Predictive factors of flares in systemic lupus erythematosus patients: data from a multiethnic Latin American cohort

Abstract

Purpose The purpose of this paper is to determine the factors predictive of flares in systemic lupus erythematosus (SLE) patients. Methods A case-control study nested within the Grupo Latino Americano De Estudio de Lupus (GLADEL) cohort was conducted. Flare was defined as an increase ≥4 points in the SLEDAI. Cases were defined as patients with at least one flare. Controls were selected by matching cases by length of follow-up. Demographic and clinical manifestations were systematically recorded by a common protocol. Glucocorticoid use was recorded as average daily dose of prednisone and antimalarial use as percentage of time on antimalarial and categorized as never (0%), rarely (>0-25%), occasionally (>25%-50%), commonly (˃50%-75%) and frequently (˃75%). Immunosuppressive drugs were recorded as used or not used. The association between demographic, clinical manifestations, therapy and flares was examined using univariable and multivariable conditional logistic regression models. Results A total of 465 cases and controls were included. Mean age at diagnosis among cases and controls was 27.5 vs 29.9 years, p = 0.003; gender and ethnic distributions were comparable among both groups and so was the baseline SLEDAI. Independent factors protective of flares identified by multivariable analysis were older age at diagnosis (OR = 0.929 per every five years, 95% CI 0.869-0.975; p = 0.004) and antimalarial use (frequently vs never, OR = 0.722, 95% CI 0.522-0.998; p = 0.049) whereas azathioprine use (OR = 1.820, 95% CI 1.309-2.531; p < 0.001) and SLEDAI post-baseline were predictive of them (OR = 1.034, 95% CI 1.005-1.064; p = 0.022). Conclusions In this large, longitudinal Latin American cohort, older age at diagnosis and more frequent antimalarial use were protective whereas azathioprine use and higher disease activity were predictive of flares.

Evaluation of belimumab treatment in patients with systemic lupus erythematosus in a clinical practice setting: Results from a 24-month OBSErve study in Argentina

“…6,7 In Latin America, studies performed by GLADEL (Grupo Latino Americano De Estudio del Lupus) demonstrated that in patients with SLE, the risk of damage accrual increases with each flare, regardless of flare severity and independently of other known risk factors, such as gender, age at diagnosis, disease duration, high disease activity, previous damage, the presence of antiphospholipid antibodies and antiphospholipid syndrome, high-dose corticosteroids and immunosuppressants, non-Caucasian race/ethnicity, and socio-economic factors. 8,9 Since 2011, belimumab, a new generation biologic therapy, has become available for adults with SLE 10,11 and children 5-17 years of age with childhood-onset SLE. 12 Belimumab is a human, immunoglobulin 1k monoclonal antibody that binds and antagonises the biological activity of circulating B-cell activating factor (BAFF), also known as B-lymphocyte stimulator (BLyS), which is elevated in patients with SLE and promotes abnormal B-cell activation and differentiation.…”

Outcomes of Systemic Lupus Erythematosus in Patients who Discontinue Hydroxychloroquine

“…Other studies have confirmed that HCQ is protective against flares in SLE. In a large case control study of 465 patients with SLE, older age at diagnosis of SLE and HCQ use were the only protective variables amongst numerous examined variables . Similarly, in a randomized, placebo‐controlled trial of 24 patients, Meinão et al found that HCQ reduced disease exacerbation rates, prednisone dose, and Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) scores in SLE .…”

Chloroquine Is Effective for Maintenance of Remission in Autoimmune Hepatitis: Controlled, Double‐Blind, Randomized Trial

“…In systemic lupus erythematosus, for which they were better studied, they have beneficial effects on general and disease-free survival, with a reduction in the risk and delay of quiescent disease reactivation, improvement of the metabolic profile, and protection against occurrence of serious infections. (5,6,16) Their possible mechanisms of action in the pathophysiology of AIH include inhibition of the processing and presentation of antigens, inhibition of cytokine release (interleukins 1, 2, and 6; tumor necrosis factor α; and interferon-γ), inhibition of the T helper 17 response (inhibition of the release of interleukins 6, 17, and 22), decreased natural killer cell activity, inhibition of polymorphonuclear chemotaxis, and inhibition of the activity of cytotoxic T lymphocytes and clusters of differentiation (CD)4+ T lymphocytes with autoreactivity. (17,18) In the current study, possible biases that could have interfered with the results were avoided.…”