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Abstract Number: 2924

Determinants of Damage in an SLE Cohort: Real World Data

Maria Francisca Moraes-Fontes1, Eliana Silva2, Nuno Riso3 and Margarida Jacinto4, 1Autoimmune Diseases Unit, Serviço Medicina 7.2, Hospital de Curry Cabral, Centro Hospitalar Lisboa Central, Lisbon, Portugal, 2Patologia Clínica, Instituto Português de Oncologia, Francisco Gentil, Lisboa, Portugal, 3Serviço de Medicina 7.2, Hospital de Curry Cabral, Centro Hospitalar Lisboa Central, Lisbon, Portugal, 4Medicina Interna - Serviço 1, Hospital Espírito Santo - Évora, Évora, Portugal

Meeting: 2015 ACR/ARHP Annual Meeting

Date of first publication: September 29, 2015

Keywords: Disease Activity, SLE and neurologic involvement

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Session Information

Date: Tuesday, November 10, 2015

Title: Systemic Lupus Erythematosus - Clinical Aspects and Treatment Poster Session III

Session Type: ACR Poster Session C

Session Time: 9:00AM-11:00AM

Background/Purpose: Across the spectra of autoimmune diseases RA stands out, as biomarkers present from the onset are associated with severity and can be a guide to therapy. In contrast, in SLE, genetic susceptibility has no clinical applicability, specific autoantibodies do not predict disease course, determinants of target organ remain unknown and clinical outcome is unpredictable for individual patients. In practice, damage accrual is therefore the best measure which is used to define SLE disease severity, found to predict future mortality. The objective of this study was to test the validity of damage determinants in a single-centre cohort.  

Methods: Prospectively followed SLE female patients (defined by the identification of at least 4 SLE ACR criteria – fulfillement 100%, n=76) over the past 5 years. Age of onset, ethnicity, disease duration, number of ACR criteria at the end of follow-up, cumulative: renal, neuropsychiatric and articular phenotypes, hypertension, dyslipidemia, smoking, hydroxychloroquine, immunosuppressive use and SLEDAI 2K were correlated to the presence and degree of irreversible damage, as measured by SLICC/SDI in its several domains. Accumulation of ACR criteria was measured in a sub-group of patients followed from disease onset (within a year of the first symptom ascribed to SLE) (n=39 – 51%); SLEDAI and SLICC were performed bi-annualy and annualy, respectively. Univariate statistical analysis was performed using the Wilcoxon Mann-Whitney, Chi-Square tests and bivariate analysis for non-parametric distributed data (Sig. 2-tailed p < 0,05).

Results: SLICC SDI index > 0 was present in 43/76 (56.6%) and significantly associated to a longer disease duration, a higher number of ACR criteria and a neuropsychiatric (NP) phenotype when compared with those with no damage. There was no effect from any other demographic or clinical features (Table I). The final number of ACR criteria accrued was positively correlated to a higher disease activity over the past 5 years of follow-up (Spearman´s rho 0.02). Mean disease activity (SLEDAI 2K ≥ 3) over the past 5 years was not correlated to damage accrual at the end of follow-up according to disease duration: ≤ 5 and < 10y (n=17); ≥ 10 and < 20y (n=32); ≥ 20 (n=27).

Table I: Univariate analysis comparing patients with and without damage according to SLICC SDI index
Characteristic SLICC < 1 (n=43) SLICC ≥ 1 (n=33) P value (Sig*) Statistical Test
Age at disease onset (years) (mean ± SD) 32 ± 11 31 ± 13 0.653 Mann Whitney (MW)
Non-Caucasian (n, %) 4 (44.4) 5 (55.6) 0.610 Pearson Chi-square (PCS)
Disease Duration (years) (mean ± SD) 14 ± 7 19 ± 8 0.007* MW
Hypertension (n, %) 16 (36.4) 27 (61.4) 0.338 PCS
Dyslipidemia (n, %) 12 (34.3) 22 (62.9) 0.201

PCS

Smoking (n, %) 7 (43.8) 9 (56.2) 1.000 PCS
Malignancy (n, %) 0 (0) 6 (100) 0.111 PCS
Infection (n, %) 16 (39) 24 (58.5) 0.809 PCS
Neuropsychiatric (n, %) 2 (11.1) 16 (88.9) 0.004* PCS
Renal (n, %) 13 (41.9) 17 (54.8) 0.614 PCS
Articular (n, %) 22 (39.3) 33 (58.9) 0.631 PCS
Anti-nuclear Ab (n, %) 32 (42.1) 43 (56.6) 1.000 PCS
Anti-dsDNA (n, %) 24 (41.4) 33 (56.9) 1.000 PCS
Mean SLEDAI (bi-annual, past 5 years) 2.2 ± 2.0 3.6 ± 2.9 0.054 MW
Cumulative ACR criteria – first 6 months after disease onset (n available) 4.1 ± 1.3 (n=21) 3.7 ± 1.5 (n=18) 0.280 MW
Cumulative ACR criteria – end of follow-up 5.0 ± 1.1 5.6 ± 1.4 0.046* MW

Conclusion: Disease duration and number of ACR criteria predict SLICC SDI as previously reported1. In our cohort, NP disease has a major impact on damage accrual.

References: 1Bruce IN et al. doi:10.1136/annrheumdis-2013-2051-71


Disclosure: M. F. Moraes-Fontes, None; E. Silva, None; N. Riso, None; M. Jacinto, None.

To cite this abstract in AMA style:

Moraes-Fontes MF, Silva E, Riso N, Jacinto M. Determinants of Damage in an SLE Cohort: Real World Data [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/determinants-of-damage-in-an-sle-cohort-real-world-data/. Accessed .
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