Impact of Air Pollution and Outdoor Temperature on the Rate of Chronic Obstructive Pulmonary Disease Exacerbations.

BACKGROUND: Environmental pollution can be one of the main risk factors for acute exacerbations of chronic obstructive pulmonary disease (COPD). AIM: To study the relationship between air pollution, outdoor temperature and exacerbations of COPD. MATERIALS AND METHODS: COPD patients (n=1432) were followed up for one year. The levels of particulate matter up to 10 µm (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2) and outside temperatures were collected from the Environmental Agency database. RESULTS: A total of 309 acute COPD exacerbations (AECOPD) were recorded in the analysis. The daily mean concentrations of PM10 were found to correlate significantly with the daily mean concentrations of NO2 and SO2 (ρ 0.34 and ρ 0.49, respectively; p=0.0001). The negative correlations between the daily mean temperature and the daily mean levels of PM10, NO2 and SO2 were also significant (ρ -0.44, ρ -0.11, and ρ -0.37, respectively; p=0.0001). The daily number of AECOPD correlated with the mean levels of PM10 in the previous six days (ρ 0.14; p=0.02) and the lower outdoor temperature (ρ -0.2; p=0.001). The negative correlation between the daily number of AECOPD and the mean daily temperature was stronger in days with levels of PM10 above 50 µg/m3 (ρ -0.3 p=0.02 vs. ρ -0.18 p= 0.01). CONCLUSION: Lower daily mean temperatures were associated with the levels of air pollutants. The level of PM10 correlated with the levels of the other air pollutants. The daily number of AECOPD was found to correlate weakly, but signifi cantly with the mean level of PM10 in the previous six days.

Stability of Frequent Exacerbator Phenotype in Patients with Chronic Obstructive Pulmonary Disease.

BACKGROUND: At present, there is little information in Bulgaria regarding the rate and stability of frequent-exacerbation phenotype in COPD patients. AIM: To study the rate and stability of frequent-exacerbation phenotype in COPD patients. MATERIALS AND METHODS: We followed up 465 COPD patients for exacerbations over a 3-year period. Exacerbations were defined as events that resulted in treatment with antibiotics and/or corticosteroids (moderate), or that led to hospitalization (severe). RESULT: Approximately 10% of the patients had two or more exacerbations per year (frequent-exacerbation phenotype), and this structure stayed stable over the study period. The exacerbation rate in the first year of follow up was 0.33 per stage I COPD patients (according to GOLD stages), 0.49 per stage II COPD patients; 0.69 - for stage III, and 1.06 for stage IV COPD patients. The frequent-exacerbation rate increased from stage I to stage IV by 4.35%, 9.17%, 10.79%, and 20.97%, respectively. A history of previous year exacerbations increased the risk of new exacerbations: with a history of one exacerbation - OR 2.1820 (95% CI: 1.4018 to 3.3965, p = 0.0005), and with a history of two exacerbations - OR 4.6460 (95% CI: 2.3286 to 9.2696; p < 0.0001). The frequent-exacerbation phenotype appeared to be unstable over the study period - up to 33% from those patients stayed in the phenotype for the next year. CONCLUSIONS: The exacerbation frequency and the rate of frequent-exacerbation phenotype increases with COPD progression. History of exacerbations in the previous year is a significant risk factor for exacerbations of COPD. The frequent-exacerbation phenotype appeared to be unstable over the study period. The pheno-type of non-exacerbators was more likely to remain stable over time.

Impact of thrombophilic genetic factors on pulmonary embolism: early onset and recurrent incidences.

The importance of genetic thrombophilic factors in the development of venous thromboembolism has been increasingly recognized. Factor V Leiden (FVL), prothrombin gene mutation G20210A (FII G20210), genetic variant C677T of the methylentetrahydrofolate reductase (MTHFR), as well as the polymorphism A2 (PlA2) in platelet glycoprotein IIb/IIIa were recently discussed. We analyzed the contribution of genetic thrombophilic factors to the pathogenesis of pulmonary embolism (PE) and their association with the early onset and recurrence of PE using DNA analysis methods. In this case control trial we found thrombophilic genetic variants in 58.8% of 51 patients with PE. FVL was found in 23.5% of the patients versus 7.1% of the 98 controls (p=0.01), PlA2 IIb/IIIa was found in 35.3% vs. 14.3% (p=0.03), and FII G20210A was found in 5.9% vs. 2.0% (NS). Patients with recurrent PE had a very high prevalence of genetic factors, 70.4%. High prevalence of FVL was found in patients under 45 years of age: 39.3% (OR=14.23, 95% CI=1.58-330.03, p=0.01) as well as in patients with recurrent incidence (37%, OR=7.647, 95% CI=2.27-26.44, p=0.001). FVL was also significantly higher in the subgroup of patients with PE combined with deep venous thrombosis (OR=6.500, 95% CI=1.81-23.76, p=0.002) in comparison with patients with isolated PE (OR=2.261, 95% CI=0.50-9.69). The carriers of FVL are at higher risk for early and recurrent PE events. High prevalence of PlA2 in PE patients evidently shows the impact of this polymorphism in PE development. A different treatment should be considered in carriers of thrombophilic defects.