Incidence and risk factors for vertebral fracture in rheumatoid arthritis: an update meta-analysis

Author(s):  
Yang Liu ◽  
Jun Jiang ◽  
Minmin Mo ◽  
Xiaohong Sun ◽  
Kailong Yu
2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Christos Bissias ◽  
Angelos Kaspiris ◽  
Athanasios Kalogeropoulos ◽  
Konstantinos Papoutsis ◽  
Nikolaos Natsioulas ◽  
...  

Abstract Objectives The increasing number of hip arthroplasties (HA), due to the growing elderly population, is associated with the risk of femoral periprosthetic fractures (FPFs). The purpose of this study was to identify potential risk factors for the development of FPFs after HA. Methods A systematic review was conducted in five data bases (Medline, Embase, Cochrane, Cinahl, ICTRP) according to the Preferred Reporting Items for Systematic reviews and Meta-analysis (PRISMA) guidelines up to May 2019, using the key words “risk factor,” “periprosthetic fracture,” and “hip replacement or arthroplasty.” Meta-analysis of the clinical outcomes of HA and subgroup analysis based on the factors that were implicated in FPFs was performed. Results Sixteen studies were included (sample size: 599,551 HA patients, 4253 FPFs, incidence 0.71%). Risk factors statistically associated with increased incidence of FPFs were female gender (+ 40%), previous revision arthroplasty surgery (× 3 times), and the presence of rheumatoid arthritis (× 2.1 times), while osteoarthritis (− 57%), cement application (− 59%), and insertion of Biomet (− 68%) or Thompson’s prosthesis (− 75%) were correlated with low prevalence of FPFs. Obesity, cardiac diseases, advanced age, bad general health (ASA grade ≥ 3), and use of Exeter or Lubinus prosthesis were not linked to the appearance of FPFs. Conclusion This meta-analysis suggested that female gender, rheumatoid arthritis, and revision arthroplasty are major risk factors for the development of FPFs after a HA. In those patients, frequent follow-ups should be planned. Further prospective studies are necessary to clarify all the risk factors contributing to the appearance of FPFs after HA.


Author(s):  
Kentaro Yamada ◽  
Akinobu Suzuki ◽  
Shinji Takahashi ◽  
Kentaro Inui ◽  
Tatsuya Koike ◽  
...  

Author(s):  
Lily W. Martin ◽  
Lauren C. Prisco ◽  
Weixing Huang ◽  
Gregory McDermott ◽  
Nancy A. Shadick ◽  
...  

2020 ◽  
pp. 219256822097822
Author(s):  
Tianyu Zhang ◽  
Yanhua Wang ◽  
Peixun Zhang ◽  
Feng Xue ◽  
Dianying Zhang ◽  
...  

Study Design: Meta-analysis. Objectives: To provide up-to-date evidence-based outcomes for the incidence and risk factors of adjacent vertebral fracture (AVF) after the vertebral augmentation. Methods: The MEDLINE, Embase, and the Cochrane Central Register of Controlled Trials were searched for studies assessing the risk factors of adjacent vertebral fracture after vertebral augmentation until June 2020. The AVF incidence and factors potentially affecting AVF were extracted and pooled. Results: A total of 16 studies, encompassing 2549 patients were included in the meta-analysis. The pooled incidence of AVF was 14% after vertebral augmentation. Female, lower T-score, thoracolumbar junction fracture, intravertebral cleft, more injected cement volume, intradiscal cement leakage significantly increased the risk of AVF. Age, body mass index, steroid medication, Cobb angle change, postoperative Cobb angle showed no significant association with AVF. Conclusions: Identifying the risk factors of AVF can facilitate prevention strategy to avoid the AVF. Female, T-score, thoracolumbar junction fracture, intravertebral cleft, more cement volume, and intradiscal cement leakage increased the risk of AVF.


2017 ◽  
Vol 20 (5) ◽  
pp. 541-549 ◽  
Author(s):  
Shuai Zhu ◽  
Wangdong Xu ◽  
Yubin Luo ◽  
Yi Zhao ◽  
Yi Liu

2011 ◽  
Vol 78 (2) ◽  
pp. 179-183 ◽  
Author(s):  
Jean-Frédéric Boyer ◽  
Pierre-Antoine Gourraud ◽  
Alain Cantagrel ◽  
Jean-Luc Davignon ◽  
Arnaud Constantin

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 420.1-420
Author(s):  
F. Wouters ◽  
M. Maurits ◽  
L. van Boheemen ◽  
M. Verstappen ◽  
X. Matthijssen ◽  
...  

Background:The HLA shared epitope (SE) and smoking are the best known genetic and environmental risk factors for rheumatoid arthritis (RA) development; however, at which pre-RA stage they exert their effect is unknown. The following stages are discerned: an asymptomatic stage in which autoimmune responses can develop, a symptomatic stage (clinically suspect arthralgia (CSA)), and development of clinically apparent inflammatory arthritis (IA). Studies in the general asymptomatic population revealed contrasting results on the associations between SE-alleles and smoking and the presence of anti-citrullinated protein antibodies (ACPA). Furthermore, studies on these risk factors in the symptomatic pre-RA phase are scarce and these data might teach us whether SE-alleles and smoking are involved in symptom development and/or progression to clinical arthritis.Objectives:We aimed to determine at which pre-RA stage SE and smoking exert their effect. In this respect, the analyses were focused on the presence of ACPA, but associations for other anti-modified protein antibodies (anti-carbamylated and anti-acetylated protein antibodies (anti-CarP and AAPA, respectively)) were also studied.Methods:Results from the literature on the association of SE and smoking with ACPA in the asymptomatic population were summarized in inverse-variance weighted meta-analyses. In addition 577 CSA-patients were studied. Associations of SE and smoking with IgG ACPA were studied at baseline (CSA-onset), to assess an effect on symptom development. Additionally, patients were monitored for the development of clinically apparent inflammatory arthritis (IA) for median 2 years and associations of SE, smoking and auto-antibodies with progression to IA were determined. Analyses were stratified for ACPA-status and associations in ACPA-positive patients were validated in meta-analyses with other arthralgia-cohorts. Finally analyses were repeated for anti-CarP and AAPA.Results:Meta-analyses showed that SE is not associated with ACPA-positivity in the asymptomatic population (OR 1.06 (95%CI 0.69-1.64)), whereas smoking was associated (OR 1.37 (1.15-1.63)). At CSA-onset, both SE and smoking associated with ACPA-positivity (OR 2.08 (1.24-3.49) and OR 2.41 (1.31-4.43), respectively). During follow-up of CSA-patients SE associated with IA-development (HR 1.86 (1.23-2.82)), in contrast to smoking. SE conferred risk for IA-development in ACPA-negative CSA-patients (HR 1.71 (0.99-2.96)) and in ACPA-positive patients (CSA-cohort HR 1.29 (0.67-2.47); meta-analysis three arthralgia-cohorts HR 1.52 (1.08-2.15)). Investigating the other autoantibodies revealed that SE and smoking were not associated with anti-CarP or AAPA-positivity at CSA-onset; longitudinally AAPA associated with progression to IA independent from ACPA and RF (HR 1.79 (1.02-3.16)), whilst anti-Carp did not.Conclusion:SE and smoking act in partly different pre-RA stages. Although SE does not associate with ACPA in the general population, it does mediate symptom-development and further progression to clinical arthritis. Smoking confers risk to development of ACPA and/or joint symptoms, but is not further involved in IA-development. The time-specific biologic pathways that are underlying need further exploration. These data enhance the understanding of the timing of key genetic and environmental risk factors in the trajectory of RA development.Disclosure of Interests:None declared


2021 ◽  
Vol 18 ◽  
pp. 147997312199456
Author(s):  
Rafal Wiater ◽  
Kjell Erik Julius Håkansson ◽  
Charlotte Suppli Ulrik

Rheumatoid arthritis (RA) is a chronic autoimmune disease primarily affecting joints but often also associated with lung involvement such as bronchiectasis (BE). The aim of the present systematic review and meta-analysis is to provide an update on the current evidence regarding the prevalence and association between RA and BE. This systematic review and meta-analysis was performed in accordance with the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines with literature search using the terms ‘Bronchiectasis AND Rheumatoid Arthritis’ without a date limitation on PubMed during May 2020. A total of 28 studies fulfilled the predefined criteria and were included in the present review, with 19 being cross-sectional studies. Twenty-three studies were included in the meta-analysis. The pooled prevalence estimate was 2.69% (95% CI 1.63–4.42) in clinically defined BE, and 24.9% (95% CI 19.21–31.67) in radiologic disease. Many inconsistencies exist regarding potential risk factors for BE in RA patients such as gender, RA duration and severity, as both negative and positive associations have been reported. Although very little is known about possible causative mechanisms between RA and BE, potential pathways might be antigenic stimulation from pulmonary mucus and/or systemic inflammation from joint disease affecting the lungs. At present, the available evidence of bronchiectasis in patients with RA is insufficient to identify RA-associated risk factors for the development of BE, possibly apart from duration of RA, and, consequently, also to fully explore a possible causal relationship between the two disease. However, the increased prevalence of BE in RA patients warrants further studies to explore the association between RA and BE.


Rheumatology ◽  
2010 ◽  
Vol 49 (7) ◽  
pp. 1303-1310 ◽  
Author(s):  
A. El Maghraoui ◽  
A. Rezqi ◽  
A. Mounach ◽  
L. Achemlal ◽  
A. Bezza ◽  
...  

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