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OBJECTIVES:To investigate the efficacy and safety of ixekizumab for up to 52 weeks in two phase 3 studies of patients with active radiographic axial spondyloarthritis (r-axSpA) who were biological disease-modifying antirheumatic drug (bDMARD)-naive (COAST-V) or tumour necrosis factor inhibitor (TNFi)-experienced (COAST-W). METHODS:Adults with active r-axSpA were randomised 1:1:1:1 (n=341) to 80 mg ixekizumab every 2 (IXE Q2W) or 4 weeks (IXE Q4W), placebo (PBO) or 40 mg adalimumab Q2W (ADA) in COAST-V and 1:1:1 (n=316) to IXE Q2W, IXE Q4W or PBO in COAST-W. At week 16, patients receiving ixekizumab continued their assigned treatment; patients receiving PBO or ADA were rerandomised 1:1 to IXE Q2W or IXE Q4W (PBO/IXE, ADA/IXE) through week 52. RESULTS:In COAST-V, Assessment of SpondyloArthritis international Society 40 (ASAS40) responses rates (intent-to-treat population, non-responder imputation) at weeks 16 and 52 were 48% and 53% (IXE Q4W); 52% and 51% (IXE Q2W); 36% and 51% (ADA/IXE); 19% and 47% (PBO/IXE). Corresponding ASAS40 response rates in COAST-W were 25% and 34% (IXE Q4W); 31% and 31% (IXE Q2W); 14% and 39% (PBO/IXE). Both ixekizumab regimens sustained improvements in disease activity, physical function, objective markers of inflammation, QoL, health status and overall function up to 52 weeks. Safety through 52 weeks of ixekizumab was consistent with safety through 16 weeks. CONCLUSION:The significant efficacy demonstrated with ixekizumab at week 16 was sustained for up to 52 weeks in bDMARD-naive and TNFi-experienced patients. bDMARD-naive patients initially treated with ADA demonstrated further numerical improvements after switching to ixekizumab. Safety findings were consistent with the known safety profile of ixekizumab. TRIAL REGISTRATION NUMBER:NCT02696785/NCT02696798.

ABSTRACT Aims/Introduction Materials and Methods Results Conclusions The relationship between economic disadvantages and the risk of developing gestational diabetes mellitus (GDM), as well as its impact on birth outcomes, remains uncertain.From the Taiwan Maternal and Child Health Database, we identified 984,712 pregnant women between 1 January 2007 and 31 December 2018. Using propensity score matching, we selected 5,068 pairs of women across four income levels: very low, low, middle and high. We used a multivariable Cox regression model to assess the risk of GDM in these pregnant women and analyzed the birth outcomes.The mean age of the pregnant women was 30.89 years. We found no significant difference in GDM risk among pregnant women with different family income. However, newborns of women with GDM and very low‐income were at higher risk for several adverse conditions, such as small for gestational age (adjusted odds ratio (aOR) 1.17, 95% confidence interval (CI) 1.04–1.31), large for gestational age (aOR 1.27, 95% CI 1.08–1.51), hypoxic–ischemic encephalopathy (aOR 3.19, 95% CI 1.15–8.86), respiratory distress (aOR 1.58, 95% CI 1.14–2. 19), congenital anomalies (aOR 1.32, 95% CI 1.08–1.62), jaundice requiring phototherapy or exchange transfusion (aOR 1.14, 95% CI 1.05–1.24) and so on.This study found that low family income alone was not associated with GDM development. However, for a GDM pregnancy, pregnant women with lower income had worse birth outcomes. Improving maternal health and nutrition among low‐income pregnant women with GDM might be critical to improving birth outcomes. [ABSTRACT FROM AUTHOR]

Aim: To assess the likelihood of dementia in individuals with type 2 diabetes (T2D), distinguishing between those with and without microvascular diseases. Methods: Leveraging the National Health Insurance Research Database in Taiwan, we identified individuals newly diagnosed with T2D from 1 January 2009 through 31 December 2014. Multivariable Cox proportional hazard models were used to compare the risk of outcomes. Results: Individuals with microvascular disease had a significantly higher risk of all‐cause dementia (adjusted hazard ratio [95% confidence interval] 1.13 [1.09, 1.17]) compared with matched individuals without microvascular disease. In addition, individuals with diabetic kidney disease and diabetic neuropathy were associated with a significantly increased risk of Alzheimer's disease (1.16 [1.02, 1.32] and 1.14 [1.03, 1.27]), vascular dementia (1.21 [1.06, 1.38] and 1.14 [1.02, 1.28]) and other dementia (1.11 [1.04, 1.19] and 1.10 [1.04, 1.16]), respectively, compared with those without microvascular disease. Conclusions: This nationwide cohort study showed that patients with T2D and microvascular disease, particularly diabetic kidney disease and diabetic neuropathy, were associated with a significantly higher risk of Alzheimer's disease, vascular dementia, other dementia and all‐cause dementia than those without microvascular disease. [ABSTRACT FROM AUTHOR]

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]