Academic literature on the topic 'Sle, Oxidative stress, Fibrinogen, Cardiovascular risk'
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Journal articles on the topic "Sle, Oxidative stress, Fibrinogen, Cardiovascular risk"
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Segal, BM, W. Thomas, X. Zhu, A. Diebes, G. McElvain, E. Baechler, and M. Gross. "Oxidative stress and fatigue in systemic lupus erythematosus." Lupus 21, no. 9 (April 16, 2012): 984–92. http://dx.doi.org/10.1177/0961203312444772.
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Objective: The objective of this study is to investigate the relationship of oxidative stress to fatigue in systemic lupus erythematosus (SLE). Methods: Patients with a confirmed diagnosis of SLE by ACR criteria and healthy controls completed validated questionnaires to assess depression and fatigue. Fatigue was measured with the Fatigue Severity Scale (FSS) and the Profile of Fatigue (Prof-F). Visual analogue scales (VAS) were also used to assess fatigue and pain. Depression was measured with the Center for Epidemiologic Studies Depression Scale (CES-D). Plasma F2-isoprostane was measured with gas chromatography/mass spectroscopy to assess oxidative stress. Evaluation included medical record review, physical exam and calculation of body mass index (BMI), disease activity (SLEDAI) and damage (SLICC) in the SLE patients. Results: Seventy-one SLE patients with low disease activity (mean SLEDAI = 1.62 standard error (SE) 0.37, range 0–8) were compared to 51 controls. Fatigue-limiting physical activity (defined as FSS ≥ 4) was present in 56% of patients and 12% of controls. F2-isoprostane was higher in SLE patients with fatigue compared to not-fatigued SLE subjects ( p = .0076) who were otherwise similar in ethnicity, disease activity and cardiovascular risk factors. Plasma F2-isoprostane was strongly correlated with FSS and Profile of Somatic Fatigue (Prof-S) ( p < .0001), VAS fatigue ( p = .005), CES-D ( p = .008) and with BMI ( p = .0001.) In a multivariate model, F2-isoprostane was a significant predictor of FSS after adjustment for age, BMI, pain and depression ( p = .0002). Conclusion: Fatigue in SLE patients with low disease activity is associated with increased F2-isoprostane. F2-isoprostane could provide a useful biomarker to explore mitochondrial function and the regulation of oxidative pathways in patients with SLE in whom fatigue is a debilitating symptom.
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Ruiz-Limon, Patricia, Nuria Barbarroja, Carlos Perez-Sanchez, Maria Angeles Aguirre, Maria Laura Bertolaccini, Munther A. Khamashta, Antonio Rodriguez-Ariza, et al. "Atherosclerosis and cardiovascular disease in systemic lupus erythematosus: effects of in vivo statin treatment." Annals of the Rheumatic Diseases 74, no. 7 (March 21, 2014): 1450–58. http://dx.doi.org/10.1136/annrheumdis-2013-204351.
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ObjectiveStatins may have beneficial vascular effects in systemic lupus erythematosus (SLE) beyond their cholesterol-lowering action, although the mechanisms involved are not completely understood. We investigated potential mechanisms involved in the efficacy of fluvastatin in preventing atherothrombosis in SLE.MethodsEighty-five patients with SLE and 62 healthy donors were included in the study. Selected patients (n=27) received 20 mg/day fluvastatin for 1 month. Blood samples were obtained before the start and at the end of treatment. Monocytes from five patients were treated in vitro with fluvastatin.ResultsIncreased prothrombotic and inflammatory variables were found in patients with SLE. SLE monocytes displayed altered mitochondrial membrane potential and increased oxidative stress. Correlation and association analyses demonstrated a complex interplay among autoimmunity, oxidative stress, inflammation and increased risk of atherothrombosis in SLE. Fluvastatin treatment of patients for 1 month reduced the SLE Disease Activity Index and lipid levels, oxidative status and vascular inflammation. Array studies on monocytes demonstrated differential expression in 799 genes after fluvastatin treatment. Novel target genes and pathways modulated by fluvastatin were uncovered, including gene networks involved in cholesterol and lipid metabolism, inflammation, oxidative stress and mitochondrial activity. Electron microscopy analysis showed increased density volume of mitochondria in monocytes from fluvastatin-treated patients, who also displayed higher expression of genes involved in mitochondrial biogenesis. In vitro treatment of SLE monocytes confirmed the results obtained in the in vivo study.ConclusionsOur overall data suggest that fluvastatin improves the impairment of a redox-sensitive pathway involved in processes that collectively orchestrate the pathophysiology of atherothrombosis in SLE.
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Baniamerian, H., F. Bahrehmand, A. Vaisi-Raygani, Z. Rahimi, and T. Pourmotabbed. "Angiotensin type 1 receptor A1166C polymorphism and systemic lupus erythematosus: correlation with cellular immunity and oxidative stress markers." Lupus 26, no. 14 (May 22, 2017): 1534–39. http://dx.doi.org/10.1177/0961203317711008.
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Angiotensin II, one of the rennin–angiotensin system components, is important in the cardiovascular hemodynamic and plays an important role in the development of cardiovascular disease in systemic lupus erythematosus (SLE) patients. The angiotensin II, through interaction with angiotensin II type 1 receptor (AGTR1), promotes proliferation, inflammation and fibrosis. The single nucleotide polymorphism of the AGTR1 (dbSNP: rs5186) gene can be associated with development and progression of SLE disease. The aims of this study were to compare the frequency of AGTR1 rs5186 in SLE patients with healthy individuals and to evaluate possible association between AGTR1 A1166C gene polymorphism and serum level of lipids, neopterin and malondialdehyde in SLE patients from a population of West Iran. One hundred SLE patients and 98 healthy subjects were studied. The AGTR1 A1166C polymorphism was detected by polymerase chain reaction– restriction fragment length polymorphism method and the serum lipid profile was obtained by enzymatic method. Neopterin and malondialdehyde were detected using high-performance liquid chromatography. We did not detect significant association between AGTR1 A1166C polymorphism and the risk of SLE. The levels of triglyceride (225 ± 118 mg/dl), neopterin (30 ± 24 nmol/l) and malondialdehyde (25 ± 9.6 nmol/l) in SLE patients were significantly higher than those in control subjects (139 ± 56 mg/dl, p = 0.03, 6.4 ± 2, p = 0.03, 9.4 ± 2.5 nmol/l, p = 0.01, respectively). Individuals with AGTR1 AC + CC genotype had higher levels of total cholesterol and malondialdehyde compared with those with AGTR1 AA genotype. SLE patients with either AGTR1 AA or AGTR1AC + CC genotype had significantly higher malondialdehyde or neopterin levels compared with the corresponding control subjects. In conclusion, although the present study did not find any association between AGTR1 A1166C polymorphism and the risk of SLE, the presence of this polymorphism was associated with higher levels of malondialdehyde and higher concentration of neopterin in patients.
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Khaliq, Shagufta, Mudassar Ali Roomi, Shaheena Naz, Komal Iqbal, Muhammad Imran Ashraf, and Muniza Saeed. "Obstructive Sleep Apnea and Cardiovascular Risk Markers (Fibrinogen & Gamma Glutamyl Transferase) in Obese Males." Pakistan Journal of Medical and Health Sciences 15, no. 12 (December 10, 2021): 3312–14. http://dx.doi.org/10.53350/pjmhs2115123312.
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Aim: To determine and compare gamma glutamyl transferase (GGT) and fibrinogen among obese males with and without obstructive sleep apnea (OSA). Second objective was to investigate correlation between blood pressure and GGT. Methodology: Sixty-four obese males aged 20-45 years with BMI > 25kg/m2 were included by convenience sampling. The study was conducted, after obtaining ethical approval from IRB, at the Department of Physiology, Post Graduate Medical Institute, Lahore from August 2014 to May 2015. Participants having acute or chronic inflammatory conditions were excluded. Participants were screened for OSA by Berlin and STOP BANG questionnaires. Diagnosis of OSA was made by overnight portable pulse oximetry. The participants were divided into two groups. Group I had 32 obese males with OSA. Group II contained 32 obese males without OSA. After an overnight fasting of 10-12 hours blood samples were drawn. Serum fibrinogen and GGT were measured by spectrophotometer. The data was analyzed using SPSS-22. Quantitative variables were compared between the two groups by Mann-Whitney U test. Spearman correlation was used to correlate blood pressure and GGT among the participants. Results: Fibrinogen was significantly raised (p=0.015) in obese males with OSA. Systolic blood pressure (p=0.003), diastolic blood pressure (p=0.001) and mean arterial blood pressure (p<0.001) showed strong positive correlation with GGT in obese males with OSA. Conclusion: Proinflammatory, procoagulant and proatherogenic marker fibrinogen levels were significantly raised in obese otherwise healthy males with OSA. Oxidative stress marker GGT showed strong positive correlation with blood pressure in obese males with OSA. Keywords: Fibrinogen, gamma glutamyl transferase, inflammation, obstructive sleep apnea, oxidative stress
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Ryan, Michael J. "Young Investigator Award Lecture of the APS Water and Electrolyte Homeostasis Section, 2008: The pathophysiology of hypertension in systemic lupus erythematosus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 4 (April 2009): R1258—R1267. http://dx.doi.org/10.1152/ajpregu.90864.2008.
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Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder that predominantly affects women during their reproductive years. Although SLE can affect any organ system, the kidneys are prominently involved in the form of immune complex glomerulonephritis. In addition, in women with SLE, risk for the development of cardiovascular disease is dramatically increased. Hypertension is a major risk factor for cardiovascular disease and is highly prevalent in women with SLE. Nevertheless, there has been little exploration of the pathophysiological mechanisms that promote SLE hypertension. This review discusses the role of several mechanisms, with an emphasis on the kidney, in SLE hypertension. These mechanisms include the renin-angiotensin system, endothelin, oxidative stress, sex steroids, metabolic changes, peroxisome proliferator-activated receptor-γ, and, perhaps most importantly, chronic inflammation and cytokines. Growing evidence suggests a link between chronic inflammation and hypertension. Therefore, elucidation of mechanisms that promote SLE hypertension may be of significant value not only for patients with SLE, but also for a better understanding of the basis for essential hypertension.
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Floris, Alberto, Matteo Piga, Arduino Aleksander Mangoni, Alessandra Bortoluzzi, Gian Luca Erre, and Alberto Cauli. "Protective Effects of Hydroxychloroquine against Accelerated Atherosclerosis in Systemic Lupus Erythematosus." Mediators of Inflammation 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/3424136.
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Cardiovascular (CV) morbidity and mortality are a challenge in management of patients with systemic lupus erythematosus (SLE). Higher risk of CV disease in SLE patients is mostly related to accelerated atherosclerosis. Nevertheless, high prevalence of traditional cardiovascular risk factors in SLE patients does not fully explain the increased CV risk. Despite the pathological bases of accelerated atherosclerosis are not fully understood, it is thought that this process is driven by the complex interplay between SLE and atherosclerosis pathogenesis. Hydroxychloroquine (HCQ) is a cornerstone in treatment of SLE patients and has been thought to exert a broad spectrum of beneficial effects on disease activity, prevention of damage accrual, and mortality. Furthermore, HCQ is thought to protect against accelerated atherosclerosis targeting toll-like receptor signaling, cytokine production, T-cell and monocyte activation, oxidative stress, and endothelial dysfunction. HCQ was also described to have beneficial effects on traditional CV risk factors, such as dyslipidemia and diabetes. In conclusion, despite lacking randomized controlled trials unambiguously proving the protection of HCQ against accelerated atherosclerosis and incidence of CV events in SLE patients, evidence analyzed in this review is in favor of its beneficial effect.
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Sciatti, Edoardo, Ilaria Cavazzana, Enrico Vizzardi, Ivano Bonadei, Micaela Fredi, Mara Taraborelli, Romina Ferizi, Marco Metra, Angela Tincani, and Franco Franceschini. "Systemic Lupus Erythematosus and Endothelial Dysfunction: A Close Relationship." Current Rheumatology Reviews 15, no. 3 (July 31, 2019): 177–88. http://dx.doi.org/10.2174/1573397115666181126105318.
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Background: Accelerated atherosclerosis, responsible for premature cardiovascular disease, has been estimated to develop or progress in 10% of systemic lupus erythematosus (SLE) patients each year and to be 6-fold more frequent in SLE compared with the general population. The mechanisms underlying accelerated atherosclerosis in SLE are complex and involve classical and “non-classical” cardiovascular risk factors. Subclinical and disseminated atherosclerosis is associated with endothelial dysfunction and arterial stiffness. Objective: The aim of this review is to analyze the association between SLE and endothelial dysfunction. Results and Conclusion: Different mechanisms have been proposed to explain the prevalence of endothelial dysfunction in SLE, which are briefly reported in this review: impaired clearance of apoptotic cells, oxidative stress markers, B cell activation with different circulating autoantibodies, different subtypes of T lymphocytes, cytokine cascade. Several studies and meta-analyses show a significant trend towards a prevalence of subclinical accelerated atherosclerosis in patients with SLE compared with healthy controls, since childhood. Based on general considerations, we suggest a multidisciplinary management to assess endothelial dysfunction at the diagnosis of the disease and to periodically search for and treat the traditional cardiovascular risk factors. Prospective studies are needed to confirm the benefits of this management.
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Harjai, Kishore J. "Potential New Cardiovascular Risk Factors: Left Ventricular Hypertrophy, Homocysteine, Lipoprotein(a), Triglycerides, Oxidative Stress, and Fibrinogen." Annals of Internal Medicine 131, no. 5 (September 7, 1999): 376. http://dx.doi.org/10.7326/0003-4819-131-5-199909070-00009.
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Kostopoulou, Myrto, Dionysis Nikolopoulos, Ioannis Parodis, and George Bertsias. "Cardiovascular Disease in Systemic Lupus Erythematosus: Recent Data on Epidemiology, Risk Factors and Prevention." Current Vascular Pharmacology 18, no. 6 (September 17, 2020): 549–65. http://dx.doi.org/10.2174/1570161118666191227101636.
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Systemic Lupus Erythematosus (SLE) is associated with increased risk for accelerated atherosclerosis and cardiovascular (CV) events including coronary heart disease, cerebrovascular and peripheral artery disease. CV events occur both early and late during the disease course, with younger patients being at much higher risk than age-matched counterparts. The risk cannot be fully accounted for by the increased prevalence of traditional atherosclerotic factors and may be due to pathophysiologic intermediates such as type I interferons and other inflammatory cytokines, oxidative stress, activated granulocytes and production of extracellular chromatin traps, antiphospholipid and other autoantibodies causing dysfunction of lipoproteins, altogether resulting in endothelial injury and pro-atherogenic dyslipidaemia. These mechanisms may be further aggravated by chronic intake of prednisone (even at doses <7.5 mg/day), whereas immunomodulatory drugs, especially hydroxychloroquine, may exert antiatherogenic properties. To date, there is a paucity of randomized studies regarding the effectiveness of preventative strategies and pharmacological interventions specifically in patients with SLE. Nevertheless, both the European League Against Rheumatism recommendations and extrapolated evidence from the general population emphasize that SLE patients should undergo regular monitoring for atherosclerotic risk factors and calculation of the 10-year CV risk. Risk stratification should include diseaserelated factors and accordingly, general (lifestyle modifications/smoking cessation, antihypertensive and statin treatment, low-dose aspirin in selected cases) and SLE-specific (control of disease activity, minimization of glucocorticoids, use of hydroxychloroquine) preventive measures be applied as appropriate. Further studies will be required regarding the use of non-invasive tools and biomarkers for CV assessment and of risk-lowering strategies tailored to SLE.
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Taylor, Erin B., and Michael J. Ryan. "Understanding mechanisms of hypertension in systemic lupus erythematosus." Therapeutic Advances in Cardiovascular Disease 11, no. 1 (July 31, 2016): 20–32. http://dx.doi.org/10.1177/1753944716637807.
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Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder that predominately affects women of reproductive age. Hypertension is an important cardiovascular risk factor that is prevalent in this patient population. Despite the high incidence of hypertension in women with SLE, the pathophysiological mechanisms underlying the development of hypertension remain poorly understood. This review will focus on disease-related factors, including inflammation, autoantibodies, and sex hormones that may contribute to hypertension in patients with SLE. In addition, we will highlight studies performed by our laboratory using the female NZBWF1 (F1 hybrid of New Zealand Black and New Zealand White strains) mouse model, a spontaneous model of SLE that mimics human disease and develops hypertension and renal injury. Specifically, using female NZBWF1 mice, we have demonstrated that multiple factors contribute to the pathogenesis of hypertension, including the inflammatory cytokine, tumor necrosis factor (TNF)-α, oxidative stress, as well as B-cell hyperactivity and autoantibody production.
Dissertations / Theses on the topic "Sle, Oxidative stress, Fibrinogen, Cardiovascular risk"
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Mannucci, Amanda. "Studio delle alterazioni post-traduzionali e funzionali del fibrinogeno in pazienti con lupus eritematoso sistemico." Doctoral thesis, 2019. http://hdl.handle.net/2158/1149940.
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Fibrinogen is a plasma glycoprotein with an average concentration of 200-400 mg/dl and a central role in coagulation, being crucial in fibrin clot assembly. Many studies in literature revealed that oxidative modifications of fibrinogen are significantly associated with altered protein function and structure in several haemostatic system disorders. However, a higher risk of thrombotic events has been also observed in autoimmunity, suggesting the emerging relation between inflammation and thrombosis. Among autoimmune disorders, Systemic Lupus Erythematosus (SLE) is an autoimmune disease with multi-systemic clinical manifestations and unpredictable course. The majority of clinical signs are due to vascular system affections; accordingly, the main cause of mortality in SLE patients with a long standing disease is represented by cardiovascular events. However, the pathophysiological mechanisms of cardiovascular risk in SLE are still under debate. Based on this background, the aim of the project was to evaluate systemic oxidative stress effects on functional and structural properties of fibrinogen purified from SLE patients. In 144 SLE patients and 190 sex- and age-matched healthy subjects, blood leukocyte intracellular ROS (Reactive Oxygen Species) levels were detected by FACS analysis. Plasma oxidative stress markers- Thiobarbituric Acid-Reactive Substances (TBARS) as an index of lipid peroxidation and Oxygen Radical Absorbance Capacity (ORAC) for the assessment of total antioxidant capacity- and fibrinogen di-tyrosine content, an indicator of protein oxidation, were measured using fluorometric assays. Furthermore, thrombin-catalyzed fibrin polymerization and plasmin-induced fibrinolysis were investigated in patients and controls. Finally, fibrinogen secondary structure and conformational properties were also explored by Circular Dichroism Spectroscopy (CD) and Intrinsic Fluorescence (FI) respectively. Our results described an altered redox status in SLE patients and a significant association of fibrinogen oxidative modification with changes in its structural and functional properties, leading to a pro-thrombotic phenotype. This evidence suggests a crucial role of oxidative stress and fibrinogen oxidation in the increased cardiovascular risk in SLE patients. Further investigations are needed in order to evaluate the effects of therapeutic supplementations with antioxidants on redox status and fibrinogen features in SLE.