Login to your account

Username *
Password *
Remember Me

Blog With Right Sidebar

    Vous êtes ici :  
  1. Accueil
  2. Blog With Right Sidebar

Family history is a risk factor for chronic obstructive pulmonary disease.

Studies have shown that family history is a risk factor for chronic obstructive pulmonary disease (COPD), but they have not accounted for family history of smoking. Therefore, we sought to identify the effects of family history of smoking and family history of COPD on COPD susceptibility.

METHODS: We compared 821 COPD cases to 776 control smokers from the COPDGene Study. Questionnaires captured parental histories of smoking and COPD, as well as childhood environmental tobacco smoke (ETS) exposure. Socioeconomic status was defined by educational achievement.

RESULTS: Parental history of smoking (85.5% cases, 82.9% controls) was more common than parental history of COPD (43.0% cases, 30.8% of controls). In a logistic regression model, parental history of COPD (OR 1.73, p<0.0001) and educational level (OR 0.48 for some college vs. no college, p<0.0001) were significant predictors of COPD, but parental history of smoking and childhood ETS exposure were not significant. The population attributable risk from COPD family history was 18.6%. COPD cases with a parental history had more severe disease, with lower lung function, worse quality of life, and more frequent exacerbations. There were non-significant trends for more severe emphysema and airway disease on quantitative chest CT scans.

CONCLUSIONS: Family history of COPD is a strong risk factor for COPD, independent of family history of smoking, personal lifetime smoking, or childhood ETS exposure. While further studies are required to identify genetic variants which influence COPD susceptibility, clinicians should question all smokers, especially those with known or suspected COPD, regarding COPD family history.

Airway Inflammation is Augmented by Obesity and Fatty Acids in Asthma.

Obesity and asthma are associated, however the mechanism(s) are yet to be elucidated.

The aim of this study was to assess airway inflammation in relation to obesity and plasma fatty acids in males and females with and without asthma. Obese (n=68) and non-obese (n=47) adults with asthma, and obese (n=16) and non-obese (n=63) healthy controls had induced sputum and venous blood samples analysed for inflammatory markers.

There was a positive interaction between obesity and asthma on %sputum neutrophils (p=0.012) and CRP (p=0.003). Although sputum %eosinophils were elevated in asthma (p=0.001), there was no effect of obesity (p=0.16). Sputum %neutrophils were positively associated with BMI in asthmatic females (β[95%CI] =1.015[0.258,1.772], p=0.009) and neutrophilic asthma was present in a greater proportion of obese compared to non-obese females (42.9 vs 16.2%, p=0.017). In asthmatic males, sputum %neutrophils were positively associated with total plasma saturated fatty acids (β[95%CI] = 0.108[0.036,0.180], p=0.004) and negatively with monounsaturated fatty acids (β[95%CI] = -0.068[-0.131,-0.005], p=0.035).

This is the first study to demonstrate an increase in neutrophilic airway inflammation in obese asthma. This relationship was only significant in asthmatic females. In males, saturated and monounsaturated fatty acids were important predictors of neutrophilic airway inflammation in asthma.

Increased arginase activity contributes to airway remodelling in chronic allergic asthma.

Airway remodelling, characterized by increased airway smooth muscle (ASM) mass, subepithelial fibrosis, goblet cell hyperplasia and mucus gland hypertrophy, is a feature of chronic asthma. Increased arginase activity could contribute to these features via increased formation of polyamines and l-proline downstream of the arginase product l-ornithine, and via reduced nitric oxide synthesis.

Using the specific arginase inhitibor 2(S)-amino-6-boronohexanoic acid (ABH), we studied the role of arginase in airway remodelling using a guinea pig model of chronic asthma. Ovalbumin-sensitized guinea pigs were treated with ABH or PBS via inhalation before each of 12 weekly allergen or saline-challenges, and indices of arginase activity and airway remodelling, inflammation and responsiveness were studied 24&emsp14;h after the last challenge. Pulmonary arginase activity of repeatedly allergen-challenged guinea pigs was increased. Allergen challenge also increased ASM mass and maximal contraction of denuded tracheal rings, which were prevented by ABH. ABH also attenuated allergen-induced pulmonary hydroxyproline (fibrosis) and putrescine, mucus gland hypertrophy, goblet cell hyperplasia, airway eosinophilia and IL-13, whereas an increased L-ornithine/L-citrulline ratio in the lung was normalized. Moreover, allergen-induced hyperresponsiveness of perfused tracheae was fully abrogated by ABH.

These findings demonstrate that arginase is prominently involved in allergen-induced airway remodelling, inflammation, and hyperresponsiveness in chronic asthma.

Vitamin D and responses to inhaled fluticasone in severe chronic obstructive pulmonary disease.

Patients with chronic obstructive pulmonary disease (COPD) demonstrate variable responses to inhaled corticosteroids (ICS). The factors contributing to this variability are not well understood. Data from patients with asthma have suggested that low 25-hydroxyvitamin D [25(OH)D] levels contribute to a lack of ICS response in asthma.

The objective of this study was to determine whether serum levels of 25(OH)D were related to ICS responses in patients with COPD.

Recognising the risk of aspirin-sensitive respiratory disease in an asthmatic patient who has previously tolerated aspirin.

Asthma is a common chronic condition composed of numerous different phenotypes. One clinically relevant phenotype is that of aspirin-sensitive respiratory disease (ASRD) which is more frequently seen in patients with difficult asthma. Reliance on a history of previous reaction to non-steroidal anti-inflammatory drugs (NSAIDs) in order to diagnose ASRD may give false reassurance.

We describe the case of a 58-year old man with late onset asthma who was suspected to have ASRD on the basis of associated clinical features despite having taken aspirin safely in the past. The diagnosis of ASRD was subsequently confirmed by an inadvertent aspirin challenge which led to a serious adverse asthma outcome.

Search

Search