Little is known about depression in SLE. To evaluate the prevalence of depression and associated factors in a large, multicenter SLE cohort (RELESSER-PROS).
Methods
Prospective longitudinal study of SLE patients answering positively to the depression question of the Lupus Impact Tracker (LIT) questionary (question number 7, LITQ7 'I was depressed') over 5 consecutive annual visits (V1 to V5). Self-perceived depression was answered from 0 ('none of the time') to 4 ('most of time'). Covariates with potential impact in depression were considered. Friedman test and GEE models were used.
Results
1463 patients were included. Mean age 55 years, 90% female. Mean disease duration: 14 years. Fibromyalgia was present in 5.7%. Glucocorticoids use ranged from 49.4% to 57%, depending on the visit. SLEDAI ranged from 0 to 2 and SDI from 1 to 2. Prevalence of 'depression any time' was 89.9% and 'most of time' in 34.6%. Up to 26.5% answered to LITQ7 'depression most of time' in the five visits. 89.7% perceived themselves as depressed at least in 2 out of 5 visits. Only 6.9% of the patients with previous diagnosis of depression answered '0' ('none of the time') to LITQ7. SLEDAI, SDI, Charlson and glucocorticoids use showed statistically significative changes during the follow up. Patients with 'depression any time' developed more damage at V5 than patients without depression (p=0.009). In the GEE binomial analysis, fibromyalgia (OR 2.79), unemployment (OR 1.95) and glucocorticoids use (OR 1.88) were significantly associated with 'depression any time'. The best model displayed a significant association with fibromyalgia (OR 2.90) and glucocorticoids (OR 1.85). Neither SDI nor unemployment reached significance (table 1). Without entering glucocorticoids, SLEDAI turns significant in the model, suggesting collinearity.
Conclusions
The prevalence of self-perceived depression is high in SLE. Our study suggests causal relationship between glucocorticoids use, fibromyalgia and self-perceived depression.
Remission and Low Disease activity state (LDAS) are physician assessed treat to target-T2T outcomes for Systemic Lupus Erythematosus (SLE). Lupus Impact Tracker (LIT), a ten-item unidimensional patient reported tool has good psychometric properties and responds to patient reported changes in health, physician based disease activity (DA) and composite response Index (SRI). Herein we report responsiveness of LIT to changes in physician (T2T) and patient assessed outcomes (DA by SLAQ and health status (EQ5D)) among SLE patients from the largest European SLE registry- cohort.
Methods
One-year longitudinal, observational, multi-center data from 1364 adult patients with SLE meeting 1997 ACR criteria were obtained from baseline and year 1 visit. This included demographics, patient reported tools (LIT, EQ5D VAS, SLAQ), SLE (activity-SLEDAI) and medications. Remission off therapy (ROFT) was defined as SLEDAI=0 without prednisone or Immunosuppressive/s. Remission on-therapy (RONT) was SLEDAI=0 and a prednisone dose 5 mg/day and/or Immunosuppressive/s (maintenance dose). LDAS (modified) was defined as SLEDAI 4, prednisone dose 9 mg/day and/or maintenance immunosuppressive/s. Non-optimal (NO) disease status was SLEDAI >4 and/or prednisone dose >9 mg/day and/or immunosuppressive/s in induction dose. Use of hydroxychloroquine was permitted in all groups. LIT values were compared using mixed models. Responsiveness was evaluated by standard response means (SRM) in groups with changes in DA (T2T, SLAQ) and EQ5D VAS as anchors. We did not have enough observations for stratified analysis for SLE patients with fibromyalgia.
Results
1232/1364 (90%) were women, and 95% were Caucasian. Mean (SD) SLEDAI and SDI were 2.6 (3.5) and 0.7 (1.1) respectively. As (i) DA was low (median 2) in LDAS, (ii) steroid use was more prevalent in RONT than LDAS, we combined RONT and LDAS into one category to analyse patient relevant differences in LIT. LIT was responsiveness in the appropriate direction with improvement and worsening in disease activity (T2T and SLAQ) and health status (EQ5D VAS) over time. Mean LIT changes to and from NO to RONT/LDAS ranged from 3–5 (table 1), while it declined by over 8.5 with change from NO to ROFT. We had limited observations for ROFT to NO change. Mean change in LIT ranged from −3 to 3 with improvement and worsening in SLAQ, and from −7.6 to 6 with improvement and worsening in EQ5D VAS.
Conclusions
LIT responds appropriately in both directions to changes in physician (T2T) as well as patient relevant (DA and health status) outcomes among Spanish SLE patients.
Background/Objectives: Interstitial lung disease (ILD) is one of the most severe complications of rheumatoid arthritis (RA). Real-world data on antifibrotic treatment are needed. Our objective was to evaluate the real-world effectiveness and tolerability of antifibrotic agents in patients with progressive fibrosing RA-ILD. Methods: A longitudinal, retrospective, observational study was conducted on a cohort of RA-ILD patients treated with either nintedanib or pirfenidone. The data collected included pulmonary function test (PFT) results, adverse events (AEs), tolerability, and drug retention. Results: Twenty-seven patients were included; 25 (92.5%) initiated nintedanib, while two initiated pirfenidone. The median follow-up duration was 25 months (IQR 7–27). The mean decline in %pFVC and %pDLCO from ILD diagnosis to the initiation of antifibrotic therapy were −8.9% and −14.8%, respectively. After 6 months of treatment, most patients achieved stabilization in PFT: a ∆%pFVC of +1.2% (p = 0.611 compared with baseline) and a ∆%pDLCO of +3.9% (p = 0.400). Eighteen patients completed one year of therapy, with a modest improvement in %pFVC (+4.7%; p = 0.023) and stabilization in %pDLCO (−3.8%; p = 0.175). This trend persisted among the nine patients who completed 2 years of treatment (%pFVC +7.7%; p = 0.037 and %pDLCO −2.2%; p = 0.621). During the follow-up period, 15% of patients died, and 4% underwent lung transplantation. Adverse events occurred in 81% of patients, leading to discontinuation in 18.5% of cases. The most frequent adverse events were gastrointestinal events and hepatitis, leading to a permanent dose reduction of 40% for nintedanib and 14% for pirfenidone. A second antifibrotic agent was prescribed for 18.5% of the patients. At the end of the follow-up period, 63% of the total cohort remained on antifibrotic therapy. Conclusions: According to our results, antifibrotic initiation was associated with a modest improvement in the trajectory of %pFVC and stabilization in %pDLCO. The discontinuation rate in our cohort (37%) was higher than that reported in clinical trials but similar to that reported in previously published real-world studies.
To estimate the incidence and analyze any cancer-associated factors in patients with systemic lupus erythematosus (SLE), differentiating between hormone-sensitive (HS) and non-HS cancers.This was a retrospective multicenter study of a patient cohort from the Systemic Lupus Erythematosus Registry of the Spanish Society of Rheumatology. Included were the first cancer post-SLE diagnosis, clinical and sociodemographic information, cumulative damage, severity, comorbidities, treatments, and refractoriness. Cancers were classified as HS (prostate, breast, endometrium, and ovarian) and non-HS (the remainder). The standardized incidence ratio (SIR) was calculated and logistic regression models were built.A total of 3,539 patients (90.4% women) were included, 154 of whom had cancer (91% female), and 44 had HS cancer (100% female). The cancer SIR was 1.37 (95% confidence interval [95% CI] 1.15-1.59), with higher values in women age <65 years (SIR 2.38 [95% CI 1.84-2.91]). The SIR in women with HS versus non-HS cancer was 1.02 (95% CI 0.13-1.91) and 1.93 (95% CI 0.98-2.89). In HS versus non-HS cancers, SLE diagnostic age (odds ratio [OR] 1.04 [P = 0.002] versus 1.04 [P = 0.019]), and period of disease evolution (OR 1.01 [P < 0.001] versus 1.00 [P = 0.029]) were associated with cancer. The Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (OR 1.27 [P = 0.022]) and angiotensin-converting enzyme (ACE) inhibitor prescriptions (OR 2.87 [P = 0.048]) were associated with non-HS cancers.Cancer incidence in patients with SLE was higher than in the Spanish population, particularly among young women. This increase might be due to non-HS cancers, which would be associated with SLE involving greater cumulative damage where more ACE inhibitors are prescribed.
Abstract Objective Previous studies have shown either a lack of effect of IRF5 polymorphisms or an association of the IRF5 gene in only a minor subset of rheumatoid arthritis (RA) patients in whom anti–citrullinated protein antibodies (ACPAs) are absent. The present study was undertaken to investigate the role of genetic variation in IRF5 in susceptibility to RA. Methods Nine IRF5 single‐nucleotide polymorphisms (SNPs) were studied in 1,338 patients with RA and 1,342 control subjects in analyses of exploratory and replication sample collections, with stratification according to sex and by the presence or absence of ACPAs, rheumatoid factor, the shared epitope, the 620W PTPN22 allele, and erosions. A meta‐analysis that included results from previous studies was also carried out. Results Our findings together with those from previous studies, in a total of 4,620 RA patients and 3,741 controls, showed a significant association of the rs2004640 IRF5 SNP in RA patients as a whole (odds ratio [OR] 0.88, 95% confidence interval [95% CI] 0.83–0.94; P = 6.5 × 10 −5 versus controls). This association was stronger in ACPA− patients, but was also present in ACPA+ patients (from 3 sample collections). Further analysis of our exploratory sample collection showed that only patients in the ACPA+ and SE− group lacked an association with IRF5 SNPs. All of the remaining RA patients (ACPA− or SE+) showed a strong association with IRF5 SNPs, which followed a complex pattern of opposing effects mediated by independent haplotypes. The susceptibility haplotype showed an OR of 1.8 (95% CI 1.4–2.3; P = 1.2 × 10 −6 versus controls), whereas the protective haplotype showed an OR of 0.76 (95% CI 0.6–0.98; P = 0.046 versus controls). Conclusion IRF5 polymorphisms seem to influence RA susceptibility in a large subgroup of patients, following a pattern of association very similar to that described in patients with systemic lupus erythematosus.