Lucy O'Malley1,2,3, Katie L Druce1,2,3, Dimitrios Chanouzas1,2,3, Matthew D Morgan1,2,3, Rachel Jones1,2,3, David R W Jayne1,2,3, Neil Basu1,2,3, Lorraine Harper4,5,6. 1. From the Institute of Clinical Sciences, University of Birmingham, Birmingham; Arthritis Research UK Centre for Epidemiology, University of Manchester, Manchester; Department of Medicine, University of Cambridge, Cambridge; Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK. 2. LH, DRJ, and RJ have received research grants and speaker fees from F. Hoffmann-La Roche. LH, RJ, DRJ, MDM have been involved in studies in which rituximab was given free of charge by Roche and MMF was given free of charge by Vifor Pharma. 3. L. O'Malley, MB ChB, Institute of Clinical Sciences, University of Birmingham; K.L. Druce, PhD, Arthritis Research UK Centre for Epidemiology, University of Manchester; D. Chanouzas, PhD, Institute of Clinical Sciences, University of Birmingham; M.D. Morgan, PhD, Institute of Clinical Sciences, University of Birmingham; R. Jones, MD, Department of Medicine, University of Cambridge; D.R. Jayne, MD, Department of Medicine, University of Cambridge; N. Basu, PhD, Institute of Infection, Immunity and Inflammation, University of Glasgow; L. Harper, PhD, Institute of Clinical Sciences, University of Birmingham. 4. From the Institute of Clinical Sciences, University of Birmingham, Birmingham; Arthritis Research UK Centre for Epidemiology, University of Manchester, Manchester; Department of Medicine, University of Cambridge, Cambridge; Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK. L.Harper@bham.ac.uk. 5. LH, DRJ, and RJ have received research grants and speaker fees from F. Hoffmann-La Roche. LH, RJ, DRJ, MDM have been involved in studies in which rituximab was given free of charge by Roche and MMF was given free of charge by Vifor Pharma. L.Harper@bham.ac.uk. 6. L. O'Malley, MB ChB, Institute of Clinical Sciences, University of Birmingham; K.L. Druce, PhD, Arthritis Research UK Centre for Epidemiology, University of Manchester; D. Chanouzas, PhD, Institute of Clinical Sciences, University of Birmingham; M.D. Morgan, PhD, Institute of Clinical Sciences, University of Birmingham; R. Jones, MD, Department of Medicine, University of Cambridge; D.R. Jayne, MD, Department of Medicine, University of Cambridge; N. Basu, PhD, Institute of Infection, Immunity and Inflammation, University of Glasgow; L. Harper, PhD, Institute of Clinical Sciences, University of Birmingham. L.Harper@bham.ac.uk.
Abstract
OBJECTIVE: Fatigue is common and burdensome in antineutrophil cytoplasmic antibody-associated vasculitis (AAV). This study aimed to understand how fatigue changes over time following treatment initiation and to determine whether individuals with the poorest prognosis can be robustly identified. METHODS: One hundred forty-nine patients with AAV and new-onset disease recruited to 2 clinical trials (RITUXVAS and MYCYC) were followed for 18 months. Fatigue was measured at baseline and 6-month intervals using the vitality domain of the Medical Outcomes Study Short Form-36 quality of life questionnaire and compared to a cohort of 470 controls. Group-based trajectory modeling (GBTM) determined trajectories of the symptom to which baseline characteristics and ongoing fatigue scores were compared. RESULTS: Fatigue levels at diagnosis were worse in patients than controls [median (interquartile range; IQR) 30 (10-48) vs 70 (55-80); p < 0.001], with 46% of patients reporting severe fatigue. Fatigue improved after 6 months of treatment but remained worse than in controls (p < 0.001). GBTM revealed varied trajectories of fatigue: low fatigue stable (n = 23), moderate baseline fatigue improvers (n = 29), high baseline fatigue improvers (n = 61), and stable baseline high fatigue (n = 37). Participants who followed stable high fatigue trajectories had lower vasculitis activity compared to improvers, but no other demographic or clinical variables differed. CONCLUSION: This study longitudinally measured fatigue levels in patients with AAV. Although most patients improved following treatment, an important subgroup of patients reported persistently high levels of fatigue that did not change. Few clinical or laboratory markers distinguished these patients, suggesting alternative interventions specific for fatigue are required. [clinicaltrialsregister.eu, RITUXVAS EudraCT number: 2005-003610-15; MYCYC EudraCT number: 2006-001663-33].
OBJECTIVE: Fatigue is common and burdensome in antineutrophil cytoplasmic antibody-associated vasculitis (AAV). This study aimed to understand how fatigue changes over time following treatment initiation and to determine whether individuals with the poorest prognosis can be robustly identified. METHODS: One hundred forty-nine patients with AAV and new-onset disease recruited to 2 clinical trials (RITUXVAS and MYCYC) were followed for 18 months. Fatigue was measured at baseline and 6-month intervals using the vitality domain of the Medical Outcomes Study Short Form-36 quality of life questionnaire and compared to a cohort of 470 controls. Group-based trajectory modeling (GBTM) determined trajectories of the symptom to which baseline characteristics and ongoing fatigue scores were compared. RESULTS: Fatigue levels at diagnosis were worse in patients than controls [median (interquartile range; IQR) 30 (10-48) vs 70 (55-80); p < 0.001], with 46% of patients reporting severe fatigue. Fatigue improved after 6 months of treatment but remained worse than in controls (p < 0.001). GBTM revealed varied trajectories of fatigue: low fatigue stable (n = 23), moderate baseline fatigue improvers (n = 29), high baseline fatigue improvers (n = 61), and stable baseline high fatigue (n = 37). Participants who followed stable high fatigue trajectories had lower vasculitis activity compared to improvers, but no other demographic or clinical variables differed. CONCLUSION: This study longitudinally measured fatigue levels in patients with AAV. Although most patients improved following treatment, an important subgroup of patients reported persistently high levels of fatigue that did not change. Few clinical or laboratory markers distinguished these patients, suggesting alternative interventions specific for fatigue are required. [clinicaltrialsregister.eu, RITUXVAS EudraCT number: 2005-003610-15; MYCYC EudraCT number: 2006-001663-33].
Entities:
Keywords:
ANCA-ASSOCIATED VASCULITIS; FATIGUE; QUALITY OF LIFE
Authors: Alexandre Moura Dos Santos; Rafael Giovani Misse; Isabela Bruna Pires Borges; Sarah Luiza Gomes da Silva; Ana Woo Sook Kim; Rosa Maria R Pereira; Samuel Katsuyuki Shinjo Journal: Rheumatol Adv Pract Date: 2022-07-21