Comment on “Efficacy of duloxetine and gabapentin in pain reduction in patients with knee osteoarthritis”

Takayasu arteritis: “bitten apple” in the aorta, odd finding in a plain X-ray

Precision medicine in rheumatoid arthritis: are we there yet?

Less IgA deposits with more severe disease: the immunoclinical paradox in Henoch-Schönlein Purpura with MEFV mutations

Monstrous gout devastating hands and feet

Increased risks of psychiatric disorders in patients with primary Sjögren’s syndrome—a secondary cohort analysis of nationwide, population-based health claim data Abstract Introduction/objectives Primary Sjögren’s syndrome (pSS) is a chronic systemic autoimmune disease. The aim of this study was to investigate the risk of five common psychiatrist-diagnosed disorders in patients with pSS. Method Using Taiwan’s National Health Insurance Research Database, 688 patients with newly diagnosed pSS between 2000 and 2012 were identified. Two comparison cohorts were assembled, namely, 3440 patients without pSS and 1302 newly diagnosed patients with rheumatoid arthritis. The incidences of depressive disorder, anxiety disorder, bipolar disorder, sleep disorder, and schizophrenia between the pSS cohort and the comparison cohorts were compared using Poisson regression models. Results Patients with pSS exhibited a significantly higher risk of developing depressive disorder (adjusted incidence rate ratio [aIRR] = 2.11, p < 0.001), anxiety disorder (aIRR = 2.20, p < 0.001), and sleep disorder (aIRR = 1.76, p = 0.012) when compared with the non-pSS cohort. The risks of developing depressive, anxiety, and sleep disorders were also significantly increased when compared to the rheumatoid arthritis comparison cohort. When the analyses were stratified by sex, depressive disorder (aIRR = 2.10, p < 0.001), anxiety disorder (aIRR = 2.02, p = 0.001), and sleep disorder (aIRR = 1.74, p = 0.022) were found to be significantly increased in female patients with pSS. However, only anxiety disorder (aIRR = 4.88, p = 0.044) was also significantly increased in male patients with pSS. The peak age group of developing depressive disorder was 65–80 years old (aIRR = 3.46, p < 0.001). Conclusions In this retrospective cohort study based on population-based claim data, significantly increased incidences of depressive disorder, anxiety disorder, and sleep disorder were observed in patients with pSS. Key Points • Patients, particularly women, with primary Sjögren’s syndrome exhibited a significantly higher risk of developing depressive disorder, anxiety disorder, and sleep disorder. • The peak age group of developing depressive disorder was 65–80 years old.

Does symptomatic knee osteoarthritis increase the risk of all-cause mortality? Data from four international population-based longitudinal surveys of aging Abstract Objective This study aimed at examining the association between symptomatic knee osteoarthritis and all-cause mortality based on four population-based longitudinal surveys. Method Data were retrieved from the English Longitudinal Study of Aging (ELSA), the Survey of Health, Aging and Retirement in Europe (SHARE), the Korean Longitudinal Study of Aging (KLoSA), and the Indonesian Family Life Survey (IFLS). The association between symptomatic knee osteoarthritis and all-cause mortality over the 8- to 12-year follow-up period was assessed using Cox-proportional hazard models. Results In the entire sample of 59,522 participants (4823 with symptomatic knee osteoarthritis; 54,699 without symptomatic knee osteoarthritis [control group]; mean age: 61.8 years; female percentage: 55.3%), 8375 died (937 in the symptomatic knee osteoarthritis group, 7438 in the control group) during the follow-up period. Patients with symptomatic knee osteoarthritis had a higher risk of all-cause mortality than control group without adjusting for potential confounders in each survey, and the unadjusted hazard ratios (HRs) of all-cause mortality were 1.32 (95% confidence interval [CI] 1.18 to 1.47) in ELSA, 1.40 (95%CI 1.24 to 1.56) in SHARE, 1.25 (95%CI 1.06 to 1.47) in KLoSA, and 1.65 (95%CI 1.31 to 2.07) in IFLS. However, with adjustment of potential confounders, the corresponding HRs dropped to 1.07 (95%CI 0.94 to 1.20) in ELSA, 1.08 (95%CI 0.97 to 1.22) in SHARE, 0.91 (95%CI 0.77 to 1.08) in KLoSA, and 0.89 (95%CI 0.66 to 1.21) in IFLS, respectively. Conclusions In these four population-based longitudinal studies, no association between symptomatic knee osteoarthritis and increased risk of all-cause mortality was observed after adjusting for potential confounders. Key Points • This study evaluated the association between symptomatic knee OA and the risk of all-cause mortality among the participants retrieved from four large population-based longitudinal studies across the world. • No association between symptomatic knee osteoarthritis and increased risk of all-cause mortality was observed after considering potential confounders, and our findings were consistent with the results derived from four independent longitudinal studies. • The present study included four international population-based longitudinal studies, comprising both developed and developing areas, which allowed the findings to be interpreted under larger circumstance.

LncRNA GAS5 overexpression downregulates IL-18 and induces the apoptosis of fibroblast-like synoviocytes Abstract Background Long non-coding RNA (lncRNA) growth arrest specific transcript 5 (GAS5) negatively regulates interleukin-18 (IL-18) in ovarian cancer, while IL-18 contributes to the development of rheumatoid arthritis (RA). Therefore, GAS5 may also participate in RA. Methods GAS5 and IL-18 in plasma of RA patients (n = 60) and healthy controls (n = 60) were measured by RT-qPCR and ELISA, respectively. Linear regression was performed to analyze the correlations between plasma levels of IL-18 and GAS5 in both RA patients and healthy controls. Results In the present study, we found that plasma GAS5 was downregulated, while IL-18 was upregulated in RA patients than in healthy controls. A significant and inverse correlation between GAS5 and IL-18 was found in RA patients but not in healthy controls. IL-18 treatment did not significantly alter the expression of GAS5 in fibroblast-like synoviocytes, while GAS5 overexpression led to the inhibited expression of IL-18. GAS5 overexpression also resulted in the promoted apoptosis of fibroblast-like synoviocytes. Conclusions Therefore, GAS5 overexpression may improve RA by downregulating IL-18 and inducing the apoptosis of fibroblast-like synoviocytes. Key points • The present study mainly showed that overexpression of GAS5 may assist the treatment of RA. • The mechanism of GAS5 for the treatment of RA involves the downregulating inflammatory IL-18 and mediating the apoptosis of fibroblast-like synoviocytes. • GAS5 and IL-8 were correlated in RA patients but not in healthy controls.

The longitudinal effect of biologic use on patient outcomes (disease activity, function, and disease severity) within a rheumatoid arthritis registry Abstract Introduction Biologics effectively manage symptoms and disease activity in rheumatoid arthritis (RA), but their long-term effects remain unclear. Method Longitudinal data were examined from the Brigham and Women’s Rheumatoid Arthritis Sequential Study (BRASS) registry. Linear regression modeled the effect of biologic exposure on changes in disease activity (Disease Activity Score-28 with C-reactive protein [DAS28-CRP]), functional status (modified Health Assessment Questionnaire [mHAQ]), and RA severity (Routine Assessment of Patient Index Data [RAPID3]). Biologic exposure was the ratio of time on a biologic relative to time participating in the BRASS cohort. Results The analysis included 1395 RA patients, 82.3% female, with 6783 unique study visits from 2003 to 2015. At the patient’s first visit, mean (SD) age was 56.3 (14.2) years and mean (SD) duration of RA was 12.7 (11.9) years. Average follow-up duration was 5.59 years (range, 1–13). Over time, DAS28-CRP, mHAQ, and RAPID3 scores decreased as the biologic exposure ratio increased. In repeated measures regression models, increased biologic exposure was significantly associated with decreased DAS28-CRP score (β = − 0.647; P < 0.001), decreased mHAQ score (β = − 0.096; P < 0.001), and decreased RAPID3 score (β = − 0.724; P < 0.001) during follow-up. Methotrexate use at baseline predicted decreased DAS28-CRP, mHAQ, and RAPID3 scores during follow-up. Biologic use at baseline predicted increased DAS28-CRP or mHAQ during follow-up. Conclusions Increased biologic exposure is associated with decreased disease activity, function impairment, and RA severity. Future studies should examine whether earlier initiation of biologics improves patient outcomes in RA. Trial Registration ClinicalTrials.gov, NCT01793103 Key Points • Biologics effectively manage symptoms and disease activity in rheumatoid arthritis (RA), but their long-term effects remain unclear. • In this analysis of longitudinal annual population samples of 1395 RA patients in the Brigham and Women’s Rheumatoid Arthritis Sequential Study (BRASS) registry, disease activity, function, and severity scores improved as time on biologic therapy increased. • In repeated measures regression models, time on biologic therapy was a significant predictor of improved outcomes for disease activity, function, and RA severity. • Further studies should examine whether earlier initiation of biologics limits the long-term effect of inflammation on RA outcomes.

Risk of pancreatic cancer in patients with systemic lupus erythematosus: a meta-analysis Abstract Object Accumulating evidences suggest that the incidence of several cancers is higher in systemic lupus erythematosus (SLE) than in general population. However, the finding on pancreatic cancer risk is inconsistent. This meta-analysis aimed to determine whether SLE patients are at risk for pancreatic cancer. Methods We searched PubMed, Embase, and the Cochrane database to screen the studies meeting our criteria. The hazard ratios (HRs) and its 95% confidence interval (CIs) were calculated from a meta-analysis. Results Eleven cohort studies were included in the final analysis. Overall, patients with SLE had an increased risk of pancreatic cancer (HR = 1.42, CI = 1.32–1.53). In subgroup analysis, hospital-based (HR = 1.43, CI = 1.32–1.54), retrospective (HR = 1.42, CI = 1.32–1.54), over 10 years followed (HR = 1.44, CI = 1.33–1.55), and low-quality studies (HR = 1.42, CI = 1.31–1.53) remained robust. Significant publication bias was not observed among the studies (p = 0.533). Conclusions The synthesized evidence from our meta-analysis demonstrated that SLE was associated with increased risk for pancreatic cancer. A well-designed, long-period followed study is needed to confirm this association. Key Points • Cancer incidence in SLE patients is increasing, but the data concerning pancreatic cancer remains inconclusive. • Our meta-analysis indicated that the risk of pancreatic cancer was significantly increased in SLE patients. • A well-designed, long-period followed study is needed to confirm the association.