Matteo Piga1, Alberto Floris1, Gian Domenico Sebastiani2, Imma Prevete2, Florenzo Iannone3, Laura Coladonato3, Marcello Govoni4, Alessandra Bortoluzzi4, Marta Mosca5, Chiara Tani5, Andrea Doria6, Luca Iaccarino6, Franco Franceschini7, Micaela Fredi7, Fabrizio Conti8, Francesca Romana Spinelli8, Mauro Galeazzi9, Francesca Bellisai9, Anna Zanetti10,11, Greta Carrara10, Carlo Alberto Scirè10, Alessandro Mathieu1. 1. Rheumatology Unit, University of Cagliari and AOU University Clinic, Cagliari. 2. UOC di Reumatologia, Azienda Ospedaliera San Camillo-Forlanini, Rome. 3. Dipartimento dell'Emergenza e dei Trapianto di Organi - Sezione di Reumatologia, Università di Bari, Bari. 4. UOC e Sezione di Reumatologia - Dipartimento di Scienze Mediche, Università degli Studi di Ferrara, Ferrara. 5. UOC di Reumatologia, Dipartimento di Medicina Clinica e Sperimentale, Università di Pisa, Pisa. 6. Rheumatology Unit, Department of Medicine, University of Padova, Padova. 7. UOC di Reumatologia e Immunologia Clinica, Dipartimento di Scienze Cliniche e Sperimentali, Università degli Studi di Brescia, ASST Spedali Civili, Brescia, Italy. 8. Reumatologia, Dipartimento di Medicina Interna e Specialità Mediche, Sapienza Università di Roma, Roma. 9. UOC di Reumatologia, Azienda Ospedaliera Universitaria Senese, Siena. 10. Società Italiana di Reumatologia, Unità Epidemiologica, Milano. 11. Divisione di Biostatistica, Epidemiologia e Salute Pubblica, Dipartimento di Statistica e Metodi Quantitativi, Università degli Studi di Milano-Bicocca, Milano, Italy.
Abstract
OBJECTIVE: To investigate risk factors for damage development in a prospective inception cohort of early diagnosed SLE patients. METHODS: The Early Lupus Project recruited an inception cohort of patients within 12 months of SLE classification (1997 ACR criteria). At enrolment and every 6 months thereafter, the SLICC/ACR Damage Index was recorded. The contribution of baseline and time-varying covariates to the development of damage, defined as any SLICC/ACR Damage Index increase from 0 to ≥1, was assessed using univariate analysis. Forward-backward Cox regression models were fitted with covariates with P < 0.05 to identify factors independently associated with the risk of damage development. RESULTS: Overall, 230 patients with a mean (s.d.) age of 36.5 (14.4) years were eligible for this study; the mean number of visits per patient was 5.3 (2.7). There were 51 (22.2%) patients with SLICC/ACR Damage Index ≥1 after 12 months, 59 (25.6%) after 24 months and 67 (29.1%) after 36 months. Dyslipidaemia [P = 0.001; hazard ratio (HR) 2.9; 95% CI 1.5, 5.6], older age (P = 0.001; HR 3.0; 95% CI 1.6, 5.5), number of organs/systems involved (P = 0.002; HR 1.4; 95% CI 1.1, 1.8) and cardiorespiratory involvement (P = 0.041; HR 1.9; 95% CI 1.0, 3.7) were independently associated with an increased risk of developing damage. Risk profiles for damage development differed for glucocorticoid-related and -unrelated damage. HCQ use (P = 0.005; HR 0.4; 95% CI 0.2, 0.8) reduced the risk of glucocorticoid-unrelated damage. CONCLUSION: We identified risk factors of damage development, but little effect of glucocorticoids, in this early SLE cohort. Addressing modifiable risk factors from the time of SLE diagnosis might improve patient outcomes.
OBJECTIVE: To investigate risk factors for damage development in a prospective inception cohort of early diagnosed SLEpatients. METHODS: The Early Lupus Project recruited an inception cohort of patients within 12 months of SLE classification (1997 ACR criteria). At enrolment and every 6 months thereafter, the SLICC/ACR Damage Index was recorded. The contribution of baseline and time-varying covariates to the development of damage, defined as any SLICC/ACR Damage Index increase from 0 to ≥1, was assessed using univariate analysis. Forward-backward Cox regression models were fitted with covariates with P < 0.05 to identify factors independently associated with the risk of damage development. RESULTS: Overall, 230 patients with a mean (s.d.) age of 36.5 (14.4) years were eligible for this study; the mean number of visits per patient was 5.3 (2.7). There were 51 (22.2%) patients with SLICC/ACR Damage Index ≥1 after 12 months, 59 (25.6%) after 24 months and 67 (29.1%) after 36 months. Dyslipidaemia [P = 0.001; hazard ratio (HR) 2.9; 95% CI 1.5, 5.6], older age (P = 0.001; HR 3.0; 95% CI 1.6, 5.5), number of organs/systems involved (P = 0.002; HR 1.4; 95% CI 1.1, 1.8) and cardiorespiratory involvement (P = 0.041; HR 1.9; 95% CI 1.0, 3.7) were independently associated with an increased risk of developing damage. Risk profiles for damage development differed for glucocorticoid-related and -unrelated damage. HCQ use (P = 0.005; HR 0.4; 95% CI 0.2, 0.8) reduced the risk of glucocorticoid-unrelated damage. CONCLUSION: We identified risk factors of damage development, but little effect of glucocorticoids, in this early SLE cohort. Addressing modifiable risk factors from the time of SLE diagnosis might improve patient outcomes.
Authors: Melissa E Munroe; Kendra A Young; Joel M Guthridge; Diane L Kamen; Gary S Gilkeson; Michael H Weisman; Mariko L Ishimori; Daniel J Wallace; David R Karp; John B Harley; Jill M Norris; Judith A James Journal: Front Immunol Date: 2022-06-03 Impact factor: 8.786