Association between systemic lupus erythematosus and thyroid dysfunction: a meta-analysis

Lupus ◽  
2018 ◽  
Vol 27 (13) ◽  
pp. 2120-2128 ◽  
Author(s):  
W Luo ◽  
P Mao ◽  
L Zhang ◽  
Z Yang

Introduction Systemic lupus erythematosus (SLE) is a chronic autoimmune disease, the pathogenesis of which remains elusive. The deficiency or excess of thyroid hormone is defined as thyroid dysfunction, including (subclinical) hypothyroidism and (subclinical) hyperthyroidism. Autoimmune factors are likely to be relevant to the development of SLE and thyroid dysfunction. Recently, many studies have indicated that the prevalence of thyroid dysfunction is higher in SLE patients than in the general population. The objective of our study was to perform a systematic review and meta-analysis to find out the relationship between SLE and thyroid dysfunction. Methods Literature databases were searched, including PubMed, Embase, Web of science, Cochrane, CNKI, CHINESE WANFANG, China Science and Technology Database (VIP). Studies comparing presence of thyroid dysfunction in SLE patients to healthy controls were extracted. All the statistical analyses were performed with STATA 12.0 software. Results Ten studies with 10,500 SLE patients and 44,170 healthy controls were included in this study. The meta-analysis results showed that the prevalence of (subclinical) hypothyroidism in SLE patients was higher than in the healthy controls (hypothyroidism: OR = 2.93, 95% CI = 1.81–4.75; subclinical hypothyroidism: OR = 5.67, 95% CI = 3.50–9.18). No statistical difference of (subclinical) hyperthyroidism was found between SLE patients and controls. Conclusion Our meta-analysis suggests that SLE is significantly associated with increased risk of (subclinical) hypothyroidism, but it has little influence on (subclinical) hyperthyroidism.

2018 ◽  
Vol 12 (2) ◽  
pp. 143-151 ◽  
Author(s):  
Zhuoxian Zhao ◽  
Natalia P. Rocha ◽  
Haitham Salem ◽  
Breno S. Diniz ◽  
Antonio L. Teixeira

Abstract A growing body of evidence indicates that systemic lupus erythematosus (SLE) is associated with increased risk of cognitive impairment and dementia. However, to date, no studies have been conducted to quantitatively summarize and evaluate the consistency of data. Objective: To quantitatively evaluate the relationship of SLE and antiphospholipid antibodies (aPL) with cognitive dysfunction and dementia. Methods: All relevant literature was retrieved from Pubmed, Scopus, and PsycINFO databases. The meta-analysis was performed using effect estimates and 95% confidence intervals (CIs) to calculate pooled risk estimates. The heterogeneity among studies was also examined. Results: The meta-analysis included 11 original studies involving a total of 81,668 patients with dementia and 407 patients with cognitive dysfunction. There were significant associations on fixed-effect models between SLE and dementia (3 studies; RR=1.50; 95% CI=1.37-1.64), SLE and cognitive dysfunction (4 studies; OR=2.97; 95% CI=1.72-5.15), and aPL and cognitive dysfunction (5 studies, OR=1.97; 95% CI=1.55-2.52). We also combined cognitive dysfunction and dementia outcomes as they both represented cognitive impairment. There were significant associations between aPL and cognitive impairment (6 studies; OR=2.03; 95% CI=1.62-2.55), and SLE and cognitive impairment (7 studies; OR=1.83; 95% CI=1.42-2.35). Moderate heterogeneity (I2=45.7%) was found in the association between SLE and cognitive impairment, low heterogeneity (I2=21.8%) in the association between SLE and dementia, and near zero heterogeneity for the other three main analyses. Conclusion: Both SLE and aPL are associated with cognitive impairment.


2021 ◽  
Vol 61 (1) ◽  
Author(s):  
Yu Fu ◽  
Qing Lin ◽  
Zhi-rong Zhang

Abstract Objective To more precisely estimate the association between the tumor necrosis factor ligand superfamily member 4 (TNFSF4) gene polymorphisms and systemic lupus erythematosus (SLE) susceptibility, we performed a meta-analysis on the association of the following single nucleotide polymorphisms (SNPs) of TNFSF4 with SLE: rs1234315, rs844648, rs2205960, rs704840, rs844644, rs10489265. Methods A literature-based search was conducted using PubMed, MEDLINE, Embase, Web of Science databases, and Cochrane Library databases to identify all relevant studies. And the association of TNFSF4 gene polymorphisms and SLE susceptibility was evaluated by pooled odds ratio (OR) with 95% confidence interval (CI). Results The meta-analysis produced overall OR of 1.42 (95% CI 1.36–1.49, P < 0.00001), 1.41 (95% CI 1.36–1.46, P < 0.00001) and 1.34 (95% CI 1.26–1.42, P < 0.00001) for the rs2205960, rs1234315 and rs704840 polymorphisms respectively, confirming these three SNPs confer a significant risk for the development of SLE. On the other hand, the meta-analysis produced overall OR of 0.92 (95% CI 0.70–1.21, P = 0.54) for the rs844644 polymorphism, suggesting no significant association. And no association was also found between either rs844648 1.11 (OR 1.11, 95% CI 0.86–1.43, P = 0.41) or rs10489265 (OR 1.17, 95% CI 0.94–1.47, P = 0.17) polymorphism with SLE susceptibility, respectively. Conclusions Our meta-analysis demonstrated that the TNFSF4 rs2205960, rs1234315 and rs844840 SNPs was significantly associated with an increased risk of SLE.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1036.3-1036
Author(s):  
M. Kosturkova ◽  
G. Mihaylova ◽  
M. Radanova

Background:Complement is strongly implicated in the pathogenesis of autoimmune diseases like systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Its component C1q plays a dualistic role, triggering the inflammatory cascade on one hand and directing the clearance of immune complexes on the other. Homozygous genetic deficiency of C1q is strongly associated with SLE and SLE-like phenotype as almost 90% of C1q deficient individuals develop SLE or similar disease. Nevertheless, there are few and inconsistent studies exploring the single nucleotide polymorphisms (SNPs) of the C1q gene cluster in relation to the pathogenesis of SLE and RA.Objectives:The aim of the study was to evaluate the possible association of five SNPs – rs292001, rs172378, rs294179, rs665691 and rs682658 in complement C1q gene cluster with susceptibility to SLE and RA in Bulgarian cohort.Methods:Fifty patients with SLE, sixty-one patients with RA and sixty-seven healthy controls were genotyped for the five SNPs by TaqMan allelic discrimination assay.Results:Frequency of genotypes and alleles of rs294179, rs665691 and rs682658 SNPs was similar between patients with SLE, RA and healthy controls. For rs172378 SNP, the minor G allele (OR = 2.73; 95% CI, 1.59-4.67, p=0.0003) and GG genotype (OR = 5.12; 95% CI, 1.60-16.49, p=0.006) were associated with susceptibility to RA. In our cohort in accordance with others, AA rs292001 SNP genotype was associated with increased risk for RA (OR = 3.32; 95% CI, 1.19-9.20, p=0.021). For SLE patients, AA rs292001 SNP genotype was low presented and did not associate with disease.Conclusion:GG genotype of rs172378 SNP in C1q gene cluster could be considered as a new risk factor for RA.References:[1]Diane Scott et al (2016). The paradoxical roles of C1q and C3 in autoimmunity. Immunobiology, 719-25. doi:10.1016/j.imbio.2015.05.001.[2]Giles JL et al (2015). Functional analysis of a complement polymorphism (rs17611) associated with rheumatoid arthritis. J Immunol., 3029-34. doi:10.4049/jimmunol.1402956.[3]Holers, V. M. (2018). Complement in the Initiation and Evolution of Rheumatoid Arthritis. Frontiers in immunology, 1057. doi:10.3389/fimmu.2018.01057.[4]Lintner, K. E. (2016). Early Components of the Complement Classical Activation Pathway in Human Systemic Autoimmune Diseases. Frontiers in immunology, 36. doi:10.3389/fimmu.2016.00036.[5]Lu, J. &. (2017). C1 Complex: An Adaptable Proteolytic Module for Complement and Non-Complement Functions. Frontiers in immunology, 592. doi:10.3389/fimmu.2017.00592.[6]Manderson, A. P. (2004). The role of complement in the development of systemic lupus erythematosus. Annual review of immunology, 431-456. doi:10.1146/annurev.immunol.22.012703.104549.[7]Martens, H. A. (2009). Analysis of C1q polymorphisms suggests association with systemic lupus erythematosus, serum C1q and CH50 levels and disease severity. Annals of the rheumatic diseases, 715–720. doi:10.1136/ard.2007.085688.[8]Namjou B, G.-M. C. (2009). Evaluation of C1q genomic region in minority racial groups of lupus. Genes Immun., 517-24. doi:10.1038/gene.2009.33.[9]Radanova M et al(2015). Association of rs172378 C1q gene cluster polymorphism with lupus nephritis in Bulgarian patients. Lupus, 280-9. doi:10.1177/0961203314555173.[10]Rafiq S et al (2010). Assessing association of common variation in the C1Q gene cluster with systemic lupus erythematosus. Clin Exp Immunol., 284-9. doi:10.1111/j.1365-2249.2010.04185.x.[11]Schejbel L et al (2011). Molecular basis of hereditary C1q deficiency-revisited: identification of several novel disease-causing mutations. Genes Immun., 626-634.[12]Trouw LA et al (2013). Genetic variants in the region of the C1q genes are associated with rheumatoid arthritis. Clin Exp Immunol., 76-83. doi:10.1111/cei.12097.[13]Trouw L. A. (2017). The complement system as a potential therapeutic target in rheumatic disease. Nature reviews. Rheumatology, 538–547. doi:10.1038/nrrheum.2017.125.[14]Walport M. J. (2002). Complement and systemic lupus erythematosus. Arthritis research, S279–S293. doi:10.1186/ar586.Disclosure of Interests:None declared


Lupus ◽  
2020 ◽  
pp. 096120332097408
Author(s):  
Zhao Jin ◽  
Cong Yang ◽  
Chu Xiao ◽  
Zizhen Wang ◽  
Suxin Zhang ◽  
...  

Objective To systematically review and summarize the available literature regarding the association between systemic lupus erythematosus (SLE) and sexual dysfunction (SD) in both sexes. Methods We retrieved relevant studies from the following databases: PubMed, Embase, Cochrane Library, and Web of Science. Two reviewers independently reviewed the studies in our sample, assessed their validity, and extracted relevant data. Sensitivity and subgroup analyses were performed to distinguish sources of heterogeneity. Results Our search resulted in a sample of eight eligible studies, which involved 758 patients in the SLE group and 1724 individuals in the control group. The pooled RR for the increased risk for SD compared to those in the control group was 1.80 (95%CI 1.12-2.87). Subgroup analysis by sex revealed that males (pooled RR = 2.98, 95%CI 2.41-3.68) had a higher risk of SD compared to females (pooled RR = 1.56, 95%CI 0.99-2.48). Females with SLE had significantly lower values in FSFI compared to the healthy individuals (WMD=-0.224, 95%CI -0.441 to -0.078). Age of participants and the quality of studies might influence the results. Conclusions Our meta-analysis suggests that SLE is significantly associated with an increased risk of sexual dysfunction. It is of great urgency to implement for active interventions that aimed to treat or prevent SD among SLE patients.


2019 ◽  
Vol 13 (13) ◽  
pp. 1137-1152 ◽  
Author(s):  
Napoleon Bellua Sam ◽  
Bao-Zhu Li ◽  
Rui-Xue Leng ◽  
Hai-Feng Pan ◽  
Dong-Qing Ye

Aim: To derive a precise estimation on plasma/serum level of SOD, GPx, CAT and GSH levels in systemic lupus erythematosus (SLE) patients. Methods: A total of 36 articles from electronic databases were finally included with 1120 SLE patients and 1024 healthy controls considered for antioxidant levels. Results: The levels of CAT and GSH were significantly lower, while SOD and GPx levels were slightly lower in patients with SLE compared with healthy controls. Subgroup analysis indicated that Arabs, ages ≥40 and SLE diseases activity index <6 had a significant association of SOD and CAT levels with SLE patients. Conclusion: The results demonstrated a significant lower CAT and GSH levels and also revealed no significant difference for SOD and GPx levels in SLE patients.


Author(s):  
Xiaolan Huang ◽  
Nan Jia ◽  
Fei Xiao ◽  
Chunrong Sun ◽  
Jia Zhu ◽  
...  

<b><i>Introduction:</i></b> The aim of this study was to assess the differences between childhood-onset and adult-onset systemic lupus erythematosus (cSLE and aSLE) for clinical manifestations and mortality using a meta-analytic approach. <b><i>Methods:</i></b> The PubMed, EMBASE, and the Cochrane library were searched for eligible studies published between January 1982 and March 2021. The odds ratio (OR) with 95% confidence interval was used to calculate the pooled effect estimates using the random-effects model. <b><i>Results:</i></b> Thirty-four studies involving 21,946 SLE patients were included. cSLE was associated with an increased risk of malar rash (OR: 1.64; <i>p</i> &#x3c; 0.001), ulcers/mucocutaneous involvement (OR: 1.22; <i>p</i> = 0.039), general neurological involvement (OR: 1.52; <i>p</i> &#x3c; 0.001), seizures (OR: 1.92; <i>p</i> &#x3c; 0.001), general renal involvement (OR: 2.08; <i>p</i> &#x3c; 0.001), proteinuria (OR: 1.35; <i>p</i> = 0.015), urinary cellular casts (OR: 1.67; <i>p</i> = 0.047), fever (OR: 2.31; <i>p</i> &#x3c; 0.001), anemia (OR: 1.91; <i>p</i> &#x3c; 0.001), thrombocytopenia (OR: 1.41; <i>p</i> &#x3c; 0.001), leucopenia (OR: 1.57; <i>p</i> = 0.017), lymphadenopathy (OR: 2.40; <i>p</i> &#x3c; 0.001), and cutaneous vasculitis (OR: 1.72; <i>p</i> = 0.001) as compared with aSLE. Moreover, cSLE versus aSLE was associated with a reduced risk of articular manifestations (OR: 0.63; <i>p</i> = 0.001), pulmonary involvement (OR: 0.54; <i>p</i> = 0.001), and pleuritis (OR: 0.61; <i>p</i> &#x3c; 0.001). There were no significant differences between cSLE and aSLE for mortality risk (OR: 1.20; <i>p</i> = 0.203). <b><i>Conclusion:</i></b> We found that certain clinical manifestations of SLE are different in cSLE and aSLE. Moreover, the mortality risk of cSLE and aSLE was not significantly different.


2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Jing Sun ◽  
Liang Yao ◽  
Yuan Fang ◽  
Ruifei Yang ◽  
Yaolong Chen ◽  
...  

Background. Evidence on the association between subclinical thyroid dysfunction and the risk of cardiovascular outcomes are conflicting. Methods and Results. PubMed, EMbase, Web of Science, Cochrane Library, and China Biology Medicine (CBM) databases were searched from inception to July 10, 2016. A total of 16 studies were included for meta-analysis. We found that subclinical hypothyroidism was not correlated with coronary heart disease (CHD) (RR = 1.17; 95% CI, 0.91–1.52), total mortality (RR = 1.02; 95% CI, 0.93–1.13), cardiovascular mortality (RR = 1.06; 95% CI, 0.77–1.45), heart failure (RR = 1.17; 95% CI, 0.87–1.57), and atrial fibrillation (RR = 1.05; 95% CI, 0.91–1.21), except CHD mortality (RR = 1.37; 95% CI, 1.03–1.84). Subgroup analysis indicated a higher estimation risk in CHD (RR = 1.54; 95% CI, 1.00–2.39), cardiovascular mortality (RR = 2.14; 95% CI, 1.43–3.22), and CHD mortality (RR = 1.54; 95% CI, 1.11–2.15) among participants < 65 years. Furthermore, subclinical hyperthyroidism was found to be associated with CHD (RR = 1.20; 95% CI, 1.02–1.42), total mortality (RR = 1.27; 95% CI, 1.07–1.51), and CHD mortality (RR = 1.45; 95% CI, 1.12–1.86). Conclusions. Subclinical hypothyroidism is likely associated with an increased risk of CHD mortality, and subclinical hyperthyroidism is likely associated with increased risk of CHD, CHD mortality, and total mortality.


2018 ◽  
Vol 24 (16) ◽  
pp. 1780-1787 ◽  
Author(s):  
Yan-Mei Mao ◽  
Song Wang ◽  
Chan-Na Zhao ◽  
Qian Wu ◽  
Yi-Lin Dan ◽  
...  

Background and Aims: Matrix metalloproteinase-9 (MMP-9) is closely related to the pathogenesis of autoimmune diseases, especially Systemic Lupus Erythematosus (SLE). However, published works about the circulating MMP-9 levels in SLE are contradictory. A meta-analysis was performed to estimate circulating MMP- 9 levels in SLE patients more accurately and explore its related influencing factors. Methods: The related literatures were systematically searched in PubMed, Embase, and The Cochrane Library database (up to 31 January 2018). Pooled Standardized Mean Difference (SMD) and 95% Confidence Interval (CI) of circulating MMP-9 levels were calculated by Stata12.0 software according to fixed-effect or randomeffect model analysis. Results: A total of 638 articles were retrieved, and 12 studies including 730 SLE cases and 759 controls were finally included in the meta-analysis. No significant differences in circulating MMP-9 levels were observed between SLE patients and healthy controls (pooled SMD = -0.209, 95% CI = -0.812 to 0.394). However, subgroup analyses indicated that age<30 years group had higher MMP-9 levels (SMD = 0.991, 95% CI: 0.504 to 1.478) and sample size (n ≥ 60) group had lower MMP-9 levels when compared with controls (SMD = -0.755, 95% CI: - 1.347 to -0.163). Conclusion: The meta-analysis of current evidence suggests that circulating MMP-9 levels do not differ between SLE patients and healthy controls, however, the results may be affected by age and sample size. Further studies are needed to clarify the relationship between SLE and circulating MMP-9 levels.


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