View clinical trials related to Lupus Erythematosus, Systemic.
Filter by:Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease that involve many different organs and display a variable clinical course.The prevalence of SLE varies across gender, race/ethnicity, and geographic regions. SLE demonstrates a striking female predominance with a peak incidence of disease during the reproductive years. In adults, the female to male ratio is 10- Renal involvement is common in SLE and is a significant cause of morbidity and mortality. It is estimated that as many as 90% of patients with SLE will have pathologic evidence of renal involvement on biopsy, but clinically significant nephritis will develop in only 50%. AII is a potent pro-inflammatory modulator with the ability to augment the immune responses in renal and non-renal tissues. Specifically in the kidney, AII stimulates mononuclear cells, favoring hyperplasia and hypertrophy of mesangial, tubular cells and interstitial fibroblasts, and increases expression and synthesis of the extracellular protein matrix leading to fibrosis. Angiotensin II and strong candidate for a mediator of the development and progression of renal disease in SLE has been found to promote glomerular cell proliferation, alter growth factor expression, and activate proinflammatory cytokines, all of which promote glomerulosclerosis
This study will evaluate the safety, tolerability, pharmacokinetics (PK), pharmacodynamics (PD), and efficacy of KP104 in participants with systemic lupus erythematosus (SLE)-Thrombotic microangiopathy (TMA). The study consists of 2 parts: Part 1 (Dose Optimization) and Part 2 (Proof of Concept). All participants will receive KP104 in combination with standard of care (SOC) for SLE-TMA.
A study of CM313 in subjects with systemic lupus erythematosus
Systemic Lupus Erythematosus (SLE) is a chronic invalidating chronic condition, with potential articular, cutaneous, renal, and neurologic involvement. Its pathophysiology is complex, and involves genetic, environmental and hormonal factors, leading to tolerance rupture. Among regulatory cells, Myeloid Derived Suppressor Cells (MDSCs) have been described as being increased during SLE, furthermore during flares. MDSCs are defined phenotypically as being HLA-DR-CD3-CD19-CD33+CD11b+, and either CD14+ (Monocytic MDSCs), CD15+ (Granulocytic MDSCs), or CD14-CD15- (Early-stage MDSCs). However, data regarding their immunosuppressive properties are conflicting, some studies identifying regulatory properties, while other have demonstrated a pro-inflammatory involvement through the induction of Th17 lymphocytes. The objectives of this study is to assess the involvement of MDSC in SLE through accurate phenotypical and functional assessment, as well as characterizing their immunometabolic profile, and to identify innovative therapeutic strategies.
The aim of the present work is to determine the frequency of critical complications of SLE patients admitted to the intensive care unit,study the risk factors and out comes.
This trial uses a double blinded, randomized 1:1 (active:sham) placebo controlled, parallel group design, investigating the effects of transcutaneous vagus nerve stimulation (tVNS) in patients with systemic lupus erythematosus (SLE). The main objective is to evaluate whether adjuvant treatment with tVNS in SLE patients with signs of autonomic dysfunction and fatigue improves patient perceived levels of fatigue. Secondary outcomes include tVNS induced changes to: patient reported outcomes, autonomic nervous system function, SLE disease activity, immunologic profile, tolerability of pain and organ (cardiac, vascular and kidney) functions. Participants are randomized to received either active non-invasive transcutaneous vagus nerve stimulation (tVNS) or inactive sham stimulation. The study period is divided in two periods. The first period investigates the effects of short-term, high-intensity tVNS treatment. The second phase investigates the effects of long-term, middle-intensity tVNS treatment.
the investigators objective is to identify the association of SNP polymorphisms in the TNFS4, and NCF gene and SLE Egyptian patients.
Systemic lupus erythematosis (SLE) is a chronic autoimmune disease characterized by production of autoantibodies and the deposition of immune complexes, affecting a wide range of organs. The clinical onset of SLE derives from the interaction between genetic predisposition and environmental, immunological and hormonal factors, with a strong predilection for women of childbearing age. SLE is usually diagnosed in young women in the third decade of life and represents the leading cause of systemic disease with secondary kidney involvement. Lupus nephritis (LN) occurs in ~50% of patients with SLE and is the most common, but not the only, cause of kidney injury in SLE. LN typically develops early in the disease course, generally within the first 6 to 36 months, and may be present at initial diagnosis. Macrophage migration inhibitory factor (MIF) is a pleiotropic inflammatory cytokine with regulatory roles in innate and adaptive immunity and is implicated in the pathogenesis of autoimmune diseases including SLE. MIF actively participates in multiple stages of the inflammatory response, acting on cells directly and/or potentiating the effects exerted by other stimuli. MIF overcomes the inhibitory effects of glucocorticoids on TNF alpha, IL-1 beta, IL-6, and IL-8 production. MIF is implicated in the pathogenesis of other autoimmune diseases including rheumatoid arthritis (RA), type 1 diabetes, multiple sclerosis and Guillain Barré syndrome.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by production of autoantibodies directed against nuclear and cytoplasmic antigens. Clinically, this disorder is characterized by periods of remission and relapse (1). The early and accurate diagnosis of SLE is challenging (2). The SLE pathogenesis involves multiple cellular components of the innate and immune systems, presence of autoantibodies and immune complexes, engagement of the complement system and cytokine dysregulation (3). About 180 autoantibodies have been identified in SLE patients, 102 of which are reported to have an organ-specific correlation with SLE disease identified in SLE patients, with SLE disease activity (4). However, with the exception of autoantibodies such as antinuclear antibody (ANA), anti double stranded DNA (dsDNA), anti-smith and antiphospholipid antibodies, currently proposed by the American college of rheumatology (ACR) (5)
1. Detection of different pattern of nail fold capillary changes in SLE patient. 2. Correlation of nail fold capillary changes in SLE patients and Anti-U1RNP antibodies. 3. Correlation of nail fold capillary changes with SLE disease activity. 4. Frequency of nail fold capillary changes in SLE patients