 3 assessments of disease activity remained similarly unchanged over 6-month intervals. When treatment was reduced, PET activity significantly worsened (p = 0.02) but clinical and serologic activity did not significantly change. Treatment of GCA with tocilizumab and of TA with tumor necrosis factor inhibitors resulted in significant improvement in imaging and clinical assessments of disease activity, but only rarely did the assessments both become normal. CONCLUSION: In addition to clinical and serologic assessments, vascular imaging has potential to monitor disease activity in LVV and should be tested as an outcome measure in randomized clinical trials.
OBJECTIVE: Disease activity in large-vessel vasculitis (LVV) is traditionally assessed by clinical and serological variables rather than vascular imaging. This study determined the effect of treatment on 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) vascular activity in relation to clinical- and serologic-based assessments. METHODS:Patients with giant cell arteritis (GCA) or Takayasu arteritis (TA) were prospectively evaluated at 6-month intervals in an observational cohort. Treatment changes were made at least 3 months before the followup visit and categorized as increased, decreased, or unchanged. Imaging (FDG-PET qualitative analysis), clinical, and serologic (erythrocyte sedimentation rate, C-reactive protein) assessments were determined at each visit and compared over interval visits. RESULTS: Serial assessments were performed in 52 patients with LVV (GCA = 31; TA = 21) over 156 visits. Increased, decreased, or unchanged therapy was recorded for 36-, 23-, and 32-visit intervals, respectively. When treatment was increased, there was significant reduction in disease activity by imaging, clinical, and inflammatory markers (p ≤ 0.01 for each). When treatment was unchanged, all 3 assessments of disease activity remained similarly unchanged over 6-month intervals. When treatment was reduced, PET activity significantly worsened (p = 0.02) but clinical and serologic activity did not significantly change. Treatment of GCA with tocilizumab and of TA with tumornecrosis factor inhibitors resulted in significant improvement in imaging and clinical assessments of disease activity, but only rarely did the assessments both become normal. CONCLUSION: In addition to clinical and serologic assessments, vascular imaging has potential to monitor disease activity in LVV and should be tested as an outcome measure in randomized clinical trials.
Authors: Himanshu R Dashora; Joel S Rosenblum; Kaitlin A Quinn; Hugh Alessi; Elaine Novakovich; Babak Saboury; Mark A Ahlman; Peter C Grayson Journal: J Nucl Med Date: 2021-06-04 Impact factor: 10.057
Authors: Emily Rose; Marcela A Ferrada; Kaitlin A Quinn; Wendy Goodspeed; Laurent Arnaud; Aman Sharma; Hajime Yoshifuji; Jeff Kim; Clint Allen; Arlene Sirajuddin; Marcus Chen; Peter C Grayson Journal: Arthritis Care Res (Hoboken) Date: 2022-04-29 Impact factor: 5.178
Authors: K S M van der Geest; G Treglia; A W J M Glaudemans; E Brouwer; M Sandovici; F Jamar; O Gheysens; R H J A Slart Journal: Eur J Nucl Med Mol Imaging Date: 2021-05-03 Impact factor: 9.236
Authors: Andrej Ćorović; Christopher Wall; Justin C Mason; James H F Rudd; Jason M Tarkin Journal: Curr Cardiol Rep Date: 2020-08-09 Impact factor: 3.955