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Secondhand Smoke Exposure and Elastin Degradation

Background:

Tobacco smoke is a major risk factor in the development of COPD. Secondhand smoke (SHS) exposure is a known risk factor in asthma, bronchitis, and coronary artery disease. Elastin is a recognized target for injury in COPD, and the amino acids desmosine and isodesmosine (D/I), which are specific for elastin degradation, are elevated in COPD. This study determined whether exposure to SHS affects elastin degradation in asymptomatic individuals.

 Methods:

Two cohorts of asymptomatic individuals without evidence of respiratory or circulatory disease, exposed to SHS, were studied. Both cohorts comprised normal nonsmokers, active smokers, and those exposed to SHS. D/I were measured in plasma and quantified by high-performance liquid chromatography and tandem mass spectrometry by published methods. Plasma cotinine, a metabolite of nicotine, was also measured.

 Results:

In each cohort, the levels of D/I in plasma were statistically significantly higher in secondhand-smoke-exposed subjects than in the normal nonexposed subjects. Smokers had the highest levels of D/I but their levels were not statistically significantly higher than those of the secondhand-smoke-exposed. Cotinine levels were elevated in secondhand-smoke-exposed subjects and active smokers but not in most nonsmoking control subjects.

 Conclusions:

Results indicate a tissue matrix effect of degradation of body elastin from SHS exposure and possible lung structure injury, which may result in COPD. Long-term studies of individuals exposed to SHS for the development of COPD are warranted.

Daily exhaled nitric oxide measurements and asthma exacerbations in children

Background: Fractional exhaled Nitric Oxide (FeNO) is a biomarker for eosinophilic airway inflammation and can be measured at home on a daily basis. A short-term increase in FeNO may indicate a higher risk of future asthma exacerbations.

Objective: To assess changes in FeNO before and after asthma exacerbations compared to a stable control period.

Methods: A post hoc analysis was performed on daily FeNO measurements over 30 weeks in children with asthma (n = 77). Moderate exacerbations were defined by an increase in symptom scores and severe exacerbations by prescription of prednisone. Individual mean and maximum FeNO, the variability of FeNO assessed by the coefficient of variation (CV), and slopes of FeNO in time were all quantified in 3-week blocks. Cross-correlation of FeNO with symptoms and autocorrelation of FeNO were assessed in relation to exacerbations and examined as predictors for exacerbations compared to reference periods using logistic regression.

Results: Fractional exhaled nitric oxide could be assessed in relation to 25 moderate and 12 severe exacerbations. The CV, slope, cross-correlation, and autocorrelation of daily FeNO increased before moderate exacerbations. Increases in slope were also randomly seen in 19% of 2-week blocks of children without exacerbations. At least 3–5 FeNO measurements in the 3 weeks before an exacerbation were needed to calculate a slope that could predict moderate exacerbations. No specific pattern of FeNO was seen before severe exacerbations.

Conclusion: Fractional exhaled nitric oxide monitoring revealed changes in FeNO prior to moderate exacerbations. Whether this can be used to prevent loss of asthma control should be further explored.

Persistent asthma, comorbid conditions and the risk of work disability: a prospective cohort study

This study examined whether asthma alone or together with chronic comorbidity is associated with an increased risk of long-term work disability.

Methods:  We examined data from 2332 asthmatic and 66 354 nonasthmatic public sector employees in Finland who responded to a survey between 1997 and 2004. Respondents were coded as persistent asthmatics based on the special reimbursement for continuous asthma medication by the Social Insurance Institution. Data on long-term work disability (sickness absences or disability pensions >90 days) were obtained from national registers. The risk of work disability was examined by Cox proportional hazard models adjusted for age, gender, socioeconomic status, type of employment contract, and type of employer.

Results:  Asthma increased the risk of all-cause long-term work disability with hazard ratio (HR) 1.8 (95% CI 1.62–2.09) compared with controls (no asthma). Asthma and one other chronic comorbidity increased the risk of long-term all-cause work disability with HR 2.2 (95% CI 1.78–2.83). Asthma together with two or more other chronic conditions increased the risk with HR 4.5 (95% CI 2.98–6.78). Asthma and depression increased the risk with HR 3.6, and the risk was especially high for permanent work disability (HR 6.8). Among those with asthma, there were more women, obese individuals (BMI ≥30), ex-smokers, and lower-grade nonmanual workers.

Conclusions:  Asthma is associated with an increased risk of long-term all-cause work disability. The risk increases further with chronic comorbidities and is especially high in patients with asthma and depression.

Late Intervention with a Myeloperoxidase Inhibitor Stops Progression of Experimental COPD.

CONCLUSIONS: We conclude that an MPO inhibitor is able to stop progression of emphysema and small airway remodeling and to partially protect against pulmonary hypertension, even when treatment starts relatively late in the course of a long-term smoke exposure, suggesting that inhibition of MPO may be a novel and useful therapeutic treatment for COPD. Protection appears to relate to inhibition of oxidative damage and downregulation of the smoke-induced inflammatory response. PMID: 21997333 [PubMed - as supplied by publisher] (Source: American Journal of Respiratory and Critical Care Medicine)

Doubling Times and CT Screen Detected Lung Cancers in the Pittsburgh Lung Screening Study (PLuSS).

CONCLUSION: Volumetric analysis of CT detected lung cancers is particularly useful in AC/BAC. Prevalent cancers have a significantly slower DT than non-prevalent cancers and a higher % of AC/BAC. These results should impact the management of indeterminant lung nodules detected on screening CT scans. PMID: 21997335 [PubMed - as supplied by publisher] (Source: American Journal of Respiratory and Critical Care Medicine)

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