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COVID-19 and EVALI share imaging findings and clinical features, including fever, respiratory, and gastrointestinal symptoms. To our knowledge, the clinical picture in patients presenting with both conditions simultaneously has not been reported. We present the case of a 17-year-old male with COVID-19 and EVALI, his hospital course, and clinical outcome.

Background: Decreased 25-hydroxyvitamin D [25(OH)D] concentrations have been associated with an increased prevalence and severity of asthma and a lower response to inhaled corticosteroids. Objective: The objective was to determine the association between serum 25(OH)D concentrations and asthma prevalence, severity, and response to asthma treatment. Design: Secondary analyses were conducted in 2 samples of adolescents 12–20 y of age: 1) NHANES 2001–2006 (n = 6487), a cross-sectional nationally representative sample of the US population, and 2) a cohort of inner-city adolescents with asthma managed prospectively for 46 wk with guidelines-based therapy in the Asthma Control Evaluation (ACE; n = 226) trial. Results: Mean (±SD) serum 25(OH)D concentrations in the NHANES and ACE samples were lower in African Americans than in non–African Americans (NHANES: 14.9 ± 6.5 compared with 23.0 ± 8.4 ng/mL, P < 0.0001; ACE: 11.2 ± 6.9 compared with 15.8 ± 7.1 ng/mL, P < 0.0001). In the NHANES sample, mean concentrations did not differ between participants without and with asthma (African Americans: 14.9 ± 6.4 compared with 15.0 ± 6.6 ng/mL, respectively, P = 0.87; non–African Americans: 23.0 ± 8.5 compared with 23.6 ± 8.2 ng/mL, respectively, P = 0.16). In the ACE models that used either a predefined cutoff (

Objectives/Hypothesis To assess laryngopharyngeal sensation, prevalence of laryngopharyngeal sensory deficit and abnormal swallowing function parameters in children with dysphagia. Study Design Retrospective chart review. Methods The medical records of children who underwent flexible endoscopic evaluation of swallowing with sensory testing (FEESST) were reviewed. Laryngopharyngeal sensory threshold (LPST) was assessed based on the threshold intensity of air pulse stimulation eliciting laryngeal adductor reflex. Swallowing function parameters including pharyngeal residue, hypopharyngeal pooling of secretions, premature spillage, laryngeal penetration, and aspiration were evaluated. Prevalence of abnormal swallowing function parameters in children with normal and impaired LPST was compared. Results Forty children with dysphagia (28 male, 12 female; age range, 3 months to 17 years) underwent FEESST. LPST was normal in six patients, moderately impaired in 20 patients, and severely impaired in 10 patients. LPST could not be measured in four patients. Children showed one or more abnormal swallowing function parameters. The prevalence of abnormal swallowing parameters in patients with normal LPST was lower than that of patients with moderately or severely impaired LPST (P

Background Asthma severity is reflected in many aspects of the disease, including impairment and future risks, particularly for exacerbations. According to the Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma, however, to assess more comprehensively the severity of asthma the level of current treatment needed to maintain a level of control should be included. Objective Development and validation of a new instrument, the Composite Asthma Severity Index (CASI), which can quantify disease severity by taking into account impairment, risk, and the amount of medication needed to maintain control. At present, there is no instrument available to measure and assess the multidimensional nature of asthma. Methods Twenty-six established asthma investigators, who are part of the National Institutes of Health–supported Inner City Asthma Consortium, participated in a modified Delphi consensus process to identify and weight the dimensions of asthma. Factor analysis was performed to identify independent domains of asthma by using the Asthma Control Evaluation trial. CASI was validated by using the Inner City Anti-IgE Therapy for Asthma trial. Results CASI scores include 5 domains: day symptoms and albuterol use, night symptoms and albuterol use, controller treatment, lung function measures, and exacerbations. At Asthma Control Evaluation trial enrollment, CASI ranged from 0 to 17, with a mean of 6.2. CASI was stable, with minimal change in variance after 1 year of treatment. In external validation, CASI detected a 32% larger improvement than did symptoms alone. Conclusion CASI retained its discriminatory ability even with low levels of symptoms reported after months of guidelines-directed care. Thus, CASI has the ability to determine the level of asthma severity and provide a composite clinical characterization of asthma.

Churg-Strauss syndrome is a vasculitis accompanied by asthma and eosinophilia. It is generally considered a disease of adults; occurrence in children has been reported infrequently. Here we report 2 pediatric patients with Churg-Strauss syndrome manifesting with prominent pulmonary involvement. One, a 16-year-old with a previous history of asthma, presented with pleuritic chest pain and a peripheral pulmonary nodule complicated by an eosinophilic pleural effusion. The other patient presented at age 6 with cough, weight loss, and radiographic infiltrates. Lung biopsies revealed elements characteristic of Churg-Strauss syndrome, including eosinophilic microabscesses and vasculitis. Three- and 5-year follow-up showed continued symptoms in both patients despite medical therapy. Both patients illustrate many of the typical features of Churg-Strauss syndrome. We report these cases to expand the scant knowledge about Churg-Strauss syndrome in pediatric patients and to heighten awareness that this serious disease may affect the pediatric population. The relevant literature on Churg-Strauss syndrome, with specific reference to childhood cases, is reviewed.

Epidemiological data indicate an increased incidence of asthma in overweight adults and children. Ozone (O3) is a common trigger for asthma. Accordingly, the purpose of this study was to compare O3-induced airway hyperresponsiveness and airway inflammation in lean, wild-type (C57BL/6J) mice and mice that are obese as a consequence of a genetic defect in the gene encoding the satiety hormone leptin ( ob/ob mice). The ob/ob mice eat excessively and weighed more than twice as much as age- and gender-matched wild-type mice. Airway responsiveness to intravenous methacholine was measured by forced oscillation. In air-exposed controls, baseline pulmonary resistance was greater, and the dose of methacholine required to double pulmonary resistance was lower in ob/ob than wild-type mice. Exposure to O3(2 parts/million for 3 h) caused AHR and airway inflammation in both groups of mice, but responses to O3were enhanced in ob/ob compared with wild-type mice. Administration of exogenous leptin did not reverse the enhanced inflammatory response observed in ob/ob mice, but augmented airway inflammation in wild-type mice. The inhaled dose of O3per gram of lung tissue was greater in ob/ob than wild-type mice. Our results indicate that O3-induced airway responses are enhanced in ob/ob mice and suggest that inhaled O3dose may be one factor contributing to this difference, but other aspects of the obese phenotype may also contribute. Our results also indicate that the hormone leptin, which is increased in the obese, has the capacity to increase airway inflammation.

To assess laryngopharyngeal sensation, prevalence of laryngopharyngeal sensory deficit and abnormal swallowing function parameters in children with dysphagia.Retrospective chart review.The medical records of children who underwent flexible endoscopic evaluation of swallowing with sensory testing (FEESST) were reviewed. Laryngopharyngeal sensory threshold (LPST) was assessed based on the threshold intensity of air pulse stimulation eliciting laryngeal adductor reflex. Swallowing function parameters including pharyngeal residue, hypopharyngeal pooling of secretions, premature spillage, laryngeal penetration, and aspiration were evaluated. Prevalence of abnormal swallowing function parameters in children with normal and impaired LPST was compared.Forty children with dysphagia (28 male, 12 female; age range, 3 months to 17 years) underwent FEESST. LPST was normal in six patients, moderately impaired in 20 patients, and severely impaired in 10 patients. LPST could not be measured in four patients. Children showed one or more abnormal swallowing function parameters. The prevalence of abnormal swallowing parameters in patients with normal LPST was lower than that of patients with moderately or severely impaired LPST (P.05). The prevalence of pharyngeal residue, hypopharyngeal pooling of secretions, and spillage in patients with severely impaired LPST was higher than that of patients with moderately impaired LPST (P.05).The majority of children with dysphagia have impaired LPST. The prevalence of abnormal swallowing function parameters in children with normal LPST is lower than that in children with moderately or severely impaired LPST. Prevalence of aspiration tends to increase when the abnormal swallowing function parameters are associated with severely impaired LPST.

Rationale: Epidemiologic data indicate an increased incidence of asthma in the obese. Objectives: To determine whether obese mice exhibit augmented pulmonary responses after allergen sensitization and challenge. Methods: Lean, wild-type (C57BL/6), obese ob/ob, and obese db/db mice were sensitized to ovalbumin (OVA), and then challenged with aerosolized OVA or phosphate-buffered saline (PBS). Changes in total pulmonary resistance (Rl) induced by intravenous methacholine were measured by forced oscillation. Blood was collected, bronchoalveolar lavage (BAL) was performed, and lungs were harvested for measurement of cytokine expression by real-time reverse transcription–polymerase chain reaction. Measurements and Main Results: OVA challenge increased baseline Rl in ob/ob, but not wild-type, mice, and airway responsiveness was greater in ob/ob than wild-type mice, regardless of the challenge. Compared with PBS, OVA challenge caused an increase in the number of BAL fluid (BALF) cells, an increase in lung Th2 cytokine expression, and an increase in serum IgE. Significantly fewer BALF cells were recovered from OVA-challenged ob/ob versus wild-type mice, whereas serum IgE levels were elevated significantly more in ob/ob versus wild-type mice. BALF and lung Th2 cytokine expression was not different in ob/ob versus wild-type mice. Airway responsiveness was greater in db/db versus wild-type mice, regardless of the challenge, and OVA caused airway hyperresponsiveness in db/db but not wild-type mice, despite reduced BALF cells in OVA-challenged db/db versus wild-type mice. Conclusions: These results demonstrate that obesity enhances OVA-induced changes in pulmonary resistance and serum IgE and that these changes are not the result of increased Th2 type airway inflammation.

Obesity is an important risk factor for asthma. We recently reported increased ozone (O3)-induced hyperresponsiveness to methacholine in obese mice (Shore SA, Rivera-Sanchez YM, Schwartzman IN, and Johnston RA. J Appl Physiol 95: 938–945, 2003). The purpose of this study was to determine whether this increased hyperresponsiveness is the result of changes in the airways, the lung tissue, or both. To that end, we examined the effect of O3 (2 parts/million for 3 h) on methacholine-induced changes in lung mechanics with the use of a forced oscillation technique in wild-type C57BL/6J mice and mice obese because of a genetic deficiency in leptin ( ob/ob mice). In ob/ob mice, O3 increased baseline values for all parameters measured in the study: airway resistance (Raw), lung tissue resistance (Rtis), lung tissue damping (G) and elastance (H), and lung hysteresivity (η). In contrast, no effect of O3 on baseline mechanics was observed in wild-type mice. O3 exposure significantly increased Raw, Rtis, lung resistance (Rl), G, H, and η responses to methacholine in both groups of mice. For G, Rtis, and Rl there was a significant effect of obesity on the response to O3. Our results demonstrate that both airways and lung tissue contribute to the hyperresponsiveness that occurs after O3 exposure in wild-type mice. Our results also demonstrate that changes in the lung tissue rather than the airways account for the amplification of O3-induced hyperresponsiveness observed in obese mice.