BackgroundAcknowledgement of COPD underdiagnosis and misdiagnosis in primary care can contribute to improved disease diagnosis. PUMA is an international primary care study in Argentina, Colombia, Venezuela and Uruguay.ObjectivesTo assess COPD underdiagnosis and misdiagnosis in primary care and identify factors associated with COPD underdiagnosis in this setting.MethodsCOPD was defined as post-bronchodilator (post-BD) forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) <0.70 and the lower limit of normal (LLN). Prior diagnosis was self-reported physician diagnosis of emphysema, chronic bronchitis, or COPD. Those patients with spirometric COPD were considered to have correct prior diagnosis, while those without spirometric criteria had misdiagnosis. Individuals with spirometric criteria without previous diagnosis were considered as underdiagnosed.Results1,743 patients were interviewed, 1,540 completed spirometry, 309 (post-BD FEV1/FVC <0.70) and 226 (LLN) had COPD. Underdiagnosis using post-BD FEV1/FVC <0.70 was 77% and 73% by LLN. Overall, 102 patients had a prior COPD diagnosis, 71/102 patients (69.6%) had a prior correct diagnosis and 31/102 (30.4%) had a misdiagnosis defined by post-BD FEV1/FVC ≥0.70. Underdiagnosis was associated with higher body mass index (≥30 kg/m2), milder airway obstruction (GOLD I–II), black skin color, absence of dyspnea, wheezing, no history of exacerbations or hospitalizations in the past-year. Those not visiting a doctor in the last year or only visiting a GP had more risk of underdiagnosis. COPD underdiagnosis (65.8%) and misdiagnosis (26.4%) were less prevalent in those with previous spirometry.ConclusionsCOPD underdiagnosis is a major problem in primary care. Availability of spirometry should be a priority in this setting.

Objective-There is a need to identify a cognitive composite that is sensitive to tracking preclinical AD decline to be used as a primary endpoint in treatment trials.Method-We capitalized on longitudinal data, collected from 1995 to 2010, from cognitively unimpaired presenilin 1 (PSEN1) E280A mutation carriers from the world's largest known earlyonset autosomal dominant AD (ADAD) kindred to identify a composite cognitive test with the greatest statistical power to track preclinical AD decline and estimate the number of carriers age 30 and older needed to detect a treatment effect in the Alzheimer's Prevention Initiative's (API) preclinical AD treatment trial. The mean-to-standard-deviation ratios (MSDRs) of change over time were calculated in a search for the optimal combination of one to seven cognitive tests/sub-* To whom correspondence should be addressed: Napatkamon Ayutyanont, PhD, Banner Alzheimer's Institute, 901 E. Willetta Street, Phoenix, AZ 85006, telephone: 602.839.6825; Napatkamon.Ayutyanont@bannerhealth.com. ** These two authors are co-senior authors.Portions of this study were presented at the 2011 Alzheimer's Association International Conference, Paris, France and the 2011 Clinical Trials on Alzheimer's Disease (CTAD), San Diego, CA.They have no conflict of interest to report. Conclusions-We have identified a composite cognitive test score representing multiple cognitive domains that has improved power compared to the most sensitive single test item to track preclinical AD decline in ADAD mutation carriers and evaluate preclinical AD treatments. This API composite cognitive test score will be used as the primary endpoint in the first API trial in cognitively unimpaired ADAD carriers within 15 years of their estimated age at clinical onset. NIH Public AccessWe have independently confirmed our findings in a separate cohort of cognitively healthy older adults who progressed to the clinical stages of late-onset AD, described in a separate report, and continue to refine the composite in independent cohorts and compared with other analytical approaches.

BackgroundCOPD, asthma, and asthma–COPD overlap increase health care resource consumption, predominantly because of hospitalization for exacerbations and also increased visits to general practitioners (GPs) or specialists. Little information is available regarding this in the primary care setting.ObjectivesTo describe the prevalence and number of GP and specialist visits for any cause or due to exacerbations in patients with COPD, asthma, and asthma–COPD overlap.MethodsCOPD was defined as post-bronchodilator forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) ratio <0.70; asthma was defined as prior medical diagnosis, wheezing in the last 12 months, or wheezing plus reversibility (post-bronchodilator FEV1 or FVC increase ≥200 mL and ≥12%); asthma–COPD overlap was defined as post-bronchodilator FEV1/FVC <0.70 plus prior asthma diagnosis. Health care utilization was evaluated as GP and/or specialist visits in the previous year.ResultsAmong the 1,743 individuals who completed the questionnaire, 1,540 performed acceptable spirometry. COPD patients had a higher prevalence of any medical visits to any physician versus those without COPD (37.2% vs 21.8%, respectively) and exacerbations doubled the number of visits. The prevalence of any medical visits to any physician was also higher in asthma patients versus those without asthma (wheezing: 47.2% vs 22.7%; medical diagnosis: 54.6% vs 21.6%; wheezing plus reversibility: 46.2% vs 23.8%, respectively). Asthma patients with exacerbations had twice the number of visits versus those without an exacerbation. The number of visits was higher (2.8 times) in asthma–COPD overlap, asthma (1.9 times), or COPD (1.4 times) patients versus those without these respiratory diseases; the number of visits due to exacerbation was also higher (4.9 times) in asthma–COPD overlap, asthma (3.5 times), and COPD (3.8 times) patients.ConclusionCOPD, asthma, and asthma–COPD overlap increase the prevalence of medical visits and, therefore, health care resource utilization. Attempts to reduce health care resource use in these patients require interventions aimed at preventing exacerbations.

Existing literature suggests that stress in early life can influence or trigger later aggressive and punishment behaviors during social interactions. However, only a few human studies have addressed this link in controlled experimental settings. Here, we assessed the impact of biological and behavioral markers of stress on economic and social interactions in healthy men using a between-group design. The Socially Evaluated Cold Pressor Test (i.e., supervised hand immersion into cold water) was applied to one group of participants (n = 19), while a second group underwent the Warm Water Test (n = 21). After the stressor or control procedure, all participants played the Inequality Game, a paradigm in which they could engage in punishment, cooperative, or aggressive behaviors towards a fair and an unfair counterpart player. Compared to the control condition, participants in the stress condition engaged in more punishment behaviors towards the unfair player and less cooperative behaviors towards both players. Critically, higher levels of cortisol in the stress group were associated with more punishment behaviors towards the unfair player. In contrast, aggressive behavior did not differ between participants in the stress vs. control condition. Overall, our findings showed that situationally induced stress might facilitate punishment behaviors in provoking situations. Further research should elucidate the role of inter-individual variables that may encourage or prevent stress-related punishment in social contexts.

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