scholarly journals Periodontitis Risk in Patients With and Without Systemic Lupus Erythematosus: A Retrospective Study

2021 ◽  
Vol 1 (1) ◽  
pp. 19-30
Author(s):  
Chinhua Hsiao

Objectives: Systemic lupus erythematosus is a systemic, long-term autoimmune condition that has chronic inflammatory effects in connective tissue throughout the body. There are numerous studies that have examined the association between systemic lupus erythematosus and chronic periodontitis, with varying conclusions. The purpose of this cross-sectional study is to evaluate and compare the risk for periodontitis in patients with SLE to patients without SLE. Materials and Methods: Medical and dental records were retrospectively reviewed for patients that had been admitted to the Temple University School of Dentistry from 2010 to 2018. A roster of 22 SLE positive patients were generated from the Temple University patient database and matched to a control population of 22 patients without SLE. Periodontal probing depths were then documented and used to evaluate periodontal statuses in both test and control groups. Sites with probing depths ≥ 5 mm were considered to be at increased risk for periodontal breakdown. Prevalence was defined as the percentage of individuals having at least one site with a ≥ 5 mm probing depth, and extent was defined as the average percentage of sites with increased periodontitis risk. The number of missing teeth in patients from each group were also recorded as a secondary outcome. Results: The prevalence of ≥ 5 mm probing depths in SLE and control groups was 50 % (10/20) and 40.9 % (9/22), respectively. Calculations of relative risk (1.22) and odds ratio (1.44) were not statistically significant between the two populations (p > 0.05). The extent of ≥ 5 mm probing depths was 1.5 % in SLE patients and 3.7 % in healthy patients, which was also not significant between groups (p > 0.05). SLE patients were missing an average of 9.6 teeth per individual compared to 3.8 in healthy patients (p < 0.05). Conclusions: The results of the present study indicate that patients with SLE do not have an increased risk for periodontitis when compared to patients without SLE. Risk analysis on the prevalence and the extent of deeper probing depths were not statistically different between SLE and control groups. Further studies with a larger sample size and elimination of unseen confounders are needed in order to validate our results. An interesting observation was the finding that SLE patients have a significantly greater number of missing teeth. The exact mechanism through which SLE patients experience periodontal breakdown and increased tooth loss is an avenue that warrants future research. Keywords: systemic lupus erythematosus (SLE); chronic periodontitis Abbreviations: SLE: Systemic Lupus Erythematosus, CP: Chronic Periodontitis, SLEDAI: Systemic Lupus Erythematosus Disease Activity Index, BOP: Bleeding on Probing, CAL: Clinical Attachment Level.

2021 ◽  
Vol 12 ◽  
Author(s):  
Ting-Yu Tu ◽  
Chiu-Yu Yeh ◽  
Yao-Min Hung ◽  
Renin Chang ◽  
Hsin-Hua Chen ◽  
...  

ObjectiveWe investigated the correlation between nontyphoidal Salmonella (NTS) infection and systemic lupus erythematosus (SLE) risk.MethodsThis case-control study comprised 6,517 patients with newly diagnosed SLE between 2006 and 2013. Patients without SLE were randomly selected as the control group and were matched at a case-control ratio of 1:20 by age, sex, and index year. All study individuals were traced from the index date back to their NTS exposure, other relevant covariates, or to the beginning of year 2000. Conditional logistic regression analysis was used to analyze the risk of SLE with adjusted odds ratios (aORs) and 95% confidence intervals (CIs) between the NTS and control groups.ResultsThe mean age was 37.8 years in the case and control groups. Females accounted for 85.5%. The aOR of having NTS infection were significantly increased in SLE relative to controls (aOR, 9.20; 95% CI, 4.51-18.78) in 1:20 sex-age matching analysis and (aOR, 7.47; 95% CI=2.08-26.82) in propensity score matching analysis. Subgroup analysis indicated that the SLE risk was high among those who dwelled in rural areas; had rheumatoid arthritis, multiple sclerosis, or Sjogren’s syndrome; and developed intensive and severe NTS infection during admission.ConclusionsExposure to NTS infection is associated with the development of subsequent SLE in Taiwanese individuals. Severe NTS infection and other autoimmune diseases such as rheumatoid arthritis, multiple sclerosis, or Sjogren’s syndrome also contributed to the risk of developing SLE.


Author(s):  
Consuelo P. C. Marques ◽  
Vandilson P. Rodrigues ◽  
Larissa C. de Carvalho ◽  
Louise P. Nichilatti ◽  
Mayra M. Franco ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Sarfaraz A. Hasni ◽  
Sarthak Gupta ◽  
Michael Davis ◽  
Elaine Poncio ◽  
Yenealem Temesgen-Oyelakin ◽  
...  

AbstractIncreased risk of premature cardiovascular disease (CVD) is well recognized in systemic lupus erythematosus (SLE). Aberrant type I-Interferon (IFN)-neutrophil interactions contribute to this enhanced CVD risk. In lupus animal models, the Janus kinase (JAK) inhibitor tofacitinib improves clinical features, immune dysregulation and vascular dysfunction. We conducted a randomized, double-blind, placebo-controlled clinical trial of tofacitinib in SLE subjects (ClinicalTrials.gov NCT02535689). In this study, 30 subjects are randomized to tofacitinib (5 mg twice daily) or placebo in 2:1 block. The primary outcome of this study is safety and tolerability of tofacitinib. The secondary outcomes include clinical response and mechanistic studies. The tofacitinib is found to be safe in SLE meeting study’s primary endpoint. We also show that tofacitinib improves cardiometabolic and immunologic parameters associated with the premature atherosclerosis in SLE. Tofacitinib improves high-density lipoprotein cholesterol levels (p = 0.0006, CI 95%: 4.12, 13.32) and particle number (p = 0.0008, CI 95%: 1.58, 5.33); lecithin: cholesterol acyltransferase concentration (p = 0.024, CI 95%: 1.1, −26.5), cholesterol efflux capacity (p = 0.08, CI 95%: −0.01, 0.24), improvements in arterial stiffness and endothelium-dependent vasorelaxation and decrease in type I IFN gene signature, low-density granulocytes and circulating NETs. Some of these improvements are more robust in subjects with STAT4 risk allele.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 857.1-857
Author(s):  
S. Bruera ◽  
R. Zogala ◽  
X. Lei ◽  
X. Pundole ◽  
H. Zhao ◽  
...  

Background:Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that carries an increased risk for both viral illnesses and malignancies, including a greater risk for both human papilloma virus (HPV) infection and cervical cancer. Due to this increased risk, the American Society of Colposcopy and Cervical Pathology guidelines for SLE patients recommend more frequent cervical cancer screening. Few studies have examined patient characteristics associated with decreased cervical cancer screening in patients with autoimmune disease, specifically SLE.Objectives:To estimate cervical cancer screening rates in women with recently diagnosed SLE, and to identify characteristics associated with decreased screening.Methods:We identified women with an initial diagnosis of SLE in the United States MarketScan Commercial Claims and Encounter (CCAE, age 18-64) administrative claims database. We included patients with at least three claims with a lupus diagnosis (first and last at least >90 days apart), no lupus claims within the year before initial claim, and who had been on antimalarial drugs for at least 90 days. We excluded all patients with a previous claim for hysterectomy.Cervical cancer screening was ascertained using diagnosis and procedure codes within 1 year before and 2 years after the first SLE claim. Our covariates included the year of first SLE claim (2001-2014), age at first SLE claim, comorbidity score, insurance type, geographical region, and prescriptions for multiple types of corticosteroids. Control patients included age-matched females without autoimmune disease. Univariate comparison and multivariate logistic regression models were built to evaluate determinants of screening.Results:We included 4,316 SLE patients (median age 45) and 86,544 control patients. The screening rate in SLE patients was 73.4% vs 58.5% in the controls (P < 0.001). The screening rate was 71% in 2001, increased to 75% in 2004, then decreased to 70% in 2014 (trend P =0.005). In the multivariate model the following factors were associated with decreased cervical cancer screening: year of first SLE claim 2012-2014 versus 2001-2005 (odds ratio (OR) 0.67, 95% confidence interval (CI) 0.53 – 0.84, P < 0.001); older age 61-64 versus 21-30 (OR 0.27, 95% CI 0.19 – 0.39, P < 0.001); comorbidity score of ≥2 versus <2 (OR 0.71, 95% CI 0.6 – 0.83, P < 0.001); and use of corticosteroids for ≥ 90 days versus <90 days (OR 0.73, 95% CI 0.59 – 0.9, P = 0.003). Insurance type and geographical region were not associated with cervical cancer screening.Conclusion:About three quarters of women with SLE underwent cervical cancer screening within 3 years of their first lupus claim, at higher rates than controls. However, there was a concerning downward trend in screening rates in recent years. In addition, higher risk populations for cervical cancer (older age, increased comorbidities, and longer duration of corticosteroids) had lower screening rates. These findings highlight the need to enhance education for healthcare providers to improve utilization of screening in women with SLE at high risk of cervical cancer.Disclosure of Interests:Sebastian Bruera: None declared, Richard Zogala: None declared, Xiudong Lei: None declared, Xerxes Pundole: None declared, Hui Zhao: None declared, Sharon Giordano: None declared, Jessica Hwang Grant/research support from: MERCK grant funding unrelated to SLE., Maria Suarez-Almazor: None declared


Genes ◽  
2018 ◽  
Vol 9 (10) ◽  
pp. 496 ◽  
Author(s):  
Bethany Wolf ◽  
Paula Ramos ◽  
J. Hyer ◽  
Viswanathan Ramakrishnan ◽  
Gary Gilkeson ◽  
...  

Development and progression of many human diseases, such as systemic lupus erythematosus (SLE), are hypothesized to result from interactions between genetic and environmental factors. Current approaches to identify and evaluate interactions are limited, most often focusing on main effects and two-way interactions. While higher order interactions associated with disease are documented, they are difficult to detect since expanding the search space to all possible interactions of p predictors means evaluating 2p − 1 terms. For example, data with 150 candidate predictors requires considering over 1045 main effects and interactions. In this study, we present an analytical approach involving selection of candidate single nucleotide polymorphisms (SNPs) and environmental and/or clinical factors and use of Logic Forest to identify predictors of disease, including higher order interactions, followed by confirmation of the association between those predictors and interactions identified with disease outcome using logistic regression. We applied this approach to a study investigating whether smoking and/or secondhand smoke exposure interacts with candidate SNPs resulting in elevated risk of SLE. The approach identified both genetic and environmental risk factors, with evidence suggesting potential interactions between exposure to secondhand smoke as a child and genetic variation in the ITGAM gene associated with increased risk of SLE.


2021 ◽  
Author(s):  
Arlley Cleverson Belo Silva ◽  
Sue Yazaki Sun ◽  
Felipe Favorette Campanharo ◽  
Letícia Tiemi Morooka ◽  
José Guilherme Cecatti ◽  
...  

Abstract Introduction: Systemic lupus erythematosus (SLE) may cause irreversible organ damage. Pregnancy with coexisting SLE may have severe life-threatening risks. Severe maternal morbidities (SMM) include maternal death, maternal near miss (MNM), and potentially life-threatening conditions (PLTC). This study aimed to determine the prevalence of SMM in patients with SLE and analyze the parameters that contributed to cases of greater severity. Methods: This is a cross-sectional retrospective study from analysis of data retrieved from medical records of pregnant women with SLE treated at São Paulo Hospital , Brazil, from 2005 to 2015. The pregnant women were divided in control group without complications, group with PLTC, and group with MNM. Results: Out of 149 pregnancies, there were 14 cases of MNM (9.4%), 56 cases of PLTC (37.6%), and no maternal death. The maternal near miss rate was 112.9 per 1,000 live births. The majority of PLTC (83.9%) and MNM (92.9%) cases had preterm deliveries with statistically significant increased risk compared with control group [p=0.0042; OR (95% CI): 12.05 (1.5-96.6) for MNM group and p=0.0001; OR (95% CI): 4.84 (2.2-10.8) for PLTC group]. SMM increases the risk of longer hospitalization [p<0,0001; OR (95% CI): 18.8 (7.0-50.6) and p <0.0001; OR (95% CI): 158.17 (17.6-1424,2) for PLTC and MNM, respectively], newborns with low birth weight [p=0.0006; OR (95% CI): 3.67 (1.7-7.9) and p=0.0009; OR (95% CI): 17.68 (2-153.6) for PLTC and MNM group, respectively] as well as renal diseases [PLTC (58.9%, 33/56; p = 0.0069) and MNM (78.6%, 11/14; p = 0.0026)]. MNM cases presented increased risk for neonatal death [p=0.0128; OR (95% CI): 38.4 (3.3-440.3)], stillbirth and miscarriage [p=0.0011; OR (95% CI): 7.68 (2.2-26.3)]. Conclusion: SLE was significantly associated with severe maternal morbidity, longer hospitalizations, and increased risk of poor obstetric and neonatal outcomes, such as prematurity, neonatal death, miscarriage and fetal loss.


2018 ◽  
Vol 77 (7) ◽  
pp. 1063-1069 ◽  
Author(s):  
Dag Leonard ◽  
Elisabet Svenungsson ◽  
Johanna Dahlqvist ◽  
Andrei Alexsson ◽  
Lisbeth Ärlestig ◽  
...  

ObjectivesPatients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) have increased risk of cardiovascular disease (CVD). We investigated whether single nucleotide polymorphisms (SNPs) at autoimmunity risk loci were associated with CVD in SLE and RA.MethodsPatients with SLE (n=1045) were genotyped using the 200K Immunochip SNP array (Illumina). The allele frequency was compared between patients with and without different manifestations of CVD. Results were replicated in a second SLE cohort (n=1043) and in an RA cohort (n=824). We analysed publicly available genetic data from general population, performed electrophoretic mobility shift assays and measured cytokine levels and occurrence of antiphospholipid antibodies (aPLs).ResultsWe identified two new putative risk loci associated with increased risk for CVD in two SLE populations, which remained after adjustment for traditional CVD risk factors. An IL19 risk allele, rs17581834(T) was associated with stroke/myocardial infarction (MI) in SLE (OR 2.3 (1.5 to 3.4), P=8.5×10−5) and RA (OR 2.8 (1.4 to 5.6), P=3.8×10−3), meta-analysis (OR 2.5 (2.0 to 2.9), P=3.5×10−7), but not in population controls. The IL19 risk allele affected protein binding, and SLE patients with the risk allele had increased levels of plasma-IL10 (P=0.004) and aPL (P=0.01). An SRP54-AS1 risk allele, rs799454(G) was associated with stroke/transient ischaemic attack in SLE (OR 1.7 (1.3 to 2.2), P=2.5×10−5) but not in RA. The SRP54-AS1 risk allele is an expression quantitative trait locus for four genes.ConclusionsThe IL19 risk allele was associated with stroke/MI in SLE and RA, but not in the general population, indicating that shared immune pathways may be involved in the CVD pathogenesis in inflammatory rheumatic diseases.


Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Emily L Gilbert ◽  
Keisa W Mathis ◽  
Marcia Venegas-Pont ◽  
Michael J Ryan

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that predominantly affects young women. Due to this partiality towards women, estrogen is commonly implicated in disease development. The potential for estrogens to promote SLE disease progression stems from data showing that removal of estrogens in young female mice with SLE (6-8 week old NZBWF1 mice) delays the development of renal injury and mortality. The primary cause of mortality in women with SLE is cardiovascular disease, and hypertension, a major cardiovascular risk factor, is highly prevalent in this patient population. Based on the presumed role of estrogen to promote SLE, we hypothesized that estrogen promotes hypertension during SLE. To test this, 30 week old SLE mice (NZBWF1) and control mice (NZW/LacJ) were subjected to either ovariectomy (OVX) or a sham operation and a subset of these mice were replete with 17β-estradiol (E2, 5μg/mouse, s.c., 2x/week). At 34 weeks of age, mean arterial pressure (MAP in mmHg) was measured by carotid catheter in conscious freely moving mice. MAP was higher in SLE sham mice compared to control shams (133±3, n=17 vs. 120±3, n=13, p<0.05). Contrary to our hypothesis, OVX at 30 weeks exacerbated the hypertension (154±3, n=9, p<0.05 vs. SLE sham) and prevalence of albuminuria in mice with SLE (83%, 10 of 12 vs 36%, 5 of 14 measured by dipstick > 100 mg/dL). OVX did not alter MAP (115±3, n=9) or albuminuria in control mice. The hypertensive response to OVX was prevented in OVX SLE mice replete with E2 (133±4, n=3) suggesting a protective role for E2 against SLE-associated hypertension. Because previous studies showed that estrogen removal in young mice delayed SLE disease progression, we tested whether OVX starting at 8 weeks of age delayed the development of hypertension. OVX in young SLE mice did not significantly alter the progression of SLE-associated hypertension (141±4, n=4 measured at 34 weeks of age). Consistent with previous work of others, OVX in young SLE mice reduced the prevalence of albuminuria (20%, 1 of 5 vs 33%, 1 of 3). These data suggest that estrogen has a complex temporal role in the pathogenesis of SLE with the potential to promote disease early in life, but protect against the progression of SLE associated hypertension later in the course of the disease.


2019 ◽  
Vol 47 (2) ◽  
pp. 188-196 ◽  
Author(s):  
Michelle J. Ormseth ◽  
Joseph F. Solus ◽  
Quanhu Sheng ◽  
Fei Ye ◽  
Qiong Wu ◽  
...  

Objective.MicroRNA (miRNA) are short noncoding RNA that regulate genes and are both biomarkers and mediators of disease. We used small RNA (sRNA) sequencing and machine learning methodology to develop an miRNA panel to reliably differentiate between rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE) and control subjects.Methods.Plasma samples from 167 RA and 91 control subjects who frequency-matched for age, race, and sex were used for sRNA sequencing. TIGER was used to analyze miRNA. DESeq2 and random forest analyses were used to identify a prioritized list of miRNA differentially expressed in patients with RA. Prioritized miRNA were validated by quantitative PCR, and lasso and logistic regression were used to select the final panel of 6 miRNA that best differentiated RA from controls. The panel was validated in a separate cohort of 12 SLE, 32 RA, and 32 control subjects. Panel efficacy was assessed by area under the receiver operative characteristic curve (AUC) analyses.Results.The final panel included miR-22-3p, miR-24-3p, miR-96-5p, miR-134-5p, miR-140-3p, and miR-627-5p. The panel differentiated RA from control subjects in discovery (AUC = 0.81) and validation cohorts (AUC = 0.71), seronegative RA (AUC = 0.84), RA remission (AUC = 0.85), and patients with SLE (AUC = 0.80) versus controls. Pathway analysis showed upstream regulators and targets of panel miRNA are associated with pathways implicated in RA pathogenesis.Conclusion.An miRNA panel identified by a bioinformatic approach differentiated between RA or SLE patients and control subjects. The panel may represent an autoimmunity signature, perhaps related to inflammatory arthritis, which is not dependent on active disease or seropositivity.


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