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Airway inflammation and bronchial hyperreactivity in steroid naive children with intermittent and mild persistent asthma.

Pediatr Pulmonol. 2013 Jun 24;

Authors: Toyran M, Bakirtas A, Dogruman-Al F, Turktas I

Abstract
BACKGROUND: Intermittent and mild persistent asthma are defined according to symptom frequency and spirometry and treated differently. To our knowledge, there is no study comparing airway inflammation between intermittent and mild persistent asthmatic children.
MATERIALS AND METHODS: Children aged 7-16 years, referred to our pediatric allergy clinic for recurrent respiratory complaints underwent a detailed clinical history and spirometry with reversibility. None of the subjects had been using regular anti-inflammatory treatment. After a 2-week run-in period during which asthma symptoms were recorded, exhaled NO measurement, bronchial provocation test with adenosine monophosphate and methacholine and sputum induction were performed. Data of patients with intermittent and mild persistent asthma and a control group were compared.
RESULTS: Thirty intermittent, 26 mild persistent asthmatic children, and 21 control subjects were studied. Sputum was obtained from 19 of intermittent asthmatics (63.3%), 18 of mild persistent asthmatics (69.2%), and 13 of control subjects (61.9%). Eosinophil count and exhaled nitric oxide were not different between asthmatic groups. Neutrophil count of children with mild persistent asthma was higher than the intermittent asthmatic group (P = 0.003). Geometric mean of PC20 methacoline values were not different between groups (P = 0.058). Geometric mean of PC20 AMP was lower among patients with mild persistent asthma (P = 0.102).
CONCLUSION: Eosinophilic airway inflammation and direct BHR may not be significantly different in intermittent asthmatic children from their peers with mild persistent disease. Neutrophilic airway inflammation and BHR to an indirect stimuli are more pronounced in the mild persistent group. Pediatr Pulmonol. © 2013 Wiley Periodicals, Inc.

PMID: 23798479 [PubMed - as supplied by publisher]

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Natural killer cells in asthma.

Front Immunol. 2013;4:159

Authors: Karimi K, Forsythe P

Abstract
The worldwide prevalence, morbidity, and mortality of asthma have dramatically increased over the last few decades and there is a clear need to identify new effective therapeutic and prophylactic strategies. Despite high numbers of NK cells in the lung and their ability to generate a variety of immunomodulatory mediators, the potential of NK cells as therapeutic targets in allergic airway disease has been largely overlooked. The fact that IgE, acting through FcγRIII, can activate NK cells resulting in cytokine/chemokine production implies that NK cells may contribute to IgE-mediated allergic responses. Indeed, current evidence suggests that NK cells can promote allergic airway responses during sensitization and ongoing inflammation. In animal models, increased NK cells are observed in the lung following antigen challenge and depletion of the cells before immunization inhibits allergic airway inflammation. Moreover, in asthmatics, NK cell phenotype is altered and may contribute to the promotion of a pro-inflammatory Th2-type environment. Conversely, driving NK cells toward an IFN-γ-secreting phenotype can reduce features of the allergic airway response in animal models. However, we have limited knowledge of the signals that drive the development of distinct subsets and functional phenotypes of NK cells in the lung and thus the role and therapeutic potential of NK cells in the allergic airway remains unclear. Here we review the potentially diverse role of NK cells in allergic airway disease, identify gaps in current knowledge, and discuss the potential of modulating NK cell function as a treatment strategy in asthma.

PMID: 23801996 [PubMed - in process]

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Cough in chronic obstructive pulmonary disease: is it important and what are the effects of treatment?

Cough. 2013 Jun 24;9(1):17

Authors: Calverley PM

Abstract
Over the last 40 years the assessment and treatment of chronic obstructive pulmonary disease has focused primarily on airflow obstruction with little significance given to the problem of cough. The reasons for this include a view that cough arises simply from the direct irritant and inflammatory effect of cigarette smoke or the presence of excess mucus in the airways. Doubt that cough is of any consequence to patients or responsive to current therapies has reinforced this opinion. At odds with this is the emerging evidence that cough impacts adversely on patients' health status and forms an important component of recently validated quality of life instruments. This article presents the arguments why the assessment and treatment of cough should have a more prominent place in the clinical management of COPD.

PMID: 23799979 [PubMed - as supplied by publisher]

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Oxygen supplementation in noninvasive home mechanical ventilation: the crucial roles of CO2 exhalation systems and leakages.

Respir Care. 2013 Jun 25;

Authors: Storre JH, Huttmann SE, Ekkernkamp E, Walterspacher S, Schmoor C, Dreher M, Windisch W

Abstract
BACKGROUND:: When supplemental oxygen is added to noninvasive positive pressure ventilation (NPPV) using non-ICU ventilators, it is usually introduced with a preset flow rate into the ventilatory circuit at a site next to the ventilator; however, the impact of different CO2 exhalation systems and leaks on actual inspired FiO2 and gas exchange has not been elucidated.
METHODS:: In a randomized, open-label, four-treatment (two-by-two), four-period crossover design, four daytime measurements (60 minutes each) were performed in 20 patients receiving home mechanical NPPV plus ≥2 L O2/min inserted proximally to the ventilator: active valve circuit or leak port circuit with or without artificial leakage (4mm I.D.). FiO2 at the ventilator, FiO2 at the mask, and blood gases were measured.
RESULTS:: Overall, FiO2-mask (29±5%) was lower compared to FiO2-ventilator (34±4%), with a mean (95%CI) difference of 5.1 (4.2 to 5.9, p<0.0001)%. With the leak port circuit, FiO2-mask decreased by 3.2 (2.6 to 3.9, p<0.0001)% when compared to the active valve circuit. When artificial leakage was introduced into the circuit, FiO2-mask decreased by 5.7 (5.1 to 6.4, p<0.0001)%, PaO2 by 10.4 (3.1 to 17.7, p=0.006) mmHg, and PCO2 increased by 1.8 (0.5 to 3.3, p=0.008) mmHg.
CONCLUSIONS:: The use of leak port circuits and the occurrence of leakages around the interface significantly reduce FiO2-mask and negatively impact on gas exchange in patients receiving home mechanical NPPV and supplemental oxygen.
REGISTERED AT:: German Clinical Trials Register (DRKS); www.drks.de REGISTRATION NUMBER:: DRKS00000449.

PMID: 23801785 [PubMed - as supplied by publisher]