International Journal of Rheumatic Diseases最新文献

Background: Hyperuricemia (HUA), marked by elevated serum urate levels, is increasingly prevalent worldwide. The relationship between lifestyle factors such as sleep duration, daytime napping, and HUA risk remains unclear. Although some studies suggest that sleep variables, including short or long sleep durations and napping, may influence serum uric acid levels, results are inconsistent.

Methods: A systematic review and meta-analysis was performed according to the PRISMA guidelines. Databases such as PubMed, Embase, Web of Science, and Cochrane Library were searched until February 2024. The data were extracted, and the quality of the study was assessed independently by two reviewers.

Results: Ten studies involving a total of 231 978 participants were included. Short sleep duration was related to higher risk of HUA (odds ratio (OR) 1.10, 95% confidence interval (CI): 1.03-1.18), while long sleep duration had no significant effect (OR 0.98, 95% CI: 0.89-1.07). The risk of HUA and daytime napping was statistically significant(OR 1.34, 95% CI: 1.12-1.61).

Conclusions: Short sleep duration and prolonged daytime napping are associated with an increased risk of HUA. These findings suggest that sleep patterns should be considered in lifestyle interventions for HUA prevention. Further research is required to establish causal relationships.

Background: N6-methyladenosine (m6A) is one of the most conserved internal RNA modifications, which has been implicated in many biological processes, such as apoptosis and proliferation. Wilms tumor 1-associating protein (WTAP), as a key component of m6A methylation, is a nuclear protein that has been associated with the regulation of proliferation and apoptosis. Rheumatoid arthritis (RA), a systemic, infiltrating autoimmune disease, is characterized by synovial hyperplasia. However, little is known about the precise role of WTAP in RA. This study investigated the role of the WTAP-mediated m6A modification of TNF-related apoptosis-inducing ligand death receptor 4 (TRAIL-DR4) in RA.

Method: Methyltransferase WTAP overexpression plasmids and small interfering RNAs were constructed and transfected into MH7A cells. Immunofluorescence (IF) staining, quantitative reverse transcription polymerase chain reaction (RT-qPCR), and Western blot were used to detect changes in the expression of WTAP, the B-cell lymphoma 2 (BCL2) gene family, BCL2-associated X (BAX) and TRAIL-DR4 expression, and the effects of WTAP overexpression on cell viability, cell cycle, apoptosis, and proliferation were assessed by a cell counting kit-8 (CCK-8), flow cytometry, and transmission electron microscopy (TEM). The m6A modification of TRAIL-DR4 was verified by m6A methylated RNA immunoprecipitation-qPCR (MeRIP-qPCR) and its stability was assessed by an actinomycin D assay.

Results: Overexpression of WTAP not only increased the levels of WTAP and BCL2, and decreased the levels of BAX and TRAIL-DR4, but also significantly inhibited MH7A cell apoptosis and promoted cell viability and proliferation, while WTAP silencing led to the opposite trend. The SRAMP online database predicted that TRAIL-DR4 has multiple potential methylation-binding sites, and fluorescence in situ hybridization (FISH) combined with IF showed that WTAP and TRAIL-DR4 were mainly expressed in both the nucleus and cytoplasm. MeRIP-qPCR and actinomycin D analysis experiments revealed that WTAP could promote the m6A level of TRAIL-DR4, decrease the stability of TRAIL-DR4 mRNA, and subsequently inhibit apoptosis.

Conclusion: This study suggests that WTAP-mediated m6A modification of TRAIL-DR4 suppresses MH7A cell apoptosis. This discovery offers a new focus and avenue for the clinical treatment of RA, while also extending our understanding of the pathophysiology of RA from the standpoint of m6A alteration.

Background: Right ventricular (RV) failure is a well-recognized pivotal prognostic factor of adverse outcomes in pulmonary artery hypertension (PAH), while RV dilation provides significant implications for adaptive or maladaptive changes. PAH is a predominant cause of mortality among patients with connective tissue disease (CTD). This study aims to elucidate the prognostic significance of RV morphology, as assessed by echocardiography (ECHO), in with CTD associated with PAH (CTD-PAH).

Methods: In this ambispective cohort study, 143 CTD-PAH patients diagnosed by right-sided heart catheterization (RHC) from 2013 to 2023 were enrolled. Clinical characteristics, laboratory data, echocardiographic parameters (right ventricular end-diastolic basal diameter index (RVDDI), tricuspid annular plane systolic excursion (TAPSE) and pulmonary arterial systolic pressure (PASP)) and therapy were recorded. The primary endpoint was defined as clinical worsening within a five-year timeframe. Analytical methods included Kaplan-Meier survival analyses, the log-rank test, and multivariable Cox proportional hazards regression to evaluate prognostic factors.

Results: The study enrolled a total of 143 patients with CTD-PAH, with a notable female predominance (95.1%) and a median age of 41.67 years; SLE-PAH (49%) and pSS-PAH (34%) were the most common subtypes, and 94% of the participants were in WHO-FC II-III. Among the participants, 34 (23.8%) patients experienced clinical worsening during a median follow-up period of 21 months. After adjusting for confounders such as age and sex, RVDDI, as determined by ECHO was correlated with clinical worsening (HR 1.090; 95% CI: 1.019-1.166; p = 0.012). RVDDI > 25.81 mm/m² predicts higher incidence of clinical worsening in CTD-PAH. In the subgroup of TAPSE/PASP > 0.19 mm/mmHg, patients with RVDDI > 25.81 mm/m² had a higher incidence of clinical worsening. The estimated event-free survival rates at 1 and 3 years were 93.5% and 53.7%, respectively.

Conclusion: The study demonstrates that RVDDI, as evaluated by ECHO, is a significant prognostic indicator for clinical worsening in CTD-PAH. Its inclusion in the assessment of RV function and risk stratification may provide valuable incremental prognostic information for this CTD-PAH population.

Objective: Since COVID-19 infections are more common in systemic lupus erythematosus (SLE) patients, most recent research has focused on the outcome of COVID-19, with fewer studies on disease activity in SLE. This research aims to evaluate flares in SLE with COVID-19 infection while investigating predictive factors.

Methods: A questionnaire survey was conducted to collect information on patients with previously diagnosed SLE from multi-center. SLE patients infected with COVID-19 after December 7, 2022, were selected. Detailed information covering demographic characteristics, SLE and COVID-19 clinical features, disease activity, and medication was collected through an electronic questionnaire. A multivariate logistic regression model was constructed to evaluate the predictive factors for SLE disease onset after COVID-19 infection.

Results: A total of 240 patients were finally included in our analysis. Thirty (12.5%) of those enrolled reported an SLE flare. Multivariate analysis with logistic models confirmed that SLE in the active stage (OR 2.617, 95% CI 1.008-6.514, p = .041) and COVID-19 duration (OR 4.140, 95% CI 1.412-11.694, p = .008) were predictors for flare in SLE patients with Covid-19 infection. In contrast, immunosuppressants were associated with a low incidence of flare of SLE (OR 0.138, 95% CI 0.042-0.46, p = .005).

Conclusions: The active phase of SLE and the progression of COVID-19 were the main risk factors for disease exacerbation in SLE patients, while the use of immunosuppressive medications was associated with a lower risk of flare-ups. These findings provide valuable insights for managing SLE patients during the COVID-19 pandemic.