Determinants of lung function changes in athletic swimmers. A review.

To summarise lung function characteristics of athletic swimmers and discuss mechanisms explaining these changes while putting forward the lack of a clear understanding of the precise physiological factors implicated. Literature search until 07.2021 on Medline and EMBASE using keywords swimming, athletes, respiratory physiology, lung development, lung function tests. Relevant articles in French and English were reviewed. We found insufficient data to perform a meta-analysis. However, there is evidence that swimmers have better expiratory flows and increased baseline lung volumes than non-athletes or non-swimmers. Although these features can result from changes in lung development following intense training over the years, the contribution of a genetic predisposition and positive selection cannot be totally excluded. Disentangling the participation of constitutional factors and years of hard training to explain the larger lung volumes of athletic swimmers is in favour of an adaptative response of the lungs to early swim training through modification of the pathway of lung development. There seems to be an optimal window of opportunity before the end of growth for these adaptational changes to occur. Precise mechanisms, and contribution of adaptative change on lung physiology, remain to be further studied

The effect of high-dose fluticasone propionate and budesonide on lung function and asthma exacerbations in patients with severe asthma

AbstractThe purpose of this study was to investigate the comparative efficacy and safety of equal doses of inhaled fluticasone propionate (FP) and inhaled budesonide (BUD) using their respective dry powder inhalers in a population of severe asthmatics requiring high doses of inhaled corticosteroid. This double-blind double-dummy parallel-group study compared the effects of 24 weeks of treatment with FP (2000 μg daily via a Diskhaler® inhaler; Glaxo Wellcome, Evreux, France) and BUD (2000 μg daily via a Turbuhaler® inhaler; Astra Pharmaceuticals, Rijswijka, Netherlands) on lung function and asthma exacerbations in 395 patients with asthma.FP was statistically significantly superior to BUD with respect to the percentage of symptom-free days (P = 0·02), the incidence of days free from rescue bronchodilator usage (P = 0·02) and the distribution of change in peak expiratory flow (PEF) expressed as a percentage of the predicted PEF (P = 0·04). During the treatment period FP was statistically significantly superior to BUD for change in forced expiratory volume in 1 sec (FEV1) at 8, 16 and 24 weeks, change in the median daytime symptom score during weeks 5–16, for incidence of symptomfree days and incidence of days free from rescue bronchodilator usage during weeks 17–24. There was no significant difference between FP and BUD with respect to the number of patients experiencing one or more asthma exacerbation (33·8 and 28·4% of patients, respectively). There was, however, evidence that the exacerbations were clinically less severe in patients treated with FP, in that the time to resolution was quicker (11·0 vs. 14·7 days; P = 0·035), mean duration of all exacerbations (for an individual patient) tended to be shorter (18·5 vs. 23·6 days; P = 0·12), the time off work was reduced (4·2 vs. 7·6 days; P = 0·012) and the lowest PEF recorded during the exacerbation was higher (301 vs. 263 1 min−1; P = 0·07). There were no clinically relevant differences in the safety (serum cortisol levels, markers of bone turnover, adverse events) of FP and BUD at these microgram equivalent doses.The patients recruited into this study, in retrospect, probably had no need for such high doses of inhaled corticosteroid but, irrespective of this, FP at microgram equivalent doses showed evidence of superior efficacy to BUD with respect to lung function and severity of asthma exacerbations without producing any greater adverse systemic effect

Optimal Management of Severe/Refractory Asthma

Asthma is a chronic inflammatory disease of the airways, affecting approximately 300 million people worldwide. Asthma results in airway hyperresponsiveness, leading to paroxysmal symptoms of wheeze, cough, shortness of breath, and chest tightness. When these symptoms remain uncontrolled, despite treatment with high doses of inhaled and ingested corticosteroids, asthmatic patients are predisposed to greater morbidity and require more health care support. Treating patients with severe asthma can be difficult and often poses a challenge to physicians when providing ongoing management. This clinical review aims to discuss the definition, prevalence and evaluation of severe asthmatics, and provides a review of the existing pharmacologic and non-pharmacologic treatment options

Manifesto on small airway involvement and management in asthma and chronic obstructive pulmonary disease:an Interasma (Global Asthma Association - GAA) and World Allergy Organization (WAO) document endorsed by Allergic Rhinitis and its Impact on Asthma (ARIA) and Global Allergy and Asthma European Network (GA2LEN)

Evidence that enables us to identify, assess, and access the small airways in asthma and chronic obstructive pulmonary disease (COPD) has led INTERASMA (Global Asthma Association) and WAO to take a position on the role of the small airways in these diseases. Starting from an extensive literature review, both organizations developed, discussed, and approved the manifesto, which was subsequently approved and endorsed by the chairs of ARIA and GA2LEN. The manifesto describes the evidence gathered to date and defines and proposes issues on small airway involvement and management in asthma and COPD with the aim of challenging assumptions, fostering commitment, and bringing about change. The small airways (defined as those with an internal diameter <2 mm) are involved in the pathogenesis of asthma and COPD and are the major determinant of airflow obstruction in these diseases. Various tests are available for the assessment of the small airways, and their results must be integrated to confirm a diagnosis of small airway dysfunction. In asthma and COPD, the small airways play a key role in attempts to achieve disease control and better outcomes. Small-particle inhaled formulations (defined as those that, owing to their size [usually <2 μm], ensure more extensive deposition in the lung periphery than large molecules) have proved beneficial in patients with asthma and COPD, especially those in whom small airway involvement is predominant. Functional and biological tools capable of accurately assessing the lung periphery and more intensive use of currently available tools are necessary. In patients with suspected COPD or asthma, small airway involvement must be assessed using currently available tools. In patients with subotpimal disease control and/or functional or biological signs of disease activity, the role of small airway involvement should be assessed and treatment tailored. Therefore, the choice between large- and small-particle inhaled formulations must reflect the physician’s considerations of disease features, phenotype, and response to previous therapy. This article is being co-published in Asthma Research and Practice and the World Allergy Organization Journal

ARIA 2016: Care pathways implementing emerging technologies for predictive medicine in rhinitis and asthma across the life cycle

The Allergic Rhinitis and its Impact on Asthma (ARIA) initiative commenced during a World Health Organization workshop in 1999. The initial goals were (1) to propose a new allergic rhinitis classification, (2) to promote the concept of multi-morbidity in asthma a

GM-CSF Induction in Human Lung Fibroblasts by IL-1 β

Fibroblast-derived cytokines may play crucial roles in airway inflammation. In this study, we analyzed expression of the inflammatory cytokine, granulocyte-macrophage colony-stimulating factor (GM-CSF), a major eosinophilopoietin, by normal human lung fibroblast (NHLF) cells and its regulation by monokines and macrophage contact. NHLFs were stimulated with interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) and were cocultured with the U937 myelomonocytic cell line. The expression of GM-CSF transcripts was analyzed by reverse transcription-polymerase chain reaction (RT-PCR), and GM-CSF protein was detected by ELISA. Nuclear translocation of nuclear factor-κB (NF-κB), an important transcription factor for inflammatory gene expression, was assessed by electrophoretic mobility shift assay (EMSA). Both IL-1β and TNF-α significantly enhanced the production of GM-CSF by NHLF. Coculturing of peripheral blood mononuclear cells (PBMC) with NHLF induced GM-CSF expression. This phenomenon was also seen on coculturing U937 cells or membranes derived from U937 with NHLF but was inhibited when the two types of cells were separated, suggesting a need for cell-cell contact. U937 membranes, as well as IL-1β and TNF-α, induced nuclear translocation of NF-κB. These data support a prominent role for macrophage-fibroblast interactions in airway inflammation and fibrosis