Search

Introduction: Primary Sjögren's syndrome (pSS) is a chronic autoimmune disorder affecting salivary and lacrimal glands, while endometriosis involves uterine‐like tissue growth outside the uterus, causing pelvic pain and infertility. Investigating their intricate relationship using real‐world data is crucial due to limited research on their connection. Material and Methods: This population‐based cohort study included patients with endometriosis and controls without endometriosis. Propensity score matching was used to balance baseline differences in demographic and clinic characteristics between the two groups. Cox proportional hazards model were used to estimate the effect of endometriosis on the risk of new‐onset pSS over time. A symmetrical cohort study, including patients with pSS and propensity score‐matched controls without pSS, was conducted to investigate the effect of pSS on the risk of endometriosis over time. To elaborate on the mechanisms linking endometriosis and pSS, Ingenuity Pathway Analysis was performed to identify activated pathways in eutopic endometrium from patients with endometriosis and parotid tissues from patients with pSS. Results: A total of 15 947 patients with endometriosis and 15 947 propensity score‐matched controls without endometriosis were included. Patients with endometriosis presented a significantly greater risk of pSS compared to non‐endometriosis controls (adjusted hazard ratio, aHR = 1.57, 95% CI = 1.29–1.91, p < 0.001). In the symmetrical cohort study, which included 4906 pSS patients and 4,906 propensity score‐matched controls without pSS, patients with pSS were found to be at a significantly higher risk of endometriosis compared to non‐pSS controls (aHR = 1.51, 95% CI = 1.12–2.04, p = 0.012). Ingenuity Pathway Analysis showed that the underlying cellular mechanisms involved autoimmune‐related pathways, including activation of dendritic cell maturation, and chronic inflammatory pathways, including the fibrosis signaling pathway. Conclusions: These findings support a bidirectional association between endometriosis and pSS, which may be driven by dendritic cell maturation and fibrosis signaling pathways. [ABSTRACT FROM AUTHOR]

Objective Patients with RA treated with Janus kinase inhibitors (JAKis) are at increased risk of herpes zoster (HZ). The objective of this study was to investigate the serological immunogenicity and safety of the HZ subunit (HZ/su) vaccine in RA patients treated with JAKi, for which little is known. Methods RA patients treated with JAKi (n  = 82) at the Department of Rheumatology, Skåne University Hospital, Lund and Malmö, Sweden, and healthy controls (n  = 51) received two doses of the HZ/su vaccine (Shingrix). Vaccine-specific antibody responses were analysed using indirect ELISA. Post-vaccination antibody levels were compared between patients and controls using analysis of covariance. Potential predictors for vaccine response were investigated using a multivariable linear regression analysis. Self-reported adverse events (AEs) and changes in RA disease activity were analysed. Results Following vaccination, vaccine-specific antibody levels increased significantly in both patients and controls (P  < 0.0001). A total of 80.5% of patients and 98.0% of controls achieved a ≥4-fold increase in antibody levels. Post-vaccination antibody levels were lower in patients than controls [ratio 0.44 (95% CI 0.31, 0.63)] and lower in patients receiving JAKi + methotrexate than JAKi monotherapy [ratio 0.43 (95% CI 0.24, 0.79)]. AEs, mostly mild/moderate, were common. One patient developed HZ and six patients (6.5%) had increased RA disease activity following vaccination. Conclusion The HZ/su vaccine was serologically immunogenic in most RA patients treated with JAKi. Moreover, the vaccine had an acceptable safety profile. These results support recommendations for use of the HZ/su vaccine in this vulnerable population. Trial registration ClinicalTrials.gov (https://clinicaltrials.gov), NCT03886038. [ABSTRACT FROM AUTHOR]

Purpose: To review cases of uterine rupture and identify risk factors associated with adverse outcomes. Methods: This study is a retrospective cohort of complete uterine ruptures diagnosed in a large hospital system in Massachusetts between 2004 and 2018. Baseline demographics, labor characteristics and outcomes of uterine rupture were collected from medical records. Results: A total of 173 cases of uterine rupture were identified. There were 30 (17.3%) women with an unscarred uterus, while 142 (82.1%) had a scarred uterus. Adverse outcomes (n = 89, 51.4% of cases) included 26 (15.0%) hysterectomies, 55 (31.8%) blood transfusions, 18 (10.4%) bladder/ureteral injuries, 5 (2.9%) reoperations, 25 (14.5%) Apgar scores lower than 5 at 5 min and 9 (5.2%) perinatal deaths. Uterine rupture of a scarred uterus was associated with decreased risk of hemorrhage (OR 0.40, 95% CI 0.17–0.93), blood transfusion (OR 0.27, 95% CI 0.11–0.69), hysterectomy (OR 0.23, 95% CI 0.08–0.69) and any adverse outcome (OR 0.34, 95% CI 0.13–0.91) compared with unscarred rupture. Uterine rupture during vaginal delivery was associated with increased risk of transfusion (OR 6.55, 95% CI 1.53–28.05) and hysterectomy (OR 8.95, 95% CI 2.12–37.72) compared with emergent C-section. Conclusions: Although rare, uterine rupture is associated with adverse outcomes in over half of cases. Unscarred rupture and vaginal delivery demonstrate increased risk of adverse outcomes, highlighting the need for early diagnosis and operative intervention. [ABSTRACT FROM AUTHOR]