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Study participants with rheumatoid arthritis (RA) have an elevated risk for nontuberculous mycobacterial pulmonary disease (NTM-PD), which limits the treatments for RA. Biomarkers for NTM-PD in study participants with RA are required. Patients with NTM-PD have been studied for small-molecule metabolites, although few have been performed for NTM-PD associated with RA. Therefore, we performed lipidomic profiling of NTM-PD in the urine specimens of study participants with RA to discover useful biomarkers. Urine specimens provided by 90 study participants with RA, with or without NTM-PD were subjected to lipidomic analysis. Univariate analysis found that the urinary concentrations of lysophosphatidic acid (LPA) 22:5 and phosphatidic acid (PA) 36:1 were altered in study participants with RA and NTM-PD (respective areas under the curves of receiver operating characteristic (AUROCs) were 0.977 and 0.811; P  = 3.83 × 10 −20 and 1.37 × 10 −5 ), when compared with the levels in urine specimens of study participants with RA without NTM-PD. The partial least squares-discriminant analysis model created from these two phospholipids validated their ability to discriminate between the study participants with or without NTM-PD (AUROC: 0.988 [95% confidence interval 0.958–1.000]). Differences between the urinary levels of the phospholipids LPA and PA in study participants with RA and with or without NTM-PD were significant. Lipidomic profiling of urine samples should be effective in the process of evaluating biomarkers for NTM-PD associated with RA.

Objective: Chronic lung diseases (CLDs), for example, interstitial lung disease, manifest as an extra-articular complication of rheumatoid arthritis (RA). The contribution of anti-bactericidal permeability-increasing protein antibodies (BPI Abs) in lung involvement in RA or primary Sjögren’s syndrome has been reported. Studies related to anti-BPI Abs in RA with CLD are infrequent. Here, the involvement of anti-BPI Abs with RA and CLD complications was evaluated. Methods: Enzyme-linked immunosorbent assays were used to measure anti-BPI Abs in RA sera. Results: Higher anti-BPI Ab amounts were present in the RA with usual interstitial pneumonia (UIP) than without CLD (mean ± standard deviation, 10.4 ± 23.5 [ng/mL] vs. 1.3 ± 3.8, p = 0.0020). Area under the curve values of receiver operating characteristic curves for anti-BPI Ab and Krebs von den lungen-6 were alike between RA with UIP and without CLD (0.8616, 95% CI 0.8184–0.9048; 0.8716, 95% CI 0.8151–0.9282, p = 0.5933, respectively). A relationship between anti-BPI Ab and anti-carbamylated protein Ab levels was observed in RA patients (rho 0.3508, p = 1.47 × 10−14). Conclusions: Anti-BPI Abs were related to UIP in RA patients and might be biomarkers for UIP. These findings predict anti-BPI Abs involvement in UIP pathogenesis in RA.

Objectives Patients with rheumatoid arthritis (RA) frequently have complications including chronic lung diseases (CLDs) consisting of airway disease (AD) or interstitial lung disease (ILD) that confer a poor prognosis. Peripheral blood leukocyte telomere length is shortened in RA with ILD. Previous studies reported rare variants in telomerase genes that were deleterious were more frequent in RA with ILD compared with controls. However, these studies were conducted in European populations. Here, we investigated associations of telomere length with ILD or AD in Japanese RA. Methods The lengths of telomeres in 108 RA patients with usual interstitial pneumonia, 134 with nonspecific interstitial pneumonia, 236 with AD, 50 with emphysema and 425 without CLDs were measured by quantitative polymerase chain reaction. Results A significantly longer telomere length was observed in RA with AD ( P  = 0.0071). Multiple logistic regression analyses indicated the association of telomere length with AD remained ( P adjusted =0.0029) when conditioned on TERT rs2736100, a single nucleotide variant related to AD in Japanese RA, and clinical characteristics, suggesting an independent association. Conclusions We report telomere length was independently associated with AD in Japanese RA patients.

Lung diseases that are chronic (emphysema [EMP], airway disease, interstitial lung disease) can complicate rheumatoid arthritis (RA) as extra-articular manifestations. Anti- ( ) antibody (Ab) has been analyzed for the diagnosis of periodontal disease and RA patients showed increased anti- Ab levels. However, amounts of anti- Ab in RA complicated with chronic lung disease (CLD) are unknown. We measured anti- Ab in cases of RA with CLD. Anti- lipopolysaccharide (LPS) Ab were measured in RA patient sera by enzyme immunoassay. Anti- LPS Ab levels in RA with EMP were significantly lower than in RA cases without CLD ( = 0.0190, mean ± standard deviation [SD], 32.7 ± 64.2 [×10 U/mL] vs. 403.5 ± 2552.7 [×10 U/mL]). Multiple logistic regression analyses revealed the independence of this association. Anti- LPS Ab amounts were increased in RA without CLD ( = 0.0412) compared with healthy controls (77.6 ± 183.7 [×10 U/mL]). Anti- LPS Ab levels in RA with EMP were lower compared with RA without CLD. Citrullinated peptides were mainly generated in the lungs of RA with EMP and the oral cavity of RA without CLD, suggesting the heterogeneity of RA.

Background: Rheumatoid arthritis (RA) is complicated with interstitial lung disease (ILD). Gastroesophageal reflux disease is prevented by Helicobacter pylori infection and is a predisposing factor for idiopathic pulmonary fibrosis. However, the prevalence of H. pylori infection in RA patients with ILD has not been sufficiently investigated. Objective: In this study, we analyzed anti-H. pylori antibodies in RA patients with ILD. Design: Case-control observational study Methods: Anti-H. pylori antibodies were analyzed in the sera of RA patients using a commercially available enzyme-linked immunosorbent assay kit. Results: The positivity of anti-H. pylori antibodies in RA with ILD (n = 30 [18.0%], P = .0227), usual interstitial pneumonia (n = 10 [14.3%], P = .0212), and airway disease (n = 30 [18.0%], P = .0227) was significantly lower than that of RA without chronic lung disease (n = 78 [27.5%]). The positivity of anti-H. pylori antibodies was also lower in RA with chronic lung disease (n = 68 [18.2%], P = .0059). Multiple logistic regression analyses showed that the presence of anti-H. pylori antibodies was independently and protectively associated with chronic lung disease in RA. Conclusion: The seroprevalence of H. pylori was lower in RA with ILD. H. pylori infection prevented ILD in patients with RA by protecting them from gastroesophageal reflux disease.

ObjectiveThe hallmarks of the chronic inflammatory disease polymyalgia rheumatica (PMR) include pain, and morning stiffness in areas of the neck, shoulder and pelvic girdle. The human leucocyte antigen (HLA) gene was reported to be an important risk factor for PMR, but it has not been analysed precisely, especially in populations other than Europeans.MethodsGenotyping of DRB1 and DQB1 was performed in Japanese PMR patients (n=270) and controls (n=413). Associations between allele carrier and genotype frequencies were determined for PMR.ResultsDRB1*04:05 was associated with a predisposition to PMR (p=0.0006, Pc=0.0193, OR 1.85, 95% CI 1.31 to 2.62). DRB1*09:01 was associated with protection against PMR (p=1.46×10−5, Pc=0.0004, OR 0.40, 95% CI 0.26 to 0.61). A shared epitope (SE) associated with PMR (p=3.07×10−6, OR 2.11, 95% CI 1.54 to 2.88). DQB1*03:03 (p=0.0010, Pc=0.0140, OR 0.52, 95% CI 0.35 to 0.77) was associated with protection against PMR and DQB1*04:01 (p=0.0009, Pc=0.0140, OR 1.82, 95% CI 1.28 to 2.58) was associated with predisposition to PMR. A gene dosage effect was observed for DRB1*09:01 and DQB1*03:03, but not for DRB1*04:05, SE or DQB1*04:01. Haplotype and logistic regression analyses suggested a protective effect for DRB1*09:01.ConclusionThis study is the first to demonstrate predisposing associations of DRB1*04:05, SE, and DQB1*04:01, and protective associations of DRB1*09:01 and DQB1*03:03 with PMR in Japanese patients. Our data indicate HLA has predisposing and protective effects on the pathogenesis of PMR.

Interstitial lung disease and airway disease (AD) are often complicated with rheumatoid arthritis (RA) and have a poor prognosis. Several studies reported genetic associations with interstitial lung disease in RA. However, few genetic studies have examined the susceptibility to AD in RA patients. Here, we investigated whether single nucleotide variants susceptible to idiopathic pulmonary fibrosis might be associated with interstitial lung disease or AD in Japanese RA patients. Genotyping of rs2736100 [C/A] in TERT and rs1278769 [G/A] in ATP11A was conducted in 98 RA patients with usual interstitial pneumonia, 120 with nonspecific interstitial pneumonia (NSIP), 227 with AD, and 422 without chronic lung disease using TaqMan assays. An association with AD in RA was found for rs2736100 (p = 0.0043, Pc = 0.0129, odds ratio [OR] 1.40, 95% confidence interval [CI] 1.11–1.77). ATP11A rs1278769 was significantly associated with NSIP in older RA patients (>65 years, p = 0.0010, OR 2.15, 95% CI 1.35–3.40). This study first reported an association of rs2736100 with AD in RA patients and ATP11A rs1278769 with NSIP in older RA patients.

Interstitial lung disease and airway disease (AD) are often complicated with rheumatoid arthritis (RA) and have a poor prognosis. Several studies reported genetic associations with interstitial lung disease in RA. However, few genetic studies have examined the susceptibility to AD in RA patients. Here, we investigated whether single nucleotide variants susceptible to idiopathic pulmonary fibrosis might be associated with interstitial lung disease or AD in Japanese RA patients. Genotyping of rs2736100 [C/A] in TERT and rs1278769 [G/A] in ATP11A was conducted in 98 RA patients with usual interstitial pneumonia, 120 with nonspecific interstitial pneumonia (NSIP), 227 with AD, and 422 without chronic lung disease using TaqMan assays. An association with AD in RA was found for rs2736100 (p = 0.0043, Pc = 0.0129, odds ratio [OR] 1.40, 95% confidence interval [CI] 1.11–1.77). ATP11A rs1278769 was significantly associated with NSIP in older RA patients (>65 years, p = 0.0010, OR 2.15, 95% CI 1.35–3.40). This study first reported an association of rs2736100 with AD in RA patients and ATP11A rs1278769 with NSIP in older RA patients.

Objectives: A common complication in patients with rheumatoid arthritis (RA) is interstitial lung disease (ILD). Antibodies (Abs) to anti-aminoacyl-transfer ribonucleic acid synthetase (ARS) are linked to ILD in patients with idiopathic inflammatory myopathies (IIM). There have been limited studies of anti-ARS Abs in RA. In this study, we examined anti-ARS Abs in ILD in patients with RA. Methods: Anti-ARS Abs in serum from patients with RA were measured. Results: There were higher anti-ARS Ab levels in RA patients with ILD (mean ± SDM, 16.3 ± 32.3 vs. 7.4 ± 7.0 (Index), p = 5.58 × 10−12), usual interstitial pneumonia (14.4 ± 24.4 vs. 7.4 ± 7.0 [Index], p = 3.14 × 10−12), and nonspecific interstitial pneumonia (17.9 ± 37.7 vs. 7.4 ± 7.0 (Index), p = 5.07 × 10−5) compared with patients without chronic lung disease. The area under the curve (AUC) of the receiver operating characteristic curve for anti-ARS Ab was too low to allow for discrimination among RA patients with/without chronic lung disease (0.608, 95% confidence interval (CI) 0.560–0.655, p = 8.69 × 10−6). Multiple logistic regression analyses of age, smoking status, anti-ARS Abs, as well as Steinbrocker stage generated an ARS-index with a high AUC value (0.707, 95%CI 0.662–0.752, p = 2.20 × 10−19). Conclusions: Anti-ARS Abs are related to ILD pathogenesis in RA and may be a biomarker for ILD.