Serum anti-citrullinated protein antibodies and rheumatoid factor increase the risk of rheumatoid arthritis–related interstitial lung disease: a meta-analysis

Author(s):  
Sisi Xie ◽  
Shu Li ◽  
Bilin Chen ◽  
Qing Zhu ◽  
Lichang Xu ◽  
...  
2016 ◽  
Vol 75 (Suppl 2) ◽  
pp. 956.2-956
Author(s):  
C. Aguilera Cros ◽  
A. Ruíz Román ◽  
M. Lisbona Muñoz ◽  
M. Luque Leόn ◽  
P. Leόn Rubio ◽  
...  

2019 ◽  
Vol 5 (1) ◽  
pp. 16
Author(s):  
EmanA Ghani Sayed Mahmoud ◽  
RagaaA Kader Mahmoud ◽  
MonaH Abdel Megid ◽  
MahmoudI Mahmoud ◽  
AbeerA El-Dousouky

BMJ Open ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. e040465
Author(s):  
Hiroyuki Kamiya ◽  
Ogee Mer Panlaqui

ObjectiveTo clarify the risk of rheumatoid arthritis-associated interstitial lung disease (RA-ILD) related to anti-cyclic citrullinated peptide (CCP) antibody.Eligibility criteriaPatients with RA with and without ILD were eligible. The primary outcome was the prevalence or incidence of ILD. Primary studies of any design aside from a case report were eligible.Information sourcesMedline, EMBASE, Science Citation Index Expanded and Cochrane Central Register of Controlled Trials were searched from the inception through 12 November 2019.Data extraction and risk of biasTwo reviewers independently selected eligible reports, extracted relevant data and assessed risk of bias using a modified Quality in Prognostic Studies tool.Data synthesisMeta-analysis was conducted using a random-effects model.Quality of evidenceThe Grades of Recommendation, Assessment, Development and Evaluation system was applied.ResultsAmong 29 out of 827 records retrieved through electronic databases and four additional reports identified from other sources, 29 studies were focused for the review. A total of 10158 subjects were included and the mean age at inclusion was between 45.8 and 63.9 years. The mean RA duration was between 4.3 and 14.9 years. The positivity of anti-CCP antibody ranged from 50.7% to 95.8%. All studies except for two were deemed as high risk of bias. A pooled analysis of univariate results demonstrated that the presence of anti-CCP antibody was significantly associated with RA-ILD with an OR of 2.10 (95% CI: 1.59 to 2.78). Similarly, the titre of anti-CCP antibody was significantly higher for RA-ILD with a standardised mean difference of 0.42 (95% CI: 0.20 to 0.65). These results were confirmed by multivariate analysis in the majority of studies and consistent by any subgroup and sensitivity analyses.ConclusionThe presence and higher titres of anti-CCP antibody were suggested to be significantly associated with an increased risk of RA-ILD. However, the quality of evidence was rated as low or very low.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Albina Tyker ◽  
Iazsmin Bauer Ventura ◽  
Cathryn T. Lee ◽  
Rachel Strykowski ◽  
Nicole Garcia ◽  
...  

AbstractRheumatoid arthritis-related interstitial lung disease (RA-ILD) is a common connective tissue disease-related ILD (CTD-ILD) associated with high morbidity and mortality. Although rheumatoid factor (RF) seropositivity is a risk factor for developing RA-ILD, the relationship between RF seropositivity, mediastinal lymph node (MLN) features, and disease progression is unknown. We aimed to determine if high-titer RF seropositivity predicted MLN features, lung function impairment, and mortality in RA-ILD. In this retrospective cohort study, we identified patients in the University of Chicago ILD registry with RA-ILD. We compared demographic characteristics, serologic data, MLN size, count and location, and pulmonary function over 36 months among patients who had high-titer RF seropositivity (≥ 60 IU/ml) and those who did not. Survival analysis was performed using Cox regression modeling. Amongst 294 patients with CTD-ILD, available chest computed tomography (CT) imaging and serologic data, we identified 70 patients with RA-ILD. Compared to RA-ILD patients with low-titer RF, RA-ILD patients with high-titer RF had lower baseline forced vital capacity (71% vs. 63%; P = 0.045), elevated anti-cyclic citrullinated peptide titer (122 vs. 201; P = 0.001), CT honeycombing (50% vs. 80%; P = 0.008), and higher number of MLN ≥ 10 mm (36% vs. 76%; P = 0.005). Lung function decline over 36 months did not differ between groups. Primary outcomes of death or lung transplant occurred more frequently in the high-titer RF group (HR 2.8; 95% CI 1.1–6.8; P = 0.028). High-titer RF seropositivity was associated with MLN enlargement, CT honeycombing, and decreased transplant-free survival. RF titer may be a useful prognostic marker for stratifying patients by pulmonary disease activity and mortality risk.


2019 ◽  
Vol 49 (3) ◽  
pp. 358-365 ◽  
Author(s):  
Namrata Singh ◽  
Jimmy Varghese ◽  
Bryant R. England ◽  
Joshua J. Solomon ◽  
Kaleb Michaud ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Cristina Regueiro ◽  
Luis Rodriguez-Rodriguez ◽  
Raquel Lopez-Mejias ◽  
Laura Nuño ◽  
Ana Triguero-Martinez ◽  
...  

Abstract The major environmental risk factor for rheumatoid arthritis (RA) is smoking, which according to a widely accepted model induces protein citrullination in the lungs, triggering the production of anti-citrullinated protein antibodies (ACPA) and RA development. Nevertheless, some research findings do not fit this model. Therefore, we obtained six independent cohorts with 2253 RA patients for a detailed analysis of the association between smoking and RA autoantibodies. Our results showed a predominant association of smoking with the concurrent presence of the three antibodies: rheumatoid factor (RF), ACPA and anti-carbamylated protein antibodies (ACarPA) (3 Ab vs. 0 Ab: OR = 1.99, p = 2.5 × 10–8). Meta-analysis with previous data (4491 patients) confirmed the predominant association with the concurrent presence of the three antibodies (3 Ab vs. 0 Ab: OR = 2.00, p = 4.4 ×10–16) and revealed that smoking was exclusively associated with the presence of RF in patients with one or two antibodies (RF+1+2vs. RF−0+1+2: OR = 1.32, p = 0.0002). In contrast, no specific association with ACPA or ACarPA was found. Therefore, these results showed the need to understand how smoking favors the concordance of RA specific antibodies and RF triggering, perhaps involving smoking-induced epitope spreading and other hypothesized mechanisms.


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