Association Between Cigarette Smoking and Systemic Lupus Erythematosus: An Updated Multivariate Bayesian Metaanalysis

2019 ◽  
Vol 47 (10) ◽  
pp. 1514-1521 ◽  
Author(s):  
Monica Hui Yan Chua ◽  
Irene Ai Ting Ng ◽  
Mike W.L.-Cheung ◽  
Anselm Mak

ObjectiveThe association between cigarette smoking and the risk of systemic lupus erythematosus (SLE) remains a matter for debate. Additionally, the effect of the change of smokers’ demographics on the risk of development of SLE over time has not been formally addressed. We aimed to examine the association between cigarette smoking and the risk of SLE by performing an updated metaanalysis.MethodsA literature search using keywords including “lupus,” “smoking,” “cigarette,” “environmental,” “autoimmune,” and “connective tissue disease” was performed in computerized databases to identify studies addressing the relationship between cigarette smoking and SLE occurrence. A Bayesian metaanalysis was conducted by computing the log-OR between current and never smokers, and between former and never smokers. The average log-OR (subsequently converted to OR) and their corresponding 95% credible intervals (CrI) were calculated. The effect of publication time, sex, and age of patients with SLE on the effect sizes was examined by multivariate metaregression.ResultsData aggregation of 12 eligible studies comprising 3234 individuals who developed SLE and 288,336 control subjects revealed a significant association between SLE occurrence and current smoking status (OR 1.54, 95% CrI 1.06–2.25), while only a non-significant trend was demonstrated between SLE occurrence and former smoking status (OR 1.39, 95% CrI 0.95–2.08). Publication time, sex, and the mean age of patients with SLE did not explain the heterogeneity of the effect sizes.ConclusionCurrent smoking status is associated with risk of SLE. Sex and age of patients with SLE had no significant effect on the risk of SLE over time.

2017 ◽  
Vol 77 (2) ◽  
pp. 196-202 ◽  
Author(s):  
Medha Barbhaiya ◽  
Sara K Tedeschi ◽  
Bing Lu ◽  
Susan Malspeis ◽  
David Kreps ◽  
...  

ObjectivesSystemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease, subtyped according to clinical manifestations and autoantibodies. Evidence concerning cigarette smoking and SLE risk has been conflicting. We investigated smoking and SLE risk, overall and by anti-double stranded DNA (dsDNA) presence, in two prospective cohort studies.MethodsThe Nurses’ Health Study (NHS) enrolled 121 701 US female nurses in 1976; Nurses’ Health Study II (NHSII) enrolled 116 430 in 1989. Lifestyle, environmental and medical data were collected through biennial questionnaires. Incident SLE was confirmed by medical record review. Cox regression models estimated HRs of SLE, overall and by dsDNA subtype, in association with time-varying smoking status and cumulative smoking pack-years through the 2-year cycle prior to diagnosis, controlling for potential confounders.ResultsAmong 286 SLE cases identified (159 in NHS (1978–2012) and 127 in NHSII (1991–2013)), mean age was 49.2 (10.3) years and 42% were dsDNA+ at SLE diagnosis. At baseline, 45% of women had ever smoked, 51% of whom currently smoked. Compared with never smokers, current smokers had increased dsDNA+ SLE risk (HR 1.86 (1.14–3.04)), whereas past smokers did not (HR 1.31 (0.85–2.00)). Women who smoked >10 pack-years (vs never) had an elevated dsDNA+ SLE risk (HR 1.60(95% CI 1.04 to 2.45)) compared with never smokers. No associations were observed between smoking status or pack-years and overall SLE or dsDNA− SLE.ConclusionStrong and specific associations of current smoking and >10 pack-years of smoking with dsDNA+ SLE were observed. This novel finding suggests smoking is involved in dsDNA+ SLE pathogenesis.


2008 ◽  
Vol 36 (6) ◽  
pp. 799-810 ◽  
Author(s):  
Hikmet Yazici

The association between the sociotropic/autonomic personality characteristics, depressive symptoms and cigarette-smoking status of 385 male and 241 female university students was examined. Depressive symptoms and sociotropic/autonomic personality were measured using the Beck Depression Inventory (adapted for use in Turkey by Hisli [1998]) and the Sociotropy-Autonomy Scale (adapted for use in Turkey by Şahin, Ulusoy, & Şahin [1993]); smoking behaviors were also assessed. Logistic regression analysis was used to assess the association between sociotropic/autonomic personality characteristics, depressive symptoms and cigarette-smoking status. Current smokers showed a trend, scoring higher than nonsmokers on depressive symptoms, and they also scored significantly higher than nonsmokers on autonomy. Results also show that depressive symptoms (OR = 1.07, 95% CI = 1.05–1.10), and autonomy (OR = 1.02, 95% CI = 1.01–1.03) were predictive variables of current smoking status.


Author(s):  
Pratik Sandesara ◽  
Wesley O’Neal ◽  
Sanjay Venkatesh ◽  
Laurence Sperling

Background: Cigarette smoking predisposes individuals to the development of cardiovascular disease by promoting inflammation, vascular dysfunction, and accelerated atherosclerosis. However, the association between smoking and outcomes in HFpEF remains unclear. Objectives: To examine the relationship between smoking and outcomes in patients with HFpEF. Methods: This analysis included 1,717 (mean age=71±10 years; 50% male; 78% white) patients with HFpEF enrolled in the Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) Trial from the Americas. Smoking was ascertained by self-reported history and was categorized as never, former, or current. Multivariable cox regression was used to examine the risk of hospitalization, hospitalization for heart failure, death, and cardiovascular death across smoking categories. Results: There were 116 (7%), 871 (51%), and 729 (42%) patients whose smoking status was classified as current, former, or never. Current smoking was associated with an increased risk for hospitalization (never: HR=1.0; former: HR=1.14, 95%CI=0.99, 1.31; current: HR=1.38, 95%CI=1.05, 1.80), hospitalization for heart failure (never: HR=1.0; former: HR=1.25, 95%CI=0.99, 1.57; current: HR=1.68, 95%CI=1.08, 2.61), death (never: HR=1.0; former: HR=1.02, 95%CI=0.81, 1.29; current: HR=1.82, 95%CI=1.19, 2.78), and cardiovascular death (never: HR=1.0; former: HR=1.00, 95%CI=0.74, 1.35; current: HR=1.85, 95%CI=1.09, 3.24) compared with former or never smokers in a multivariable model adjusted for cardiovascular risk factors. The cumulative incidence estimates for hospitalization for heart failure across smoking categories are shown in Figure 1 (log-rank p=0.0029). Similar effect estimates were observed for smoking categories and the outcomes examined when further adjusted for quantity of cigarette use. Conclusion: Current smoking is associated an increased risk for adverse outcomes in HFpEF, including hospitalization for heart failure. Smoking cessation possibly has role to reduce the risk for hospital admission and death in these high-risk patients.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Sharon Cox ◽  
Jamie Brown ◽  
Loren Kock ◽  
Lion Shahab

Abstract Introduction Up-to-date monitoring of non-combustible nicotine products (e.g. e-cigarettes, nicotine replacement therapies (NRT), heated tobacco products (HTP); NNP) is important to assess their impact. To date, there is little evidence on the association between ever regular use (defined here as 1 year or more) of NNP and current smoking status. Aims/methods The purpose of this study was to examine the prevalence, and sociodemographic, alcohol and smoking status correlates, of ever regular use of NNP in England in 2020. A cross-sectional survey of adults in England was conducted between February and June 2020. Results A total of 8486 adults were surveyed; 94.9% (8055) were complete cases. The weighted prevalence of ever regular NNP use was 5.4% (n = 436; 95% CI 5.0–6.0), of which 82% (n = 360; 95% CI 78.7–85.8) was single and 18% (n = 79; 95% CI 14.8–22) multiple product use. Amongst ever regular NNP users, the prevalence of ever regular NRT, e-cigarette and HTP use was 64.7% (95% CI 60.1–69), 43.4% (95% CI 38.8–48) and 2.5% (95% CI 1.4–4.5), respectively. In adjusted analysis, ever regular NNP use was associated with smoking status, being significantly higher among current (22.3%; adjusted OR (aOR) 34.9, 95% CI 24.0–50.8) and ex-smokers (12.7%, aOR 19.8, 95% CI 11.1–14.4) than among never-smokers (0.6%). More advantaged occupational grade (aOR, 1.27 95% CI 1.02–1.57) and at least hazardous alcohol use (aOR, 1.38 95% CI 1.06–1.78) were associated with greater prevalence of ever regular NNP use. Conclusions Ever regularly using NNP was highest among smokers and ex-smokers and rare among never-smokers. Among people who have ever regularly used NNP, NRT is the most popular.


2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S150-S150
Author(s):  
H Li ◽  
M Arslan ◽  
Z Fu ◽  
H Lee ◽  
M Mikula

Abstract Introduction/Objective A subset of patients with an established diagnosis of UC develops signs of CD (de novo CD) following IPAA. While the etiology and risk factors of de novo CD remain largely unknown, preliminary studies have shown controversial results regarding family history of inflammatory bowel disease (IBD) and smoking history. Methods Patients that underwent IPAA for UC, with at least 1 year of follow-up, were identified (n=161; 1996 to 2018). We retrospectively reviewed the electronic medical records. Patients that were diagnosed with de novo CD during the follow-up period were further identified. Smoking history and family history of IBD were evaluated. Chi square test was performed to compare the frequencies. Odds ratio (OR) and 95% confidence intervals (CIs) were estimated by logistic regression model. P<0.05 was considered statistically significant. Results 29 de novo CD were identified. At the time of proctocolectomy, the family history of IBD and smoking history was documented in 152 UC patients including 27 that subsequently developed de novo CD. 23 of 152 had a family history of IBD (12 UC, 9 CD and 2 IBD, NOS). 19/129 (14.7%) UC patients without a family history of any type of IBD, 4/9 (44.4%) with a family history of CD, and 4/12 (33.3%) with a family history of UC developed de novo CD. Patients with a family history of CD were more likely to develop de novo CD post IPAA than those without a family history of any type of IBD (OR 4.63, 95% CI 1.14-18.82, p=0.03). Family history of UC did not correlate with development of de novo CD (OR 2.90; 95% CI 0.79-10.57, p=0.108). At the time of proctocoletomy, 11 were current smokers, 25 were former smokers, and 116 never smoked. In de novo CD group, there were 4/27 (14.8 %) former smokers and 23/27 (85.2 %) never smokers. No de novo CD patient was current smoker. In the UC group that remained as UC following IPAA, 11/125 (8.8%) were current smokers, 21/125 (16.8 %) former smokers, and 93/125 (74.4 %) were never smokers. Current smoking status was not associated with development of de novo CD (p = 0.214). Conclusion Family history of CD may be a risk factor for developing de novo CD following IPAA for UC. Current smoking status was not associated with development of de novo CD following IPAA for UC.


2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Xiaohua Zhu ◽  
Lin Xie ◽  
Haihong Qin ◽  
Jun Liang ◽  
Yongsheng Yang ◽  
...  

Aims. This study is aimed at exploring the relation between IL-33 single-nucleotide polymorphisms (SNPs) and the risk of systemic lupus erythematosus (SLE). Methods. SNPStats (online software) was used to test the Hardy-Weinberg equilibrium in controls. Generalized multifactor dimensionality reduction (GMDR) was adopted to screen the preferable interaction between IL-33 SNPs and current smoking. Results. Logistic regression analysis based on the fundamental data of age, gender, BMI, current smoking, and alcohol drinking showed that both rs1929992-G and rs1891385-C alleles were correlated with an increasing risk of SLE, the ORs (95% CI) of which were 1.62 (1.21-2.05) and 1.64 (1.22-2.10), respectively. One two-locus model (rs1929992×current smoking) had a testing accuracy of 60.11% (P=0.0010). Through an overall multidimensional model, optimum cross-validation consistency was obtained. The analysis indicated that current smoking status influenced the SLE risk depending on the genotypes at rs1929992. Pairwise LD analysis indicated that haplotype rs1929992G-rs7044343T was statistically related to the elevating risk of SLE (P<0.05). Those subjects with the G-T haplotype had a higher SLE risk than those with other haplotypes, after correction with factors, including gender, alcohol drinking, age, BMI, and current smoking. Conclusions. The rs1929992-G and rs1891385-C allele, interaction between the rs1929992 gene and current smoking, and haplotype rs1929992G-rs7044343T were all risk factors of SLE.


2009 ◽  
Vol 36 (12) ◽  
pp. 2691-2693 ◽  
Author(s):  
IRINA TURCHIN ◽  
SASHA BERNATSKY ◽  
ANN E. CLARKE ◽  
YVAN ST-PIERRE ◽  
CHRISTIAN A. PINEAU

Objective.To evaluate the association between cigarette smoking and cutaneous damage in systemic lupus erythematosus (SLE).Methods.Our study was performed in SLE clinic registry cohort patients, all of whom fulfilled revised American College of Rheumatology criteria for SLE; patients are followed prospectively with annual assessments that include collection of demographic variables, smoking history, disease activity (SLE Disease Activity Index version 2000, SLEDAI-2K), medications, and damage scores (Systemic Lupus International Collaborating Clinics/ACR Damage Index). Cumulative cutaneous damage scores were used for the primary analyses. Logistic and logit regression models were performed to examine potential associations between current smoking and cutaneous damage, controlling for age, sex, race, lupus disease duration, antimalarial or immunosuppressant use, and anti-DNA and anti-SSA antibody status.Results.Of our sample (N = 276), 92% were women and 73.7% were Caucasian; the mean age was 45.1 years, mean disease duration 13.5 years, and 17.5% were current smokers. In the regression analyses, current cigarette smoking was associated with total cutaneous damage (OR 2.73, 95% CI 1.10, 6.81) and with scarring (OR 4.70, 95 CI 1.04, 21.2). In additional analyses, current smoking was also associated with active lupus rash (OR 6.18, 95% CI 1.63, 23.3).Conclusions.Current cigarette smoking may be associated with cutaneous damage and active lupus rash in SLE, suggesting another reason to emphasize smoking cessation in patients with SLE.


Lupus ◽  
2021 ◽  
pp. 096120332098860
Author(s):  
Trevor McKown ◽  
Maria Schletzbaum ◽  
Rachna Unnithan ◽  
Xing Wang ◽  
Nnenna Ezeh ◽  
...  

Objectives To investigate the relationship between smoking history and pack-year exposure on the rate of end-organ damage in systemic lupus erythematosus (SLE). Methods The SLE incident cohort included patients who met American College of Rheumatology (ACR) 1997 or SLE International Collaborating Clinics (SLICC) 2012 SLE criteria and had rheumatology encounters at a US academic institution (2008–16). The primary outcome was median time to SLICC/ACR damage index (SLICC/ACR-DI) increase or death. Main explanatory variables were smoking status and pack-years. Covariates included age, sex, race, ethnicity, receipt of Medicaid, neighborhood area deprivation index, and baseline SLE damage. Damage increase-free survival was evaluated by smoking status and pack-years using Kaplan-Meier and Cox proportional hazards methods. Results Patients of Black race and Medicaid recipients were more commonly current smokers ( p’s < 0.05). Former smokers were older and more likely to have late-onset SLE (54% versus 33% of never and 29% of current smokers, p = 0.001). Median time to SLICC/ACR-DI increase or death was earlier in current or former compared to never smokers (4.5 and 3.4 versus 9.0 yrs; p = 0.002). In multivariable models, the rate of damage accumulation was twice as fast in current smokers (HR 2.18; 1.33, 3.57) and smokers with a >10 pack-year history (HR 2.35; 1.15, 3.64) versus never smokers. Conclusions In this incident SLE cohort, past or current smoking predicted new SLE damage 4-5 years earlier. After adjustment, current smokers and patients with a pack-year history of >10 years accumulated damage at twice the rate of never smokers.


2021 ◽  
pp. 1-8
Author(s):  
Francesca Galluzzi ◽  
Veronica Rossi ◽  
Cristina Bosetti ◽  
Werner Garavello

<b><i>Introduction:</i></b> Smell and taste loss are characteristic symptoms of SARS-CoV-2 infection. The aim of this study is to investigate the prevalence and risk factors associated with olfactory and gustatory dysfunctions in coronavirus disease (COVID-19) patients. <b><i>Methods:</i></b> We conducted an observational, retrospective study on 376 patients with documented SARS-CoV-2 infection admitted to the San Gerardo Hospital in Monza, Italy, from March to July 2020. All patients answered a phone questionnaire providing information on age, sex, smoking status, and clinical characteristics. Adjusted odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated through logistic regression models including relevant covariates. <b><i>Results:</i></b> The prevalence of olfactory and gustatory dysfunctions in COVID-19 patients was 33.5 and 35.6%, respectively. Olfactory dysfunctions were significantly directly associated with current smoking and history of allergy, the multivariable ORs being 6.53 (95% CI 1.16–36.86) for current smokers versus never smokers, and 1.89 (95% CI 1.05–3.39) for those with an allergy compared to those without any allergy. Respiratory allergy in particular was significantly associated with olfactory dysfunctions (multivariable OR 2.30, 95% CI 1.02–5.17). Significant inverse associations were observed for patients aged 60 years or more (multivariable OR 0.33, 95% CI 0.19–0.57) and hospitalization (multivariable OR 0.22, 95% CI 0.06–0.89). Considering gustatory dysfunctions, after allowance of other variables a significant direct association was found for respiratory allergies (OR 2.24, 95% CI 1.03–4.86), and an inverse association was found only for hospitalization (OR 0.21, 95% CI 0.06–0.76). <b><i>Conclusion:</i></b> Our study indicates that current smoking and history of allergy (particularly respiratory) significantly increase the risk for smell loss in COVID-19 patients; the latter is also significantly associated to taste loss. Hospitalization has an inverse association with the risk of olfactory and gustatory dysfunctions, suggesting that these may be symptoms characteristics of less severe SARS-CoV-2 infection.


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