Development and Dynamic Responsiveness of the Acute Asthma Exacerbation Survey in Patients With Moderate to Severe Disease.

BACKGROUND: The recall periods and response scales of existing surveys of asthma control are poorly suited for studying acute exacerbations. OBJECTIVE: To develop an instrument able to predict exacerbations after the onset of acute symptoms and with a recall window sufficiently short to study recovery. METHODS: We developed the six-item Acute Asthma Exacerbation Survey (AAES). Data were collected at baseline, acute, and recovery visits within an established longitudinal protocol for participants with severe asthma. Participants scheduled acute study visits at the first sign of a cold. Nasal lavage samples and lung function measurements were also collected. The AAES data were analyzed using Cronbach α, Spearman correlations, and Kruskal-Wallace methods. We used logistic regression for predictors of bursts of oral corticosteroids (OCS). RESULTS: Of 130 participants studied at baseline, 52 returned for an acute visit. The AAES scores were elevated at the acute visit and returned to baseline after recovery independently of respiratory virus detection. Cronbach α for the AAES was 0.853, 0.822, and 0.889 at the three respective visits. Compared with participants not needing burst OCS, those with exacerbations had higher acute AAES scores (16 [13.5-18] vs 11.5 [8.2-14], median [interquartile range]; P = .017) and a larger reduction from baseline in lung function. For each 3-point increase in AAES scores, the odds ratio for burst OCS use was 1.64 (95% CI, 1.04-2.57; P = .030). CONCLUSIONS: The AAES is internally consistent and dynamically responsive during acute asthma exacerbations. Additional validation studies are warranted to support future trials and aid in clinical decision-making.

A 48-Year-Old Amateur Bodybuilder With History of Provoked DVT With Subacute Progressive Shortness of Breath.

CASE PRESENTATION: A 48-year-old man presented with 6 months of progressive shortness of breath, intermittent exertional left-sided chest pain, and bilateral lower extremity edema. During the 2 days before admission, he experienced new onset confusion, fatigue, and malaise that prompted evaluation. He denied fever, chills, cough, or sputum production. He used anabolic steroids for 20 years as part of his bodybuilding hobby. Recently, he also began injecting mineral oil into his pectoral, bicep, and shoulder muscles for an improved muscular appearance. Additionally, he had a history of provoked DVT after traumatic fracture, schizophrenia, hypertension, and epilepsy. He was a former cigarette smoker with 2.5 pack-year history, having quit 10 years earlier. The patient's occupation was construction, installing aluminum gutters. He specifically denied exposures to sand-blasting, coal, beryllium, hard metals, silicone, and fine particles. He had no recent travel, sick contacts, or animal exposures.

Pupillary response abnormalities in depressive disorders.

Depressive disorders lack objective physiological measurements to characterize the affected population and facilitate study of relevant mechanisms. The melanopsin-mediated light signaling pathway may contribute to seasonal variation and can be measured non-invasively by pupillometry. We prospectively studied changes in melanopsin-mediated pupillary constriction in 19 participants with major depressive disorder (MDD) and 10 control across the summer and winter solstices. The melanopsin-mediated response, as measured by the pupil's sustained constriction six s after a high intensity blue light stimulus, was marginally attenuated in those with MDD relative to controls (p=0.071). The participants with MDD unexpectedly showed a significantly reduced transient pupillary response to low intensity red (p=0.011) and blue light (p=0.013), but not high intensity red and blue light. Sustained pupillary constriction in response to high intensity blue light was more pronounced with increasing daylight hours (p=0.037) and was more strongly related to objectively measured versus estimated light exposure. Melanopsin-mediated impairments in pupil response may serve as a biological marker for vulnerability to depression in low light conditions. Assessment of these and other responses to light stimuli, such as response to low intensity light, may be useful for the study of the neurobiology of MDD and related mood disorders.