Fungal bronchitis is a distinct clinical entity which is responsive to antifungal therapy.

Chronic productive cough in the context of exacerbations of airway disease can be associated with positive sputum cultures for fungi, in particular Aspergillus fumigatus and Candida spp., suggesting fungal bronchitis, a condition not widely recognised, as a possible cause for the exacerbation. Our objective was to determine the response to antifungal therapy in patients with suspected fungal bronchitis. Retrospective analysis of data extracted from case records of patients under secondary care respiratory clinics who had been treated with triazole therapy for suspected fungal bronchitis between 2010-2017. Primary outcome was lung function response after 1 month of treatment. Nineteen patients with fungal bronchitis due to A. fumigatus and 12 patients due to Candida spp., were included in the study. Most of the patients, particularly in the Aspergillus group, had allergic fungal airway disease on a background of asthma. All but one of the patients in each group were recorded as showing clinical improvement with antifungal therapy. In the majority of patients this was reflected in an improvement in lung function. Aspergillus group: FEV1 (1.44 ± 0.8 L vs 1.6 ± 0.8 L: p < 0.02), FVC (2.49 ± 1.08 L vs 2.8 ± 1.1 L: p = 0.01), and PEF (260 ± 150L/min vs 297 ± 194ml/min: p < 0.02). Candida group: FEV1 (1.6 ± 0.76 L vs 2.0 ± 0.72 L: p < 0.004), FVC (2.69 ± 0.91 L vs 3.13 ± 0.7 L: p = 0.05), and PEF (271± 139L/min vs 333 ± 156 L/min: p = 0.01). Side effects of treatment were common, but resolved on stopping treatment. This service improvement project supports the idea that fungal bronchitis is a distinct clinical entity which is responsive to treatment. Controlled clinical trials to confirm the clinical impression that this is relatively common and treatable complication of complex airway disease are required.

Lung function decline and variable airway inflammatory pattern: longitudinal analysis of severe asthma.

BACKGROUND: Eosinophilic airway inflammation measured by using induced sputum is an important treatment stratification tool in patients with severe asthma. In addition, sputum eosinophilia has been shown to be associated with severe exacerbations and airflow limitation. OBJECTIVES: We sought to identify whether eosinophilic inflammation in sputum is associated with FEV1 decrease in patients with severe asthma and whether we could identify subgroups of decrease behavior based on the variation of eosinophilic airway inflammation over time. METHODS: Ninety-seven patients with severe asthma from the Glenfield Asthma Cohort were followed up with scheduled 3-month visits; the median duration of follow-up and number of visits was 6 years (interquartile range, 5.6-7.6 years) and 2.7 visits per year. Induced sputum was analyzed for eosinophilic inflammation at scheduled visits. Linear mixed-effects models were used to identify variables associated with lung function and overall decrease. In addition, using individual patients' mean and SD sputum eosinophil percentages over time, a 2-step cluster analysis was performed to identify patient clusters with different rates of decrease. RESULTS: FEV1 decrease was -25.7 mL/y in the overall population. Postbronchodilator FEV1 was also dependent on exacerbations, age of onset, height, age, sex, and log10 sputum eosinophil percentages (P < .001). Three decrease patient clusters were identified: (1) noneosinophilic with low variation (mean decrease, -14.0 mL/y), (2) eosinophilic with high variation (mean decrease, -40.9 mL/y), and (3) hypereosinophilic with low variation (mean decrease in lung function, -19.2 mL/y). CONCLUSION: The amplitude of sputum eosinophilia was associated with postbronchodilator FEV1 in asthmatic patients. In contrast, high variability rather than the amplitude at baseline or over time of sputum eosinophils was associated with accelerated FEV1 decrease.

Airway dysfunction and inflammation in pool- and non-pool-based elite athletes.

PURPOSE: This study sought to determine and compare the levels of airway dysfunction and inflammation in a large cohort of symptomatic international athletes from pool- and non-pool-based sporting backgrounds. In total, 118 athletes were recruited. METHODS: All subjects had symptoms of exercise asthma and were steroid naïve. They completed baseline spirometry, a symptom score, exhaled nitric oxide, a eucapnic voluntary hyperventilation (EVH) test, and a postchallenge induced sputum and urine test. RESULTS: Pool-based athletes had better lung function (FEV1 = 110% vs 102% predicted, mean difference = 8.200 ± 2.339, P = 0.0006 and FVC = 5.64 vs 4.75 L, mean difference = 0.8855 ± 0.1951, P < 0.0001) and more marked airways hyper-reactivity (AHR) (percent drop in FEV1 after EVH = 18.14 vs 11.47, mean difference = 6.67, 95% confidence interval = 2.89-10.53, P = 0.0009). More pool-based athletes had a positive EVH test (72% pool vs 39% nonpool), but there was no difference between groups with respect to eosinophilic inflammation (sputum eosinophil percentage: pool = 2.07, nonpool = 2.28, P = 0.77; exhaled nitric oxide: pool = 32.54, nonpool = 35.77, P = 0.60). Athletes with a positive EVH test had less neutrophilic inflammation (P = 0.01) and more epithelial cells (P = 0.03) in their sputum. CONCLUSIONS: Pool-based endurance athletes have greater evidence of AHR than non-pool-based athletes but no evidence of greater eosinophilic airway inflammation. Athletes who test positive on EVH are more likely to be eosinophilic and have higher levels of epithelial cells in their sputum.