Over the last decades new therapies have been approved and new treatment strategies have been proposed in the treatment of SLE. In particular, recently, EULAR recommendations1 and the Treat to… Click to show full abstract
Over the last decades new therapies have been approved and new treatment strategies have been proposed in the treatment of SLE. In particular, recently, EULAR recommendations1 and the Treat to Target2 approach established a new paradigm for the treatment of SLE based on the early introduction of immunosuppressive treatment and glucocorticoids (GC) minimization.to evaluate changes in therapeutic approach and outcomes over the last three decades in a monocentric cohort of SLE patients.This is a retrospective analysis of prospectively collected data from a monocentric cohort of patients with SLE with disease diagnosis between 1990 and 2020. Based on the year of diagnosis, patients were divided in three groups, each of them corresponding to a decade: group 1: decade 1990-1999; group 2: decade 2000-2009; group 3: decade 2010-2020. For each patient, epidemiological and demographic characteristics, cumulative organ involvement and serology, previous and ongoing therapies, comorbidities were collected and compared among the 3 groups. Organ damage was evaluated by the SLICC-DI (SDI)3 at 1 and 5 years from diagnosis, as comorbidities we considered hypertension, diabetes, osteoporosis and cardiovascular (CV) events occurred during the follow-up.A total of 262 SLE patients were enrolled in the study (97% Caucasian, 90.5% females): 69 patients in group 1, 100 in group 2 and 93 in group 3. Demographic and clinical characteristics of whole cohort and of the three groups are summarized in table 1. Differences in therapies during the first year from diagnosis among the groups are summarized in table 1. In group 3 the use of Micophenolate Mofetil was significantly more common with respect to the group 1 (25% vs 1.4%, p= 0.001) and similar to group 2 (25% vs 25.5%, p=ns); on the contrary, in group 3, Azathioprine (AZA) and Cyclosporine (Cya) were less used (13.2% vs 27.5%, p=0.003 and 3.3% vs 14.3%, p= 0.019 respectively). As Cyclophosphamide (CYC) is concerned, it was used with the same frequency in the three decades, but in group 1, the total dose of CYC was significantly higher than second and third group (4.8 g vs 2.3 and 0.9, p=0.02 and p=0.001 respectively). In group 2 and 3, during the first year of disease, biological drugs (Rituximab or Belimumab) have been used more frequently (2% and 2.2% vs 0%, p=0.04). Any differences have not been showed for GC among the groups. However, in group 3 a significantly higher proportion of patients stopped GC therapy within 5 years from diagnosis (34.5% vs 8.8% and 12.5%, p=0.001) and in the same group the duration of GC therapy was significantly shorter with respect to previous two decades (3.1 years vs 16.8 and 10.5 respectively, p=0.001). As regard damage accrual, at 1 and 5 years from diagnosis, no significant differences among groups were observed; however, hypertension resulted significantly less common in group 3 (10% vs 26% and 37.3%, p=0.001), even adjusting for age (OR=0.2); less CV events were recorded in group 3, but significance is lost adjusting for age.Table 1.Whole cohortGroup 1Group 2Group 3pPatients (n)2626910093Caucasian (%)97%99%98%94.6%.n.s.Females (%)90.5%94.2%95%92.5%n.s.Median age at diagnosis IQR)29 (20-36)27 (20-32)28.5 (20-36)34 (23-44)0.001Cumulative organ involvementRenal48.1%52.2%57%35.5%0.007Articular74.4%75.3%66%82.8%n.s.Serositic19.5%20.3%22%16.1%n.s.Neuropsychiatric8%11.6%6%7.5%n.s.Cutaneous63%70%60%61.3%n.s.Hematological58.4%51.5%61%61.3%n.s.Therapies 1styearAZA17.2%8.7%27.5%13.2%0.003MMF18.7%1.4%25.5%25.3%0.001CYC22.5%21.7%27%17%n.s.Cya9.9%13%14.3%3.30.019Biologicals1.5%0%2%2.2%n.sThese data show that new therapies and new treatment strategies have actually been implemented in clinical practice over the past 30 years; further studies with a longer follow-up are necessary to appreciate the impact of these advancement on clinical outcomes.[1]Bertsias G, et al. Ann Rheum Dis 2008.[2]van Vollenhoven RF, et al.Ann Rheum Dis 2014.[3]Gladman DD, et al. J Rheumatol 2000.None declared
               
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