Background: Although hallux valgus is known to cause lower-back pain, the association between hallux valgus and spinal degenerative disease remains unclear. Methods: A retrospective cohort study was conducted between 1 January 2000 and 31 December 2015 using data from the Longitudinal Health Insurance Database in Taiwan. After propensity score matching for age, sex, and some potential comorbidities, 1000 individuals newly diagnosed with hallux valgus were enrolled in the study group, while 1000 individuals never diagnosed with hallux valgus served as the control group. Both groups were followed up until 2015 to evaluate the incidence of hallux valgus. Kaplan-Meier analysis was used to determine the cumulative incidence of hallux valgus, while the Cox proportional hazard model was adopted to estimate the hazard ratio (HR) and adjusted hazard ratio (aHR) with 95% confidence intervals (CIs). Results: The incidence densities of spinal degeneration in the hallux valgus and non-hallux valgus groups were 73.10 and 42.63 per 1000 person-years, respectively. An increased risk of spinal degenerative changes was associated with hallux valgus (adjusted HR = 1.75, 95% CI = 1.50–2.05). Age- and sex-stratified analyses showed a significantly higher risk of spinal degeneration in the hallux valgus group. Moreover, sub-outcome evaluations revealed significantly higher risks of spondylosis (aHR = 2.01, 95% CI = 1.55–2.61), intervertebral disorder (aHR = 2.27, 95% CI = 1.62–3.17), and spinal stenosis (aHR = 1.24, 95% CI = 1.47–1.76). There was also an increased risk of spinal degenerative change in those with hallux valgus without surgical intervention (aHR = 1.95, 95% CI = 1.66–2.99, p < 0.001). Conclusions: Hallux valgus was associated with increased risk of degenerative spinal changes and other spinal disorders.

Purpose Type 2 diabetes mellitus (T2DM) is associated with elevated risks of osteoporosis and fractures, but the contribution of diabetic microvascular complications remains poorly defined—especially in Asian populations. Prior studies have suggested links between diabetes-related complications and skeletal fragility, but most were limited by small sample sizes, cross-sectional designs, or inadequate adjustment for key confounders such as medication use, fall history, and comorbidities. Methods Using Taiwan’s National Health Insurance Research Database, we conducted a large-scale, population-based cohort study of individuals newly diagnosed with T2DM (2008–2020) to assess associations between microvascular complications and the risk of new-onset osteoporosis and osteoporotic fractures using multivariable Cox proportional hazards models. Results In this East Asian cohort, patients with diabetic neuropathy (DN), retinopathy (DR), or kidney disease (DKD) exhibited a graded increase in the risk of both osteoporosis and major osteoporotic fractures, including those of the hip, spine, humerus, and radius/ulna. Compared to patients without microvascular disease, those with DR and DN had significantly higher risks of osteoporosis (adjusted hazard ratio [aHR]: 1.14 [95% CI: 1.09–1.19] and 1.25 [1.22–1.28], respectively; p < 0.001). Furthermore, amongst the microvascular complications, DN showed the strongest and most consistent associations with osteoporosis and spine fractures. Conclusions This nationwide cohort focused exclusively on newly diagnosed T2DM patients and comprehensively adjusted for confounders. Our findings suggest that microvascular complications may serve as independent predictors of skeletal fragility and support their incorporation into fracture risk assessment models, particularly for Asian individuals with T2DM.

Background/Aims: Mirabegron, a selective β3-adrenergic receptor agonist used to treat overactive bladder (OAB), can promote adipose tissue browning and alter systemic metabolism, raising interest in its potential relationship with cancer development. However, clinical evidence regarding cancer risk remains limited and inconsistent. We compared the risks of obesity-related and site-specific cancers between patients with OAB initiating mirabegron and those initiating antimuscarinic medications. Methods: We conducted a multicenter emulated target trial using the TriNetX Global Collaborative Network. Adults aged ≥20 years with OAB or related symptoms who newly initiated mirabegron or an antimuscarinic medication were included using a new-user, active-comparator design. Patients with pre-existing malignancy were excluded. Propensity score matching was performed 1:1, and a 1-year lag period after treatment initiation was applied for cancer outcomes to reduce potential reverse causation from occult malignancy. Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) under an intention-to-treat analog. Results: A 365-day lag/landmark period was applied before propensity-score matching. Patients with a recorded neoplasm or death during this period, or without follow-up extending through day 366, were excluded. Subsequent 1:1 propensity-score matching yielded 106,500 patients in each treatment group. Mirabegron initiation was not associated with the composite of obesity-related neoplasms compared with antimuscarinic initiation (HR, 1.011; 95% CI, 0.954–1.071). The individual neoplasm outcomes also showed no significant between-group differences. However, among patients eligible for the 1-year landmark mortality analysis, mirabegron initiation was associated with higher subsequent all-cause mortality (HR, 1.083; 95% CI, 1.044–1.124). Exploratory negative-control analysis of Hodgkin lymphoma showed no significant association. Conclusions: Among patients with OAB, mirabegron initiation was not associated with a significant difference in overall obesity-related neoplasm risk compared with antimuscarinic initiation. The observed associations with all-cause mortality should be interpreted cautiously given the observational design, multiple comparisons, and potential residual confounding. These findings are hypothesis-generating and require confirmation in prospective studies.

Background: The palatine tonsils and adenoids are critical inductive sites for the mucosa-associated lymphoid tissue (MALT) system, educating B cells for salivary defense. While their removal is common, the long-term impact on mucosal autoimmunity remains unclear. We hypothesized that disrupting this lymphoid network increases susceptibility to Sjögren’s syndrome (SS). Methods: Using the TriNetX US Collaborative Network (2006–2023), we conducted a retrospective cohort study matching 302,737 patients who underwent tonsillectomy/adenoidectomy with 302,737 non-surgical controls (propensity score-matched 1:1). Hazard ratios (HR) for incident SS were estimated using Cox proportional hazards models. Results: The surgical cohort exhibited a significantly elevated risk of SS (HR 1.52; 95% CI 1.23–1.87; p<0.001) compared to controls. This risk was most profound in individuals operated on before age 18 (HR 2.27) and in African American patients (HR 2.26). Sensitivity analyses using negative outcome controls (e.g., burns, injuries) confirmed the specificity of the association. Conclusion: Tonsillectomy is independently associated with an increased risk of SS. These findings suggest that early-life removal of nasopharyngeal lymphoid tissue may disrupt the MALT axis, impairing oral tolerance and predisposing to salivary autoimmunity.