A Functional Ser413/Ser413 PAI-2 Polymorphism Is Associated With Susceptibility and Damage Index Score in Systemic Lupus Erythematosus

2008 ◽  
Vol 15 (2) ◽  
pp. 233-238 ◽  
Author(s):  
Claudia A. Palafox-Sánchez ◽  
Mónica Vázquez-Del Mercado ◽  
Gerardo Orozco-Barocio ◽  
Ignacio García-De la Torre ◽  
Norma Torres-Carrillo ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Healthy Subjects ◽  
Damage Index ◽  
Index Score ◽  
Systemic Lupus ◽  
Risk Of Mortality ◽  
Increased Risk ◽  
Significant Difference

Systemic lupus erythematosus in some cases is characterized for development of thrombotic events with a significantly increased risk of mortality. The frequencies and clinical associations of Ser413/Cys413 PAI-2 polymorphism in 40 systemic lupus erythematosus, 50 rheumatoid arthritis patients, and 100 healthy subjects were investigated. The Ser413/Ser413 genotype frequency was 53% (lupus), 36% (rheumatoid arthritis), and 35% (healthy subjects). The Ser413 allele was associated with systemic lupus erythematosus ( P = .04, odds ratio = 1.76, 95% confidence interval = 1.01-3.06). In all, 4 patient carriers of Ser413/Ser413 genotype, developed thrombotic events. The lupus patients identified with Ser 413/Ser413 genotype showed an increased damage (57%), compared with Ser413/Cys413 and Cys413/Cys413 genotypes, with significant difference ( P = .03). These findings suggest an association of Ser413/Ser413 genotype with greater damage index score and Ser413 allele with systemic lupus erythematosus. Besides, PAI-2 polymorphism could be related with thrombotic phenomena in systemic lupus erythematosus

scholarly journals Erratum to: MRI pattern of arthritis in systemic lupus erythematosus: a comparative study with rheumatoid arthritis and healthy subjects

2014 ◽  
Vol 44 (2) ◽  
pp. 267-267 ◽  
Author(s):  
Chiara Tani ◽  
Dario D’Aniello ◽  
Niccolò Possemato ◽  
Andrea Delle Sedie ◽  
Davide Caramella ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Comparative Study ◽  
Lupus Erythematosus ◽  
Healthy Subjects ◽  
Systemic Lupus

scholarly journals Novel gene variants associated with cardiovascular disease in systemic lupus erythematosus and rheumatoid arthritis

2018 ◽  
Vol 77 (7) ◽  
pp. 1063-1069 ◽  
Author(s):  
Dag Leonard ◽  
Elisabet Svenungsson ◽  
Johanna Dahlqvist ◽  
Andrei Alexsson ◽  
Lisbeth Ärlestig ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Cardiovascular Disease ◽  
General Population ◽  
Lupus Erythematosus ◽  
Risk Allele ◽  
Snp Array ◽  
Inflammatory Rheumatic Diseases ◽  
Systemic Lupus ◽  
Increased Risk

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.

scholarly journals Measuring Disease Activity and Damage with Validated Metrics: A Systematic Review on Mortality and Damage in Systemic Lupus Erythematosus

2018 ◽  
Vol 45 (10) ◽  
pp. 1448-1461 ◽  
Author(s):  
Stephanie O. Keeling ◽  
Ben Vandermeer ◽  
Jorge Medina ◽  
Trish Chatterley ◽  
Tatiana Nevskaya ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Disease Activity ◽  
Lupus Erythematosus ◽  
Activity Index ◽  
Damage Index ◽  
Disease Activity Index ◽  
Evaluation Methodology ◽  
Systemic Lupus ◽  
Increased Risk ◽  
Damage Accrual

Objective.To identify the effect of disease activity and damage, measured by validated indices, on mortality and damage accrual, in order to inform upcoming Canadian systemic lupus erythematosus (SLE) recommendations.Methods.Following GRADE (Grading of Recommendations Assessment, Development and Evaluation) methodology to fill in evidence-to-decision tables to create recommendations for “minimal investigations needed to monitor SLE patients at baseline and subsequent visits,” a systematic literature review was performed. The effect of disease activity and damage, measured by validated metrics, on mortality and damage was systematically reviewed, with metaanalyses performed when available.Results.A title/abstract screen of 5599 articles identified 816 articles for full paper review, with 102 meeting inclusion criteria and 53 with extractable data. Thirty-three articles describing outcomes related to disease activity and 20 articles related to damage were identified. Mortality was associated with higher SLE Disease Activity Index-2000 scores in 6 studies (HR 1.14, 95% CI 1.06–1.22) and higher Systemic Lupus International Collaborating Clinics/ACR Damage Index scores in 6 studies (HR 1.53, 95% CI 1.28–1.83). Higher SLE Activity Measure scores were associated with increased risk of damage in 3 studies (OR 1.06, 95% CI 1.04–1.08). British Isles Lupus Assessment Group was associated with mortality in 1 study with HR of 1.15.Conclusion.Active SLE disease and damage are associated with and predict greater mortality and damage. The use of validated disease activity and damage metrics is important in the assessment of disease activity and damage and will inform upcoming Canadian recommendations for the assessment of SLE.

scholarly journals AB0002 ASSOCIATION OF C1Q GENETIC POLYMORPHISMS WITH SUSCEPTIBILITY TO RHEUMATOID ARTHRITIS IN BULGARIAN COHORT

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1036.3-1036
Author(s):  
M. Kosturkova ◽  
G. Mihaylova ◽  
M. Radanova
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Autoimmune Diseases ◽  
Gene Cluster ◽  
Lupus Erythematosus ◽  
Annual Review ◽  
Healthy Controls ◽  
Systemic Lupus ◽  
Allelic Discrimination Assay ◽  
Increased Risk

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

scholarly journals The problem of accelerated atherosclerosis in systemic lupus erythematosus: Insights into a complex co-morbidity

2011 ◽  
Vol 106 (11) ◽  
pp. 849-857 ◽  
Author(s):  
Nekeithia Wade ◽  
Amy Major
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Cardiovascular Disease ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Inflammatory Responses ◽  
Systemic Lupus ◽  
Accelerated Atherosclerosis ◽  
Increased Risk ◽  
Co Morbidity

SummaryRheumatic autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus (SLE), are associated with antibodies to “self” antigens. Persons with autoimmune diseases, most notably SLE, are at increased risk for developing accelerated cardiovascular disease. The link between immune and inflammatory responses in the pathogenesis of cardiovascular disease has been firmly established; yet, despite our increasing knowledge, accelerated atherosclerosis continues to be a significant co-morbidity and cause of mortality in SLE. Recent animal models have been generated in order to identify mechanism(s) behind SLE-accelerated atherosclerosis. In addition, clinical studies have been designed to examine potential treatments options. This review will highlight data from recent studies of immunity in SLE and atherosclerosis and discuss the potential implications of these investigations.

Ibuprofen-Induced Aseptic Meningitis in Rheumatoid Arthritis

1997 ◽  
Vol 31 (9) ◽  
pp. 1009-1011 ◽  
Author(s):  
Amy C Horn ◽  
Steven W Jarrett
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Aseptic Meningitis ◽  
Lupus Erythematosus ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Systemic Lupus ◽  
Antiinflammatory Drugs ◽  
Stiff Neck ◽  
Laboratory Findings ◽  
Increased Risk

Objective To report a case of aseptic meningitis related to ibuprofen ingestion. Case Summary We discuss the case of a 56-year-old white man with a history of rheumatoid arthritis and hypertension who became confused, nauseated, and began to vomit within 2 hours of the ingestion of ibuprofen. A diagnosis of ibuprofen-induced aseptic meningitis was made based on the patient's physical and laboratory findings, the quick onset and resolution of symptoms, and his medical history. Discussion Ibuprofen-induced aseptic meningitis has been most frequently reported in patients with systemic lupus erythematosus. However, there have been reports of this reaction in patients with other underlying disease states. Various nonsteroidal antiinflammatory drugs have been reported to cause this reaction, but ibuprofen is the most common offending agent. A drug-related cause should be considered in any patient who presents with typical meningitis symptoms, such as fever, headache, and stiff neck, that occur within hours of ingesting a drug. Conclusions Although persons with systemic lupus erythematosus appear to have an increased risk for this type of reaction, the development of signs and symptoms in other patients warrants the consideration of nonsteroidal antiinflammatory drugs as the cause of aseptic meningitis.

scholarly journals FRI0556 INCREASED RISK OF MORTALITY AND CANCER IN SYSTEMIC LUPUS ERYTHEMATOSUS: RESULTS FROM A LUPUS COHORT STUDY FROM 1998 TO 2015

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 880.1-880
Author(s):  
G. Y. Ahn ◽  
J. Lee ◽  
J. M. Shin ◽  
Y. K. Lee ◽  
J. H. Kim ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
General Population ◽  
Cerebrovascular Disease ◽  
Lupus Erythematosus ◽  
Cytotoxic Agents ◽  
Mortality Data ◽  
Systemic Lupus ◽  
Risk Of Mortality ◽  
Increased Risk ◽  
Age And Sex

Background:Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune inflammatory disease with increased risk for mortality and cancers possibly because of the effects of systemic inflammation and immunodeficiency due to disease itself and/or cytotoxic agents for SLE management. Although there has been improvement in the prognosis of SLE over decades with the treatment advance including standardized treatment strategy for lupus nephritis and less cytotoxic agents, the improvement also is fixed nowadays.Objectives:In this study, we we are to investigate the mortality and cancer of SLE patients in a longitudinal SLE cohort and compare the morality ratio and incidence of cancer with general population over time.Methods:This study was conducted in Hanyang BAE lupus cohort during the period of 1998 to 2015. Mortality data and malignancy data were derived in connection with data from the Korean National Statistics Office and the Korea Central Incidence Database, respectively. The Standardized Mortality Ratio (SMR) and Standardized Incidence Ratio (SIR) was estimated yearly by dividing the observed number deaths/cancers by the expected number of deaths/cancers of age- and sex- matched general population from matched year.Results:Mortality data were available in 1284 patients and total 71 deaths were observed. The most common cause of death was SLE itself (52.1%) followed by infection (18.3%), cerebrovascular disease (8.5%) and suicide (7.0%). The total age and sex adjusted SMR was 3.4 [95% CI (Confidential Interval) 2.6-4.1]. When we conduct subgroup analysis by age, the sex-adjusted SMR was significantly increased in young and middle aged adult patients: the SMR in patients younger than 20 was 12.2, but it was not significant due to the small number of young patients (observed death 3, expected death 0.3, 95% CI 0-26.0). The adjusted SMR in patients aged 20-39, aged 40-59 and aged over 60 were 9.8 (observed death 35, expected death 4.8, 95% CI 6.5-13.0), 3.7 (observed death 24, expected death 11.5, 95% CI 2.2-5.2), and 1.0 (observed death 9, expected death 10.3, 95% CI 0.3-1.6), respectively. Compared with alive patients, died patients had more serositis and more neurologic disorder according to American College of Rheumatology classification criteria for SLE despite the shorter observational period (5.6 years vs. 9.4 years).Malignancy data were available in 1,020 patients and 56 primary cancers were diagnosed. Solid tumor was developed in 51 patient and hematologic malignancy was developed in 5 patients (3 non-Hodgkin’s lymphoma, 1 solitary plasmacytoma and 1 acute lymphoblastic leukemia). Thyroid cancer was the most common solid cancer (24 patients) followed by colorectal (5 patients), breast (4 patients), cervical cancer (4 patients) and hepatocellular carcinoma (3 patients). The total age and sex adjusted SIR was 1.1 (95% CI 0.8-1.4).Conclusion:Patients with SLE had higher risk of mortality than general population and the younger patients had the higher risk of mortality. The leading cause of death was SLE itself followed by infection and cerebrovascular disease. The risk for cancer in patient with SLE was similar with that of general population.Disclosure of Interests:None declared

Plasma interleukin-22 level, variants in interleukin-22 gene polymorphism, and the severity of systemic lupus erythematosus among Egyptian pediatric and adolescents

Lupus ◽  
2021 ◽  
pp. 096120332110423
Author(s):  
Zeinab R Attia ◽  
Mohamed M Zedan ◽  
Thuraya M Mutawi ◽  
Entsar A Saad ◽  
Mohamed A El Basuni
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Regression Analysis ◽  
Gene Polymorphism ◽  
Lupus Erythematosus ◽  
Nucleotide Polymorphisms ◽  
Systemic Lupus ◽  
Interleukin 22 ◽  
Increased Risk ◽  
Significant Difference ◽  
First Time

Objectives Our purpose was to investigate, for the first time, genotypes and alleles distribution of two single nucleotide polymorphisms (SNPs) of interleukin 22 (IL-22) (rs1012356 and rs2227485) in Egyptian pediatric and adolescents with systemic lupus erythematosus (SLE) and to evaluate the plasma IL-22 levels and their association with gene polymorphism and SLE risk and severity. Methods The TaqMan™ SNP genotyping assay on a real-time polymerase chain reaction (PCR) system was employed to evaluate the polymorphism’s genotypes. Plasma IL-22 levels were determined by using an enzyme-linked immunoabsorbent assay (ELISA). Results The frequencies and genotypes of rs2227485 and rs1012356 in IL-22 between SLE patients and controls also haplotypes formed by the same SNPs revealed no statistically significant difference ( p > 0.05). Otherwise, logistic regression analysis revealed that patients carrying rs1012356 “TA + AA” genotype had increased risk for prediction of SLE activity (OR = 1.610, 95% CI = 1.339–2.760, p = 0.034) by lowering plasma IL-22 level. Conclusions Among Egyptian pediatric and adolescents, we confirm a combined model “TA + AA” in rs1012356 (A/T) of IL-22 in regression analysis, as an independent predictor for SLE activity by lowering IL-22 plasma levels. Despite neither SNP rs2227485 A/G in IL-22 gene nor haplotypes formed by the same two SNPs (rs2227485 A/G and rs1012356 A/T) were significantly associated with the clinical and/or laboratory manifestations of SLE.

scholarly journals AB1213 DIFFERENT IMMUNOSUPPRESSIVE REGIMENS WITH NO EFFECT ON INFLUENZA-LIKE ILLNESS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1898.3-1898
Author(s):  
M. I. Freixa ◽  
H. Inácio ◽  
M. Amaral ◽  
M. Martins ◽  
C. Costa ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Vaccine Coverage ◽  
Multivariate Logistic Regression Analysis ◽  
Infection Risk ◽  
Systemic Lupus ◽  
Influenza Like Illness ◽  
Increased Risk ◽  
Biologic Dmard

Background:Autoimmune disease (AID) has been associated with increased risk of influenza and influenza-like illness (ILI) and its worse clinical outcomes complications.Objectives:We aimed to assess the influence and difference of several immunosuppressive (IS) treatments in the incidence of ILI, including glucocorticoids (GC), classic DMARDs and biologic DMARDs.Methods:We conducted a cross-sectional study in two autoimmune clinics. Patients were invited to answer a survey reporting ILI symptoms between October 2017 and March 2018. ILI definition was considered according to the European Center for Disease Control. Data regarding current IS, diagnostic, disease activity, comorbidities, and vaccination coverage were collected from electronic registry. Patients with history of cancer, HIV, IGIV treatment, or lack of information were excluded. Univariate and multivariate logistic regression analysis were used to access predictors of ILI.Results:We included 109 patients, with mean age 51 years and 81% female gender. The majority of patients had autoimmune arthropathy (n=54) or a connective tissue disease (n=44). Active disease was present in in 39% of patients. IS treatment was: GC 31%, classic DMARD 44%, biologic DMARD 28%. Vaccine coverage was 51%. Overall 41% reported ILI. We did not find any association between studied variables and ILI, including univariate and multivariate analysis. Univariate odds ratio calculation for IS treatment were: GC [OR 1,68 IC 0,7-3,8], classic DMARD [OR 1,03 IC 0,5-2,2], and biologic DMARD [OR 0,86 IC 0,4-2,0]. Comorbidity of pulmonary disease (n=8) may contribute to higher risk to ILI [OR 2,76 IC 0,8-10,0].Conclusion:There was no difference in risk of ILI within different IS treatment regimens, although GC may increase the risk. The study is limited by the subjectivity of the ILI survey and the small size of the sample. The stratification of influenza risk will help in designing better vaccine coverage strategies in this population.References:[1]Nakafero G, Grainge MJ, Myles PR, Mallen CD, Zhang W, Doherty M, Nguyen-Van-Tam JS, Abhishek A. Predictors and temporal trend of flu vaccination in auto-immune rheumatic diseases in the UK: a nationwide prospective cohort study. Rheumatology (Oxford). 2018 Oct 1;57(10):1726-1734.[2]Danza A, Ruiz-Irastorza G. Infection risk in systemic lupus erythematosus patients: susceptibility factors and preventive strategies. Lupus. 2013 Oct;22(12):1286-94.[3]McLean-Tooke A, Aldridge C, Waugh S, Spickett GP, Kay L. Methotrexate, rheumatoid arthritis and infection risk: what is the evidence? Rheumatology (Oxford). 2009 Aug;48(8):867-71.[4]Lacaille D, Guh DP, Abrahamowicz M, Anis AH, Esdaile JM. Use of non biologic disease-modifying antirheumatic drugs and risk of infection in patients with rheumatoid arthritis. Arthritis Rheum. 2008 Aug 15;59(8):1074-81.[5]Bernatsky S, Hudson M, Suissa S. Anti-rheumatic drug use and risk of serious infections in rheumatoid arthritis. Rheumatology (Oxford). 2007 Jul;46(7):1157-60.[6]Doran MF, Crowson CS, Pond GR, O’Fallon WM, Gabriel SE. Predictors of infection in rheumatoid arthritis. Arthritis Rheum. 2002 Sep;46(9):2294-300.[7]Fessler BJ. Infectious diseases in systemic lupus erythematosus: risk factors, management and prophylaxis. Best Pract Res Clin Rheumatol. 2002 Apr;16(2):281-91. Review.[8]Singh JA, Wells GA, Christensen R, Tanjong Ghogomu E, Maxwell L, Macdonald JK, Adverse effects of biologics: a network meta-analysis and Cochrane overview. Cochrane Database Syst Rev. 2011 Feb 16;(2):CD008794.Acknowledgments:None.Disclosure of Interests:None declared

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