ObjectivesPrimary objective was to investigate clinical features and biomarkers associated with severe systemic lupus erythematosus (SLE). The secondary objective was to identify patterns of SLE remission. ’MethodsA retrospective study of 200 SLE patients (2014–20) from ImmunoCure Center was conducted. Patients fulfilled ACR criteria 1997 for SLE classification. SLEDAI-2K categories mild-moderate (score <=10) and severe (score >10) were used as outcome for the primary objective. Predictors of severe SLE were evaluated by multivariate logistic regression analysis. For the secondary objective, we evaluated 94 records with follow-up time >1year. Remission status (Yes/No) was based on DORIS criteria. Survival regression was performed using Kaplan Meier curve.ResultsSignificant predictors of severe SLE were male gender (OR 4.1; 95% CI: 1.2, 13.5), oral ulcers (OR 6.9; 95% CI: 2.8, 17.1), alopecia (OR 2.1; 95% CI 1.0-4.1), nephritis (OR 4.5; 95% CI: 1.9-11.4), ESR >30mm/hour (OR 2.3; 95% CI: 1.2-4.4) and aCL antibodies (OR 2.4, 95% CI 1.0 -5.9). The mean duration of follow-up was 41±19 months. Remission on treatment was achieved in 66% of 94 patients, while off treatment in 21% with a mean post-remission follow-up of 18±15 months. For every one-month increase in the duration of follow-up, the hazard of time to remission increased by 4% (95% CI 0.95-0.98;P<0.001). Factor analysis identified 4 SLE subtypes.ConclusionA clinical model including aCL antibodies is presented here that predicts severe SLE. Remission is possible even in severe SLE in LMIC with adequate immunosuppression and persistent follow-up.
BackgroundUndifferentiated Arthritis (UA) is a group of inflammatory disorders where early synovitis (duration less than 12 months) is present, however patients do not meet criteria for established rheumatologic disorders such as Rheumatoid arthritis, Lupus or Spondyloarthritis (1). On long term follow up, a subpopulation of UA patients converge into definitive Rheumatologic disorders. Up to 50% of early arthritis in European cohorts has been reported to be UA (1, 2).ObjectivesIdentify Anti-nuclear antibody (ANA) Subset antibodies in patients presenting with early UA.MethodsOver a 1-year period (2017-18) patients with early UA were prospectively evaluated. This included clinical exam, routine laboratory investigations including ESR and CRP, RF and anti-CCP as well as Musculoskeletal ultrasound (MSKUS) (3). These patients underwent further testing for ANA Subset antibodies. ANA subsets (17 antibodies) were performed using standard immunoblot assays (EUROIMMUN) at our clinical laboratory (4).Results110 UA patients were found to have positive ANA subsets. The most frequent antibodies were Ku (77.3%) and Mi2 (73.6%) followed by dsDNA (30%) and Nucleosome antibody (29%) (Figure 1). Low frequency antibodies included Sm (n=1), Ribosomal-P and PCNA (n=2 each), Jo-1 (n=3), PM-Scl100 (n=4) and SSB (n=5), whereas Scl70 antibodies were absent. SSA (n=9) and Ro-52 (n=14) together constituted 21% frequency. These antibodies had high signal intensities (mean ± SD SSA = 52±35 and Ro-52 = 46±25). Ku (17±11) and Mi2 (22±15) had modest signal intensities (Figure 2). Clinically 42 patients were classified as RA (RF+ = 33%; anti-CCP+ = 14%) and 41 patients met ACR criteria for SLE while 2 patients met criteria for both and were classified as Rhupus. ANA subset antibody frequencies did not statistically differ between the RA and SLE groups signifying that the clinically classified RA patients in fact had early Rhupus which did not meet ACR criteria for SLE.ConclusionEarly UA is difficult to categorize clinically, sometimes even after long term follow up, though a substantial portion converge into RA. This study shows that there is a significant portion of early Rhupus in the RA group whose steroid discontinuation leads to a disease flare. ANA Subset antibody profile in such patients may help in their more accurate diagnoses and treatment.References[1] van Aken J, van Bilsen JH, Allaart CF, Huizinga TW, Breedveld FC. The Leiden Early Arthritis Clinic. Clin Exp Rheumatol. 2003 Sep-Oct;21(5 Suppl 31):S100-5. PMID: 14969059.[2] Hülsemann JL, Zeidler H. Undifferentiated arthritis in an early synovitis out-patient clinic. Clin Exp Rheumatol. 1995 Jan-Feb;13(1):37-43. PubMed PMID: 7774101.[3] Horton SC, Tan AL, Wakefield RJ, Freeston JE, Buch MH, Emery P. Ultrasound-detectable grey scale synovitis predicts future fulfilment of the 2010 ACR/EULAR RA classification criteria in patients with new-onset undifferentiated arthritis. RMD Open. 2017;3(1):e000394. PMID: 28469936.[4] Op De Beéck K, Vermeersch P, Verschueren P, Westhovens R, Mariën G, Bl...
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