View clinical trials related to Lupus Erythematosus, Systemic.
Filter by:This project is intended to identify the routes on which BAFF and APRIL act in order to detect possible future candidates to Belimumab treatment among patients diagnosed of SLE.
This is a 36 months, randomized, double-blind, placebo-controlled, parallel-groups, equivalence multicenter trial in patients with inactive Systemic Lupus Erythematosus to evaluate if low disease activity can be sustained with withdrawal of glucocorticoids in patients on stable clinical remission or low disease activity.
Systemic lupus erythematosus (SLE) is systemic autoimmune disease characterized by various immunological abnormalities, including dysregulated activation of both T and B lymphocytes with overt production of autoreactive antibodies.The chemokine CXC ligand 13 protein (CXCL13), also known as B cell-attracting chemokine-1 (BAC-1) or B lymphocyte chemoattractant (BLC), CXCL13 serum levels were correlated with disease activity using the SLE Disease Activity Index (SLEDAI) and to lupus nephritis
Systemic lupus erythematosus is systemic autoimmune disease characterized by a wide range of clinical manifestations, from skin and mucosal lesions to severe injuries in the central nervous system, kidneys and other organs. The presence of high titres of autoantibodies against nuclear components, immune complexes deposition, complement deficiency and lymphocytes infiltration in affected tissues, which causes tissue and organ damage are the main characteristics of the disease. Nowadays, many studies elucidate the essential role of autophagy in the occurrence, development and severity of systemic lupus erythematosus.
The primary objective of the study is to assess the efficacy of DHA in patients with SLE.
This study is to evaluate the safety and efficacy of human umbilical cord derived mesenchymal stem cells transplantation in systemic lupus erythematosus.
Systemic lupus erythematosus , the archetypal multisystem autoimmune disease, presents many diagnostic and management challenges. One such challenge is the excess cardiovascular disease observed in patients with Systemic lupus erythematosus . Coronary heart disease and other manifestations of atherosclerosis continue to be a major cause of death in patients with Systemic lupus erythematosus.Regulatory B-cells have been identified as a negative regulator of the immune system that inhibit pathological immune response by suppressing both uncontrolled protective immune response and damaging autoimmune responses
Systemic lupus erythematosus is a chronic inflammatory autoimmune disease with an unknown cause and many challenges. Whilst corticosteroids and effective immunosuppressive therapy have transformed the management of patients with active systemic lupus erythematosus, one of the major causes of morbidity in Systemic lupus erythematosus patients is chronic, debilitating fatigue. Despite frequent occurrence of fatigue in Systemic Lupus Erythematosus, to the best of our knowledge, no studies have been directly performed to examine fatigue-related changes in cortical motor function in Systemic lupus erythematosus. In this study, we hypothesized that Systemic lupus erythematosus patients with fatigue and depression versus Systemic lupus erythematosus patients without fatigue and depression would present an alteration of motor cortex excitability.
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease affecting many organ systems. SLE includes a wide spectrum of severity, ranging from relatively mild manifestations (e.g. skin rash or non-erosive arthritis) to seriously disabling or even life threatening complications, such as lupus nephritis (LN) and neuropsychiatric disorders . LN is one of the most serious SLE complications since it is the major predictor of poor prognosis . Lupus nephritis is a common major organ manifestation and main cause of morbidity and mortality of the disease . It is occurred in 30-50% of SLE patients at initial diagnosis and more prevalent in Asians and Blacks than other races . Approximately, 10-30% of LN patients will develop the end-stage renal disease (ESRD) within 15 years after diagnosis. The 5-year survival rate of a patient with severe LN is less than70-80%. Therefore, an involvement of renal disease activity is one of the most important prognostic factors for patients with SLE, and the diagnosis of SLE patients with LN has an important clinical implication in guiding the treatment of SLE in clinical settings.
Systemic Lupus Erythematosus (SLE) is the most common systemic autoimmune disease. The clinical manifestations are severe and affect multiple target organs such as the kidney, central nervous system, skin, heart and joints. Despite the progress made in the therapeutic approach with new immunosuppressive regimens, morbi-mortality is still high. Therefore, it's important to identify new biomarkers to help clinicians to predict severity and evolution of the disease for better adaptation of treatments and try to improve the prognosis. RAGE (Receptor for Advanced Glycation Endproducts) : RAGE (Receptor for Advanced Glycation Endproducts) is an ubiquitous membrane receptor, involved in development of many diseases such as diabetes, chronic renal failure but also in vascular remodelling, inflammatory, infectious deseases and cancer. RAGE regulates a number of crucial cell processes like inflammation, and tissue and cellular homeostasis. RAGE is able to bind not only the advanced glycation end products (AGEs) such as pentosidine, carboxymethyllysine (CML), methyl-glyoxal-hydroimidazolone-1 (MG- H1), but also other ligands such as HMGB1 (high mobility group box1), and S100A8/A9 proteins which have been correlated in recent studies to the activity index of SLE. The activation of RAGE leads to a cascade of intracellular signaling and activation of the transcription factor NF-ΚB . NF-ΚB enable the traduction of proinflammatory cytokines such as IL-6, IL-1α ,IFN-γ. In SLE, these cytokines involved in perpetuation of inflammation and tissue damages including lupus nephritis. Moreover, the activation of RAGE induces the expression of adhesion molecule such as sICAM -1 and sVCAM -1 wich were recently involved in SLE vasculitis. Soluble forms of RAGE, sRAGE and esRAGE : RAGE is a proinflammatory membrane receptor. But RAGE also exists in soluble plasma forms, esRAGE (secreted form) and sRAGE (a truncated form as cleaved by MMP9 and ADAM10 enzymes). esRAGE and sRAGE have the same ligand-binding specificity as RAGE and may function as a 'decoy receptor' by binding pro-inflammatory ligands and preventing them from accessing cell surface RAGE (Kierdorf and Fritz, 2013). Therefore, both soluble forms have an anti-inflammatory action. Several studies have shown a decrease in circulating levels of sRAGE in patients with Rheumatoid Arthritis, or Sjögren Syndrome compared with healthy controls. However, the role of RAGE in SLE remains unknown. RAGE and Systemic Lupus Erythematosus, recent advances : Our team (Laboratory of Nephrology, CNRS UMR 7369, URCA) showed in a study in lupus RAGE knockout mice (B6/ MRL-FAS lpr/J RAGE-/-) a strong involvement of RAGE in systemic manifestations SLE. Recently, another report showed that sRAGE has an anti-inflammatory effect on the lupus nephritis and could be a potent therapy in mice. In humans, two studies show a correlation between the plasma level of sRAGE and lupus phenotype ( Nienhuis et al. , 2008). Working hypothesis : Based on the results and those of the current studies, the investigators think that RAGE axis and its soluble forms play a crucial role in the complex pathogenesis of SLE. The investigators hypothesize that plasma levels sRAGE and esRAGE are a reflection of the activity and the development of SLE in humans. Soluble forms of RAGE and ligands may be novel biomarkers of SLE and sRAGE a potent therapeutic target.