ABSTRACT
OBJECTIVE: To assess how race, ethnicity, primary language, clinical and other sociodemographic factors predict surgical treatment for pelvic organ prolapse (POP) in a minority-majority Hispanic population. METHODS: We identified patients with POP ICD-10 codes from Oct 2019 to Dec 2022 at our Urogynecology academic practice. Data were collected by chart review. Covariates were obtained by manual abstraction. Continuous and categorical variables were analyzed using t-test and chi-square test, and Wilcoxon rank-sum test for non-parametric data. A logistic regression model was fitted to identify independent predictors of surgery. RESULTS: Of 943 patients over 38 months, 441 (46.8%) underwent surgery. On univariate analysis, younger age, Hispanic/Latino ethnicity, Spanish as primary language, private insurance, stage of prolapse and obesity correlated with higher rates of surgical treatment. On multivariate regression, only age and prolapse compartment remained significant predictors. Younger age and apical prolapse increased the likelihood of surgery (OR=.98 [.96-.99], P = <.001; R=2.31 [1.13-4.72], P = <.001, respectively). CONCLUSION: Controlling for confounders, age, and apical prolapse compartment predicted surgical treatment for POP in our Hispanic minority-majority population. Previously identified barriers to care including minority status and non-English primary language do not appear to exist in our population. This may be related to linguistic, ethnic, and racial concordance between healthcare staff and patients, alongside protective aspects of ethnic enclaves. Further research is warranted to understand the impact of cultural barriers, such as provider language, on patient-provider dynamics and surgical decision-making.
ABSTRACT
Introduction: Indoor nitrogen dioxide (NO2) sources include gas heating, cooking, and infiltration from outdoors. Associations with pulmonary function, systemic inflammation, and oxidative stress in patients with chronic obstructive pulmonary disease (COPD) are uncertain. Methods: We recruited 144 COPD patients at the VA Boston Healthcare System between 2012 and 2017. In-home NO2 was measured using an Ogawa passive sampling badge for a week seasonally followed by measuring plasma biomarkers of systemic inflammation (C-reactive protein [CRP] and interleukin-6 [IL-6]), urinary oxidative stress biomarkers (8-hydroxy-2'deoxyguanosine [8-OHdG] and malondialdehyde [MDA]), and pre- and postbronchodilator spirometry. Linear mixed effects regression with a random intercept for each subject was used to assess associations with weekly NO2. Effect modification by COPD severity and by body mass index (BMI) was examined using multiplicative interaction terms and stratum-specific effect estimates. Results: Median (25%ile, 75%ile) concentration of indoor NO2 was 6.8 (4.4, 11.2) ppb. There were no associations observed between NO2 with CRP, 8-OHdG, or MDA. Although the confidence intervals were wide, there was a reduction in prebronchodilator FEV1 and FVC among participants with more severe COPD (FEV1: -17.36 mL; -58.35, 23.60 and FVC: -28.22 mL; -91.49, 35.07) that was greater than in patients with less severe COPD (FEV1: -1.64 mL; -24.80, 21.57 and FVC: -6.22 mL; -42.16, 29.71). In participants with a BMI <30, there was a reduction in FEV1 and FVC. Conclusions: Low-level indoor NO2 was not associated with systemic inflammation or oxidative stress. There was a suggestive association with reduced lung function among patients with more severe COPD and among patients with a lower BMI.