Background: Rurality, race, and age at diagnosis are important predictors in head and neck cancer (HNC) prognosis. However, literature on the associations of rurality and race with age at HNC diagnosis is limited. Data on geographical, racial, and gender disparities in young HNC patients (diagnosed £ 45 years) are also scarce. Materials and Methods: This retrospective study assesses rural-urban, racial, and gender disparities in age at HNC diagnosis, using electronic medical records (Cerner) data of 4258 HNC patients (1538 residing in rural counties and 2720 in urban counties) from National Cancer Institute-designated cancer center in Alabama. Rurality was defined based on 2010 U.S. Census Bureau's rural-urban classification. Logistic regression was used to assess the association of young HNC diagnosis with demographical, behavioral, and clinical variables. ArcGIS 10.2 was used to map geospatial distribution of age and population-adjusted HNC case across rural and urban counties. Results: Patients from rural counties were less likely to be diagnosed at younger age (£ 45 years) compared with urban counties (odds ratio [OR] [95% confidence interval (CI)]: 0.74 [0.58-0.93]). Most patients present at stage III/IV (64.9% in rural and 60.2% in urban). Compared with white patients, black patients were 70% more likely to get diagnosed at a young age (95% CI: 1.23-2.35). Young patients were more likely to be females and blacks compared with older patients (p < 0.0001). Among oral cavity cancer patients, rural patients were 51% less likely to get diagnosed at young age compared with urban patients (95% CI: 0.27-0.89). Conclusions: Head and neck cancer screening is not routinely conducted so most show up at later stage of cancer. There is also evidence of disparities in age at HNC diagnosis based on rurality, race, and gender; targeted screening can help in reducing these disparities.
Blinded randomized controlled trials (RCT) require participants to be uncertain if they are receiving a treatment or placebo. Although uncertainty is ideal for isolating the treatment effect from all other potential effects, it is poorly suited for estimating the treatment effect under actual conditions of intended use-when individuals are certain that they are receiving a treatment. We propose an experimental design, randomization to randomization probabilities (R2R), which significantly improves estimates of treatment effects under actual conditions of use by manipulating participant expectations about receiving treatment. In the R2R design, participants are first randomized to a value, π, denoting their probability of receiving treatment (vs. placebo). Subjects are then told their value of π and randomized to either treatment or placebo with probabilities π and 1-π, respectively. Analysis of the treatment effect includes statistical controls for π (necessary for causal inference) and typically a π-by-treatment interaction. Random assignment of subjects to π and disclosure of its value to subjects manipulates subject expectations about receiving the treatment without deception. This method offers a better treatment effect estimate under actual conditions of use than does a conventional RCT. Design properties, guidelines for power analyses, and limitations of the approach are discussed. We illustrate the design by implementing an RCT of caffeine effects on mood and vigilance and show that some of the actual effects of caffeine differ by the expectation that one is receiving the active drug. (PsycINFO Database Record
Background Microbial etiology for community-acquired pneumonia (CAP) is evolving with pathogens known for high CAP mortality e.g., Pseudomonas species. Chronic obstructive pulmonary disease (COPD) patients are at risk for hospitalization for CAP. Understanding regional patterns and risk factors for multidrug-resistant (MDR) Pseudomonas acquisition has implications for antimicrobial stewardship. Objectives To evaluate the regional epidemiology of MDR Pseudomonas CAP and its association with COPD. Methods We queried the electronic medical records of the University of Alabama at Birmingham Healthcare System to identify patients hospitalized for CAP with Pseudomonas positive respiratory samples between 01/01/2013–12/31/2019. Log binomial regression models were used to examine associations between COPD diagnosis and risk of Pseudomonas/MDR Pseudomonas CAP. Results Cohort consisted of 913 culture positive CAP cases aged 59-year (IQR:48–68), 61% (560) male, 60% (547) white, 65% (580) current/past smokers, and 42% (384) COPD. Prevalence of Pseudomonas CAP in culture positive CAP was 18% (167), MDR Pseudomonas CAP in Pseudomonas CAP was 22% (36), and yearly incidence of MDR Pseudomonas CAP was stable (p = 0.169). COPD was associated with Pseudomonas CAP (RR 1.39; 95% CI 1.01, 1.91; p = 0.041) but not with MDR Pseudomonas CAP (0.71; 95% CI 0.35, 1.45; p = 0.349). Stroke (RR 2.64; 95% CI 1.51, 4.61; p = 0.0006) and use of supplemental oxygen (RR 2.31; 95% CI 1.30, 4.12; p = 0.005) were associated with MDR Pseudomonas CAP. Conclusion Incidence of MDR Pseudomonas CAP was stable over time. COPD was associated with Pseudomonas CAP but not with MDR Pseudomonas CAP. Larger cohort studies are needed to confirm findings.
Study design ICD codes were used to identify children with Kawasaki disease admitted to a tertiary Southeast U.S. center. Subjects diagnosed and treated according to AHA criteria were included. Demographic, laboratory, clinical and echocardiographic data from EMR (2000-2015) were compared between Blacks and Whites. Results Data from 369 subjects (52% Whites and 48% Blacks) were included in our analysis. No significant differences related to timely admission, IVIG treatment or, coronary artery abnormalities during hospitalization were observed, Blacks showed lower IVIG response rates for those administered IVIG within 10 days of fever onset (86.6% vs 95.6%, P = 0.007). Blacks received more ancillary drugs (9.6% vs 2.6%, P value 0.003), and endured longer hospitalizations (5±3.9 v s 3.4±2.2 days, P = 0.001). Blacks presented with higher C-reactive protein, erythrocyte sedimentation rate and; lower hemoglobin, albumin and, sodium. Blacks showed a greater proportion of persistent coronary artery abnormalities at follow-up when compared with Whites (14.5% vs 6.3%, P = .03, second follow-up ECHO; 21.2% vs 6.9%, P = 0.01 third follow-up ECHO). Conclusion Black children with Kawasaki disease had higher IVIG refractory prevalence, severe inflammation, received more ancillary treatments and, longer hospitalizations than White children. Despite no racial differences in time to diagnosis or initial treatment, there was higher coronary artery abnormality persistence among Black children at follow-up.
Objective: We observed an overall increase in the use of third- and fourth-generation cephalosporins after fluoroquinolone preauthorization was implemented. We examined the change in specific third- and fourth-generation cephalosporin use, and we sought to determine whether there was a consequent change in non-susceptibility of select Gram-negative bacterial isolates to these antibiotics. Design: Retrospective quasi-experimental study. Setting: Academic hospital. Intervention: Fluoroquinolone preauthorization was implemented in the hospital in October 2005. We used interrupted time series (ITS) Poisson regression models to examine trends in monthly rates of ceftriaxone, ceftazidime, and cefepime use and trends in yearly rates of nonsusceptible isolates (NSIs) of select Gram-negative bacteria before (1998–2004) and after (2006–2016) fluoroquinolone preauthorization was implemented. Results: Rates of use of ceftriaxone and cefepime increased after fluoroquinolone preauthorization was implemented (ceftriaxone RR, 1.002; 95% CI, 1.002–1.003; P < .0001; cefepime RR, 1.003; 95% CI, 1.001–1.004; P = .0006), but ceftazidime use continued to decline (RR, 0.991, 95% CI, 0.990–0.992; P < .0001). Rates of ceftazidime and cefepime NSIs of Pseudomonas aeruginosa (ceftazidime RR, 0.937; 95% CI, 0.910–0.965, P < .0001; cefepime RR, 0.937; 95% CI, 0.912–0.963; P < .0001) declined after fluoroquinolone preauthorization was implemented. Rates of ceftazidime and cefepime NSIs of Enterobacter cloacae (ceftazidime RR, 1.116; 95% CI, 1.078–1.154; P < .0001; cefepime RR, 1.198; 95% CI, 1.112–1.291; P < .0001) and cefepime NSI of Acinetobacter baumannii (RR, 1.169; 95% CI, 1.081–1.263; P < .0001) were increasing before fluoroquinolone preauthorization was implemented but became stable thereafter: E. cloacae (ceftazidime RR, 0.987; 95% CI, 0.948–1.028; P = .531; cefepime RR, 0.990; 95% CI, 0.962–1.018; P = .461) and A. baumannii (cefepime RR, 0.972; 95% CI, 0.939–1.006; P = .100). Conclusions: Fluoroquinolone preauthorization may increase use of unrestricted third- and fourth-generation cephalosporins; however, we did not observe increased antimicrobial resistance to these agents, especially among clinically important Gram-negative bacteria known for hospital-acquired infections.
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