Background Significant gender differences in drug and alcohol use have been reported, however little is known about gender differences in prescription opioid misuse and dependence. This study compared correlates, sources and predictors of prescription opioid non-medical use, as well as abuse or dependence among men and women in a nationally-representative sample. Methods Participants were 55,279 (26,746 men, 28,533 women) non-institutionalized civilians aged 12 years and older who participated in the National Survey on Drug Use and Health. Results Rates of lifetime and past year non-medical use of prescription opiates were 13.6% and 5.1%, respectively. Significantly more men than women endorsed lifetime (15.9% vs. 11.2%) and past year use (5.9% vs. 4.2%; ps < .0001). Among past year users, 13.2% met criteria for current prescription opiate abuse or dependence, and this did not differ significantly by gender. Polysubstance use and treatment underutilization were common among both men and women, however significantly fewer women than men had received alcohol or drug abuse treatment (p = .001). Men were more likely than women to obtain prescription opioids for free from family or friends, and were more likely to purchase them from a dealer (ps < .01). Gender-specific predictors of use as compared to abuse/dependence were also observed. Conclusions The findings highlight important differences between men and women using prescription opiates. The observed differences may help enhance the design of gender-sensitive surveillance, identification, prevention and treatment interventions.

The average delay in adopting hearing aids after hearing aid candidacy was 8.9 years. Nonwhite race and better speech recognition (in a more difficult task) significantly increased the delay to treatment. Poorer hearing and more self-assessed hearing handicap in social situations significantly decreased the delay to treatment. These results confirm the assumption that adults with hearing loss significantly delay seeking treatment with hearing aids.

Objective Administrative data is used for research, quality improvement, and health policy in severe sepsis. However, there is not a sepsis-specific tool applicable to administrative data with which to adjust for illness severity. Our objective was to develop, internally validate, and externally validate a severe sepsis mortality prediction model and associated mortality prediction score. Design Retrospective cohort study using 2012 administrative data from five US states. Three cohorts of patients with severe sepsis were created: 1) ICD-9-CM codes for severe sepsis/septic shock, 2) ‘Martin’ approach, and 3) ‘Angus’ approach. The model was developed and internally validated in ICD-9-CM cohort and externally validated in other cohorts. Integer point values for each predictor variable were generated to create a sepsis severity score. Setting Acute care, non-federal hospitals in NY, MD, FL, MI, and WA Subjects Patients in one of three severe sepsis cohorts: 1) explicitly coded (n=108,448), 2) Martin cohort (n=139,094), and 3) Angus cohort (n=523,637) Interventions None Measurements and Main Results Maximum likelihood estimation logistic regression to develop a predictive model for in-hospital mortality. Model calibration and discrimination assessed via Hosmer-Lemeshow goodness-of-fit (GOF) and C-statistics respectively. Primary cohort subset into risk deciles and observed versus predicted mortality plotted. GOF demonstrated p>0.05 for each cohort demonstrating sound calibration. C-statistic ranged from low of 0.709 (sepsis severity score) to high of 0.838 (Angus cohort) suggesting good to excellent model discrimination. Comparison of observed versus expected mortality was robust although accuracy decreased in highest risk decile. Conclusions Our sepsis severity model and score is a tool that provides reliable risk adjustment for administrative data.

With the recent emphasis on evidence-based practice and healthcare reform, understanding the cost of dysphagia management has never been more important. It is helpful for clinicians to understand and objectively report the costs associated with dysphagia when they advocate for their services in this economy. Having carefully estimated cost of illness, inputs are needed for cost-effectiveness analyses that help support the value of treatments. This study sought to address this issue by examining the 1-year cost associated with a diagnosis of dysphagia post-stroke in South Carolina. Furthermore, this study investigated whether ethnicity and residence differences exist in the cost of dysphagia post-stroke. Data on 3,200 patients in the South Carolina Medicare database from 2004 who had ICD-9 codes for ischemic stroke, 434 and 436, were retrospectively included in this study. Differences between persons with and without dysphagia post-stroke were compared with respect to age, gender, ethnicity, mortality, length of stay, comorbidity, rurality, discharge disposition, and cost to Medicare. Univariate analyses and a gamma-distributed generalized linear multivariable model with a log link function were completed. We found that the 1-year cost to Medicare for persons with dysphagia post ischemic stroke was $4,510 higher than that for persons without dysphagia post ischemic stroke when controlling for age, comorbidities, ethnicity, and proportion of time alive. Univariate analysis revealed that rurality, ethnicity, and gender were not statistically significantly different in comparisons of individuals with or without dysphagia post-stroke. Post-stroke dysphagia significantly increases post-stroke medical expenses. Understanding the expenditures associated with post-stroke dysphagia is helpful for optimal allocation and use of resources. Such information is needed to conduct cost-effectiveness studies.

Background and Purpose Little is known about the contribution of aphasia to the cost of care for patients who experience stroke. Methods We retrospectively examined a cohort of South Carolina Medicare beneficiaries who experienced an ischemic stroke in 2004 to determine the attributable cost of aphasia. Univariate analyses were used to compare demographic, comorbidity, and severity differences between individuals with post-stroke aphasia and those without aphasia. Differences in payments by Medicare due to stroke were examined using a Gamma distributed generalized linear multivariable model. Results 3,200 Medicare beneficiaries experienced an ischemic stroke in South Carolina in 2004 and 398 had post-stroke aphasia. Patients with aphasia experienced longer length of stays, greater morbidity, and greater mortality. In adjusted models that controlled for relevant covariates, the attributable one-year cost of aphasia was estimated at $1703. Conclusions Aphasia adds to the cost of stroke-related care, above the cost of stroke alone.

Summary There are likely to be gender differences in determinants of relapse to drug use following abstinence in cocaine-dependent individuals. Cocaine-dependent women are more likely to attribute relapse to negative emotional states and interpersonal conflict. Cocaine dependence has also been linked to dysregulation of stress response and the hypothalamic pituitary adrenal (HPA) axis which may differ between genders. Subjective and HPA axis responses to a social evaluative stressor, the Trier Social Stress Test (TRIER), and in vivo cocaine-related cues were examined in the present study. Results There were no gender differences in magnitude of craving responses to the TRIER or the CUE. Both genders had a greater craving response to the CUE than to the TRIER, but the magnitude of the difference was greater for men than women (p=0.04). Cocaine-dependent subjects, compared to the control group, had significantly higher response throughout the TRIER (p<0.0001) and CUE (p<0.0001) testing sessions. There were no gender differences and no gender by cocaine interaction for ACTH responses to the TRIER, although women had lower baseline ACTH (p=0.049). On the CUE task, in contrast, female cocaine-dependent subjects had a more blunted ACTH response than did the other three groups (p=0.02). Female cocaine-dependent subjects also had a lower odds of a positive cortisol response to the TRIER as compared to the other three groups (OR=0.84, 95% CI=[0.02, 1.01]). During the CUE task, cocaine-dependent subjects had overall higher mean cortisol levels (p=0.0001), and higher odds of demonstrating a positive cortisol response to the CUE (OR=2.61, 95% CI=[1.11, 6.11]). No gender differences were found in ACTH responses to the CUE. The results are reviewed in the context of the existing literature on gender differences in cocaine dependence and potential implications for treatment are discussed.

We examined the influence of gender and smoking status on reactivity in two human laboratory stress paradigms. Participants were 46 (21 men, 25 women) healthy individuals who completed the Trier Social Stress Task (i.e., performed speech and math calculations in front of an audience) and a pharmacological stress provocation (i.e., administration of corticotrophin releasing hormone (CRH)) after an overnight hospital stay. Approximately half (53%) of the participants were smokers. Cortisol, adrenocorticotrophin hormone (ACTH), physiologic measures (heart rate, blood pressure), and subjective stress were assessed at baseline and at several time points post-task. Men demonstrated higher baseline ACTH and blood pressure as compared to women; however, ACTH and blood pressure responses were more pronounced in women. Women smokers evidenced a more blunted cortisol response as compared to non-smoking women, whereas smoking status did not affect the cortisol response in men. Finally, there was a more robust cardiovascular and subjective response to the Trier as compared to the CRH. Although preliminary, the findings suggest that women may be more sensitive than men to the impact of cigarette smoking on cortisol response. In addition, there is some evidence for a more robust neuroendocrine and physiologic response to acute laboratory stress in women as compared to men.

Context Corticotropin-releasing hormone (CRH), through the hypothalamic pituitary adrenal (HPA) axis and other brain stress systems, is involved in the emotional dysregulation associated with cocaine dependence. Little is known about the response of cocaine-dependent individuals to CRH administration. Objective The primary objective was to examine the HPA axis, subjective and physiologic response to CRH in cocaine-dependent individuals and controls. Design Case-control study Setting Subjects were admitted to a General Clinical Research Center (GCRC) for testing and abstinence verified with urine drug screening. Participants Participants were control males (n=23), control females (n=24), cocaine-dependent males (n=28), and cocaine-dependent females (n=25). Individuals with dependence on other substances (except caffeine, nicotine) or with major depression, PTSD, bipolar, psychotic and eating disorders were excluded. Intervention Subjects received i.v. CRH (1ug/kg). Main Outcome Measures Primary outcomes included plasma ACTH and cortisol, heart rate, and subjective measurements. Results Cocaine-dependent individuals exhibited higher stress (P < 0.001) and craving to CRH compared to controls. A positive correlation (rs=.51, P=0.0002) between stress and craving was found in cocaine dependent subjects. CRH elevated heart rates in all groups, however cocaine dependent females, demonstrated a significantly higher heart rate at all time points (P=0.05). Women had higher cortisol response to CRH (P=0.028). No effect of cocaine status was observed. ACTH response to CRH was independent of gender and cocaine. Cortisol and ACTH were positively correlated in the controls and cocaine-dependent males, but not in cocaine-dependent females (rs = 0.199; P = 0.4). Conclusion There is an increased subjective and heart rate response to CRH and a relationship between stress and craving in cocaine-dependent individuals. The lack of difference in HPA axis response between the cocaine and control groups suggests that the heart rate and subjective responses in the cocaine group may be mediated by sensitization of non-hypothalamic stress-responsive CRH systems.