scholarly journals Asymptomatic Carotid Atherosclerosis Cardiovascular Risk Factors and Common Hypertriglyceridemia Genetic Variants in Patients with Systemic Erythematosus Lupus

2020 ◽  
Author(s):  
Marta Fanlo-Maresma ◽  
Beatriz Candás-Estébanez ◽  
Virginia Esteve-Luque ◽  
Ariadna Padró-Miquel ◽  
Francesc Escrihuela-Vidal ◽  
...  

Abstract Background and aims: SLE is a systemic autoimmune disease associated with an increased cardiovascular risk which is related with the characteristic dyslipidemia of SLE. This consists of an alteration of triglyceride-rich lipoprotein metabolism and an increased concentration of apoB containing particles. The objective of this study is to know the prevalence of carotid atherosclerosis and to analyze its relationship with dyslipidemia and its related genetic factors in a population of SLE patients.Methods: Seventy-one SLE female were recruited. A carotid ultrasound was performed to evaluate the presence of atheromatous plaques and cIMT. Lipid profile and analysis of ZPR1, APOA5 and GCKR genes were carried out. SLE patients were analyzed according to the presence or absence of carotid plaques. Statistical analyses were performed to evaluate the relationship between lipid parameters and these allelic variants involved in triglyceride metabolism.Results: SLE patients with carotid plaque had higher concentrations of plasma triglyceride than SLE patients without carotid plaque (1.5 vs 0.9 mmol/L, respectively, p=0.001), Non-HDLC (3.5 vs 3.1 mmol/L, p= 0.025) and apoB (1.0 vs 0.9 g/L, p=0.010). GCKR (c.1337C>T) C-allele was observed in 83.3% and 16.7% (p=0.047) of patients with and without carotid plaque, respectively. The GCKR (c.1337C>T) CC genotype (OR= 0.03; [95% CI] [0.002 to 0.53], p=0.016), and triglyceride concentrations (OR= 7.57; [95% CI] [1.43 to 40.19], p=0.017) were independently associated with the diagnosis of carotid plaque.Conclusions: plasma triglyceride concentration and CGKR CC homozygosity for CGKR gene are independent predictive factors of carotid atherosclerosis in women with systemic lupus erythematosus.Keywords: triglycerides, CGKR gene, Non-HDLC, atherosclerosis, systemic lupus erythematosus.

Medicina ◽  
2020 ◽  
Vol 56 (10) ◽  
pp. 533
Author(s):  
Naomi Martin ◽  
Xiaodie Tu ◽  
Alicia J. Egan ◽  
Cordula Stover

Systemic lupus erythematosus is a classical systemic autoimmune disease that overactivates complement and can affect all organs. Early diagnosis and effective management are important in this immune-complex-mediated chronic inflammatory disease, which has a strong component of vasculitis and carries an increased risk of thrombosis, even in the absence of antiphospholipid antibodies. Development of lupus nephritis can be life limiting but is managed with dialysis and renal transplantation. Therefore, data have become available that cardiovascular risk poses a serious feature of systemic lupus erythematosus that requires monitoring and prospective treatment. Cell-derived microparticles circulate in plasma and thereby intersect the humoral and cellular component of inflammation. They are involved in disease pathophysiology, particularly thrombosis, and represent a known cardiovascular risk. This viewpoint argues that a focus on characteristics of circulating microparticles measured in patients with systemic lupus erythematosus may help to classify certain ethnic groups who are especially at additional risk of experiencing cardiovascular complications.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1187.2-1188
Author(s):  
J. Santana Peralta ◽  
T. Polanco Mora ◽  
A. Cornelio ◽  
Y. Cruz ◽  
E. Rodriguez Bautista ◽  
...  

Background:Systemic lupus erythematosus (SLE) is a multisystemic autoimmune disease. 1 Atherosclerosis is considered an alteration of the arteries by the abnormal deposit of lipids and fibrous tissue. 2 Cardiovascular disease is one of the leading causes of morbidity and mortality, especially due to its precocity, which occurs in women during childbearing age, is associated with a higher prevalence of cardiovascular disease (CVD), due to accelerated atherosclerosis3,4,5. Patients with rheumatic diseases have an increased cardiovascular risk due to systemic inflammation and endothelial dysfunction, which promotes accelerated atherosclerosis2.Objectives:Evaluate the frequency of atheromatous plaques in patients with systemic lupus erythematosus.Methods:Observational, prospective, cross-sectional study. Carotid Doppler was performed on patients with SLE from the external consultation of the rheumatology service from November 2019 to 2020. Inclusion criteria: > 18 years old, diagnosis SLE with the classification criteria ACR 2007, realization of Doppler. Controls: no disease, equated by age and sex. The data was analyzed with SPSS V23.Results:116 patients met inclusion criteria, including 116 female controls. Mean sick time was 6.23 years. 14.65% (17) had atheromaus plates, 29.4% calcified plates (5). 34.7% Dyslipidemia (63.1%) (73), obesity 34.7% (33), high blood pressure 23.1% (22), diabetes 3.44% (4), smokers 0% (0). The activity rate using SLEDAI showed 68.96% (80) without activity, 13.79% (16) low, 11.20% (13) moderate, 6.03% (7) high activity. About control group (116), 19.82% (23) showed atheromatous plates, 39.13% (9) calcified plates.Conclusion:Our study shows that less than a quarter of patients have atheromatous plaques in the carotid Doppler. In relation to LES activity, the vast majority are in low activity. We suggest the realization of Carotid Doppler in patients with low activity SLE for evaluation and monitoring of cardiovascular risk. Our study showed that there is no increased risk of atheroma plaque formation in SLE patients, compared to the general population.References:[1]Hernández Muñiz, Y., Guibert Toledano, Z. and Reyes Llerena, G., 2015. Correlation of C Reactive Protein Figures and Atherosclerosis In Patients with Systemic Lupus Erythematosus.[2]Saldarriaga Rivera, L., Ventura Ríos, L., Hernández Díaz, C. and Pineda Villaseñor, C., 2016. Measurement of the thickness of the intimate-half carotid: utility and ultrasound diagnosis of subcline atherosclerosis in rheumatic diseases. Literature review. Rev Col Reum, 23(2), pp.92-101.[3]Telles, R., Lanna, C., Ferreira, G., Souza, A., Navarro, T. and Ribeiro, A., 2008. Carotid atherosclerotic alterations in systemic lupus erythematosus patients treated at a Brazilian university setting. Lupus, 17(2), pp.105-113.[4]Nienhuis, H., by Leeuw, K., Bijzet, J., van Doormaal, J., van Roon, A., Smit, A., Graaff, R., Kallenberg, C. and Bijl, M., 2010. Small artery elasticity is decreased in patients with systemic lupus erythematosus without increased intima media thickness. Arthritis Research & Therapy, 12(5), p.R181.[5]Frerix et al. Arthritis Research & Therapy 2014, 16: R54.[6]Marta, M., Joan T., Stefano B., Chapt 2 - Assessment of Disease Activity in Systemic Lupus Erythematosus, Systemic Lupus Erythematosus, Mosby, 2007.Disclosure of Interests:None declared


2020 ◽  
Vol 26 ◽  
Author(s):  
Marija Vavlukis ◽  
Daniela Pop-Gjorceva ◽  
Lidija Poposka ◽  
Emilija Sandevska ◽  
Sasko Kedev

Background: Accelerated atherosclerosis is widely present in patients with systemic lupus erythematosus. Objective: The aim of this review is to analyze the relationship between systemic lupus erythematosus and cardiovascular diseases, with the emphasis on acute myocardial infarction. Results: Various molecular mechanisms triggered by infection/inflammation are responsible for endothelial dysfunction and development of atherosclerosis at an earlier age. Contributing factor is the cumulative effect of traditional cardiovascular risk factors interaction with disease related characteristics. Myocardial infarction rates are 2- to 10-fold higher compared to the general population. Young women have the highest relative risk, however, men carry at least 3- fold higher risk than women. Coronary involvement varies from normal coronary artery with thrombosis, coronary microartery vasculitis, coronary arteritis, and coronary atherosclerosis. Typical clinical presentation is observed in men and older women, while atypical is more frequent in young women. Treatment is guided by the underlying mechanism, engaging invasive procedures alone, or accompanied with immunosuppressive and/or antiinflammatory therapy. There are significant gender differences in pathophysiology and clinical presentation. However, they receive the same therapeutic treatments. Conclusion: Systemic lupus erythematosus is a major contributor to atherosclerotic and non-atherosclerotic mechanisms involved in the development of myocardial infarction, which should be taken into account during therapeutic treatment. Although Systemic lupus erythematosus per se is a “female” disease, males are at increased cardiovascular risk and worse outcome. Method: We conducted a literature review through PubMed and Cochrane, using key words: SLE, atherosclerosis, atherothrombosis, coronary artery disease, myocardial infarction, prognosis, sex specifics.


2012 ◽  
Vol 39 (12) ◽  
pp. 2286-2293 ◽  
Author(s):  
ADNAN N. KIANI ◽  
JENS VOGEL-CLAUSSEN ◽  
ARMIN ARBAB-ZADEH ◽  
LAURENCE S. MAGDER ◽  
JOAO LIMA ◽  
...  

Objective.A major cause of morbidity and mortality in systemic lupus erythematosus (SLE) is accelerated coronary atherosclerosis. New technology (computed tomographic angiography) can measure noncalcified coronary plaque (NCP), which is more prone to rupture. We report on a study of semiquantified NCP in SLE.Methods.Patients with SLE (n = 147) with no history of cardiovascular disease underwent 64-slice coronary multidetector computed tomography (MDCT). The MDCT scans were evaluated quantitatively by a radiologist, using dedicated software.Results.The group of 147 patients with SLE was 86% female, 70% white, 29% African American, and 3% other ethnicity. The mean age was 51 years. In our univariate analysis, the major traditional cardiovascular risk factors associated with noncalcified plaque were age (p = 0.007), obesity (p = 0.03; measured as body mass index), homocysteine (p = 0.05), and hypertension (p = 0.04). Anticardiolipin (p = 0.026; but not lupus anticoagulant) and anti-dsDNA (p = 0.03) were associated with higher noncalcified plaque. Prednisone and hydroxychloroquine therapy had no effect, but methotrexate (MTX) use was associated with higher noncalcified plaque (p = 0.0001). In the best multivariate model, age, current MTX use, and history of anti-dsDNA remained significant.Conclusion.Our results suggest that serologic SLE (anti-dsDNA) and traditional cardiovascular risk factors contribute to semiquantified noncalcified plaque in SLE. The association with MTX is not understood, but should be replicated in larger studies and in multiple centers.


2012 ◽  
Vol 39 (4) ◽  
pp. 735-742 ◽  
Author(s):  
MARK J. HARRISON ◽  
YASMEEN AHMAD ◽  
SAHENA HAQUE ◽  
NICOLA DALE ◽  
LEE-SUAN TEH ◽  
...  

Objective.Preference-based measures, such as the Short Form-6D (SF-6D), allow quality-adjusted life-years, used in cost-utility evaluations, to be calculated. We investigated the construct and criterion validity of the SF-6D in patients with systemic lupus erythematosus (SLE).Methods.Female patients with SLE were recruited from outpatient clinics at 2 timepoints, 5 years apart. Cross-sectional correlation of the SF-6D with domains of the disease-specific LupusQol health-related quality of life (HRQOL) measure, the Systemic Lupus International Collaborating Clinics Damage Index (SDI; for damage) and Systemic Lupus Erythematosus Disease Activity Index (SLEDAI; for activity) measures, and patient characteristics was tested. The ability to discriminate between groups defined by smoking status, presence/absence of carotid plaque, depression, and fatigue was tested using the t-test.Results.In total 181 patients were recruited at baseline. The SF-6D correlated moderately to strongly with all domains of the LupusQoL (0.6–0.8) apart from intimate relationships (0.42) and body image (0.34). Correlations of the SF-6D with the demographic and disease-specific measures at baseline were small for the SDI score (−0.23) and age (−0.19) and in the expected direction. The SF-6D did not correlate with disease activity (SLEDAI −0.08). The SF-6D could distinguish those who smoked, had carotid plaque, had depression, and reported fatigue from those who did not, with the largest effect size being for depression (0.75).Conclusion.The SF-6D displays construct and criterion validity for use in patients with SLE, but the low correlation with aspects of intimate relationships and body image represents a concern and reinforces the need to collect disease-specific measures of HRQOL alongside generic preference-based instruments.


2013 ◽  
Vol 71 (Suppl 3) ◽  
pp. 677.4-677
Author(s):  
I.J. Colunga-Pedraza ◽  
D.A. Galarza-Delgado ◽  
F. Gόngora-Rivera ◽  
S.L. Segarra-Linares ◽  
M.A. Garza-Elizondo

2021 ◽  
Vol 10 (20) ◽  
pp. 4788
Author(s):  
Katarzyna Pawlak-Buś ◽  
Wiktor Schmidt ◽  
Piotr Leszczyński

Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease characterized by the production of multiple autoantibodies, resulting in tissue and organ damage. Recent studies have revealed that interleukin-23 (IL-23) and interleukin-27 (IL-27) may be therapeutically relevant in selected SLE manifestations. This study aimed to identify associations between serum IL-27 and IL-23 levels and disease activity in Polish patients with different manifestations of SLE: neuropsychiatric lupus (NPSLE), and lupus nephritis (LN). Associations between interleukin levels and oligo-specific antibodies against double-stranded DNA (dsDNA), dose of glucocorticoids, and type of treatment were also analyzed. An enzyme-linked immunosorbent assay was used to assess anti-dsDNA antibodies and analyze the serum concentration of IL-27 and IL-23 from 72 patients aged 19–74 years with confirmed active SLE. Disease activity was measured using the Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI 2-K). No significant correlations between interleukin levels and SLEDAI score, anti-dsDNA, corticosteroid dose, or type of treatment were noted. Patients with NPSLE and LN presented the highest median scores of SLEDAI.


2021 ◽  
Vol 13 (3) ◽  
pp. 109-112
Author(s):  
Parviz Torkzaban ◽  
Amir Talaie

Systemic lupus erythematosus is a systemic autoimmune disease that involves multi organs. Genetic, endocrine, immunological, and environmental factors influence the loss of immunological tolerance against self-antigens leading to the formation of pathogenic autoantibodies that cause tissue damage through multiple mechanisms. The gingival overgrowth can be caused by three factors: noninflammatory, hyperplastic reaction to the medication; chronic inflammatory hyperplasia; or a combined enlargement due to chronic inflammation and drug-induced hyperplasia. Drug-Induced Gingival Overgrowth is associated with the use of three major classes of drugs, namely anticonvulsants, calcium channel blockers, and immunosuppressants. Due to recent indications for these drugs, their use continues to grow.


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