Prevalence, Risk Factors, and Treatment for Overactive Bladder in a Racially Diverse Population.

OBJECTIVE: To evaluate differences in prevalence, overactive bladder (OAB) risk factors, and OAB treatment in a diverse population of underrepresented racial/ethnic groups. METHODS: This is a retrospective cohort study of women ≥ 18 years who had an OAB diagnosis code from June 1, 2013 to June 30, 2016. Women who had neurogenic bladder or pelvic cancer were excluded. OAB risk factors included age, body mass index, socioeconomic status, diabetes, and smoking. OAB treatment included consultation with a specialist, diagnostic testing, medication, and third-line therapy (neuromodulation or chemodennervation). ANOVA and Chi-square were used to compare continuous and categorical variables. Multivariable logistic regression models were developed to examine the association between racial/ethnic groups and OAB management while controlling for risk factors. RESULTS: OAB prevalence was 4.41% (5407/122,606) and was highest in Hispanic women. Black and Hispanic women were significantly younger, had a higher median body mass index, higher rate of diabetes, and lower socioeconomic status compared to White women. There was no racial difference in OAB prescriptions. Black women were less likely to consult with a specialist in multivariable analysis. CONCLUSION: OAB prevalence and presence of OAB risk factors was highest in Hispanic and Black women. Black women were less likely to consult with a specialist suggesting that Black women receive initial therapy from primary care physicians. Future studies will evaluate if racial differences in OAB treatment are due to patient preference or provider practices.

Prevalence, risk factors, and treatment for women with stress urinary incontinence in a racially and ethnically diverse population.

AIMS: Black women may have lower rates of SUI than Whites, whereas the rate of SUI in Hispanic women varies. Most studies have been conducted in predominantly White populations, making it difficult to evaluate race and SUI. The objective of this study was to estimate the prevalence of SUI in a diverse population and examine racial/ethnic differences in risk factors and treatment. METHODS: This is a retrospective cohort study of women ≥21 years with SUI seen at our medical center from June 1, 2013 to June 30, 2016. Risk factors measured included age, BMI, SES, diabetes, smoking, Charlson comorbidity index, hysterectomy, and pregnancy. SUI management included consultation with a specialist and active treatment (physical therapy, pessary use, or incontinence surgery). ANOVA, chi-square, and multivariable logistic regression were used to evaluate race and SUI. RESULTS: The prevalence rate was 4.65 per 100 women (5557 cases/119 452 women). Hispanics comprised the majority (54.13% n = 3008), followed by Blacks (23.54% n = 1308), Other (12.74% n = 708), and Whites (9.59% n = 532). Black women were less likely to consult with a specialist or undergo treatment compared to White and Hispanic women, which persisted in multivariable analysis. Women classified as other were more likely to undergo active treatment in the logistic regression model. CONCLUSION: SUI prevalence was highest in Hispanics, despite risk factors being more common in Black women. Black women were less likely to consult with a specialist. Mixed or unknown race/ethnicity women were more likely to undergo active treatment. Future studies will evaluate if racial/ethnic differences in SUI management are due to patient preference or provider practices.

The Hemoglobin Homolog Cytoglobin in Smooth Muscle Inhibits Apoptosis and Regulates Vascular Remodeling.

OBJECTIVE: The role of hemoglobin and myoglobin in the cardiovascular system is well established, yet other globins in this context are poorly characterized. Here, we examined the expression and function of cytoglobin (CYGB) during vascular injury. APPROACH AND RESULTS: We characterized CYGB content in intact vessels and primary vascular smooth muscle (VSM) cells and used 2 different vascular injury models to examine the functional significance of CYGB in vivo. We found that CYGB was strongly expressed in medial arterial VSM and human veins. In vitro and in vivo studies indicated that CYGB was lost after VSM cell dedifferentiation. In the rat balloon angioplasty model, site-targeted delivery of adenovirus encoding shRNA specific for CYGB prevented its reexpression and decreased neointima formation. Similarly, 4 weeks after complete ligation of the left common carotid, Cygb knockout mice displayed little to no evidence of neointimal hyperplasia in contrast to their wild-type littermates. Mechanistic studies in the rat indicated that this was primarily associated with increased medial cell loss, terminal uridine nick-end labeling staining, and caspase-3 activation, all indicative of prolonged apoptosis. In vitro, CYGB could be reexpressed after VSM stimulation with cytokines and hypoxia and loss of CYGB sensitized human and rat aortic VSM cells to apoptosis. This was reversed after antioxidant treatment or NOS2 (nitric oxide synthase 2) inhibition. CONCLUSIONS: These results indicate that CYGB is expressed in vessels primarily in differentiated medial VSM cells where it regulates neointima formation and inhibits apoptosis after injury.