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Thrombocytosis is associated with increased short and long term mortality after exacerbation of chronic obstructive pulmonary disease: a role for antiplatelet therapy?

Introduction

Evidence suggests that platelets play a significant role in inflammation in addition to their role in thrombosis. Systemic inflammation is linked to poor short and long term outcomes in COPD. Increased platelet activation has been reported in acute exacerbations of COPD (AECOPD). We investigated whether thrombocytosis is independently associated with poor outcomes following AECOPD.

 Methods

An observational cohort study of patients hospitalised with AECOPD was performed. Patients were >40 years with spirometry confirmed COPD admitted between 2009 and 2011. Platelet count was recorded on admission. The primary outcome was 1-year all-cause mortality. Secondary outcomes included inhospital mortality and cardiovascular events. Analyses were conducted using logistic regression after adjustment for confounding variables.

 Results

1343 patients (49% male) were included. Median age was 72 years (IQR 63–79 years). 157 (11.7%) had thrombocytosis. Thrombocytosis was associated with both 1-year mortality and inhospital mortality; OR 1.53 (95% CI 1.03 to 2.29, p=0.030) and OR 2.37 (95% CI 1.29 to 4.34, p=0.005), respectively. Cardiovascular hospitalisation was not significantly increased (OR 1.13 (95% CI 0.73 to 1.76, p=0.600)) in patients with thrombocytosis. Aspirin or clopidogrel treatment correlated with a reduction in 1-year mortality (OR 0.63 (95% CI 0.47 to 0.85, p=0.003)) but not inhospital mortality (OR 0.69 (95% CI 0.41 to 1.11, p=0.124)).

 Conclusions

After adjustment for confounders thrombocytosis was associated with increased 1-year mortality after exacerbation of COPD. Antiplatelet therapy was associated with significantly lower 1-year mortality and may have a protective role to play in patients with AECOPD.

The impact of azithromycin therapy on the airway microbiota in asthma

Introduction

There is interest in the use of macrolide antibiotics in asthma. Macrolides have been shown to improve airway hyper-responsiveness (AHR) and measures of airway inflammation.1 The degree of AHR may relate to the microbiota present in the airways,2 with a recent study reporting that patients with asthma with a significant improvement in AHR following treatment with clarithromycin had a higher bacterial diversity prior to treatment.3 To our knowledge, the impact on the asthmatic airway microbiota of an antibiotic has not been reported and we therefore set out to establish if macrolide therapy was associated with a change in airway microbiota in asthma.

 Methods

Five adult patients with moderate/severe asthma (British Thoracic Society step 4–5) (see online supplementary table S1) and no evidence of respiratory infection or bronchiectasis underwent bronchoscopy before and after 6 weeks of daily 250 mg azithromycin therapy. Patients...

The devastating power of platelets in COPD exacerbations: can aspirin save lives in COPD?

The human and societal burden of COPD is alarming. Despite large reductions in smoking rates across industrialised nations, COPD mortality has increased by 60% over the past 20 years, making it the second leading cause of morbidity and mortality in the USA and elsewhere.1 Most of the COPD-related deaths occur during or shortly following acute exacerbations (or ‘lung attacks’). Unfortunately, severe lung attacks are common, with one in six patients requiring hospitalisation for urgent care each year.2 Despite best therapy, 1 in 12 of these patients will succumb to their disease in hospital.3 Even those who survive will experience persistent morbidity from their recent lung attack and never regain their lost health status. Furthermore, one in three patients will have another lung attack in 6–12 months.3 Regrettably, acute and chronic treatments for COPD are suboptimal. Despite global drug expenditures that exceed $36 billion...

Improving Adherence for Management of Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

Related Articles

Clinical practice guidelines recommend 40-60 mg of prednisone equivalent for 10-14 days for patients with acute exacerbations of chronic obstructive pulmonary disease (COPD). However, the amount of corticosteroid prescribed varies widely in clinical practice. Using the electronic health record (EHR), we implemented an evidence based orderset to standardize treatment of patients hospitalized with acute exacerbations of COPD.

METHODS: This is a pre- and post- intervention study on patients hospitalized between January 1, 2009 and September 30, 2012 with primary discharge diagnosis of COPD (ICD-9 code: 491.xx, 492.xx and 496) and receipt of at least one dose of corticosteroid at our tertiary care hospital. Data on baseline demographics, dose of corticosteroid in prednisone equivalent administered during the first 48 hours and during the entire hospitalizations were collected from the electronic health record. Evidence-based guidelines were used to build and implement acute exacerbations of COPD management electronic ordersets in our electronic health record, Epic(®). We divided the study into two time periods (January 1, 2009 through February 28, 2011 as pre- (n= 203) and March 1, 2011 through September 30, 2012 as post-intervention periods (n=217)). The primary outcome measure was corticosteroid dose administered in the first 48 hours. Secondary outcome measures were corticosteroid dosage during the entire hospitalization, length of stay, hospital follow-up rates, and 30-day readmission rates.

RESULTS: A total of 420 patients with acute exacerbations of COPD were included in the study. In the post-intervention period, the median amount of corticosteroid used in the first 48 hours was significantly reduced (306.2 mg vs. 156.25 mg, p<0.0001), as was that used during the entire hospitalization (352.5 mg vs. 175 mg, p<0.0001). There was no difference in hospital follow-up rates, length of stay, or 30-day readmission rates between the two periods.

CONCLUSIONS: Evidence-based electronic ordersets improve compliance with clinical practice guidelines and reduce the total dose of corticosteroid administered in patients hospitalized with acute exacerbations of COPD.

Oxidative stress and lung function profiles of male smokers free from COPD compared to those with COPD: a case-control study.

Oxidative StressThe mechanisms of smoking tobacco leading to chronic obstructive pulmonary disease (COPD) are beginning to be understood. However, conclusions about the role of blood or lung oxidative stress markers were disparate.

Aims: To investigate the oxidative stress in blood or lung associated with tobacco smoke and to evaluate its effect on pulmonary function data and its relation with physical activity.

Methods: It is a case-control study. Fifty-four male-smokers of more than five pack-years (PY) and aged 40-60 years were included (29 Non-COPD, 16 COPD). Physical activity score was determined. Blood sample levels of malondialdehyde (MDA), protein-cys-SH (PSH), and Glutathione (GSH) were measured. Fractional exhaled nitric oxide (FeNO) and plethysmographic measurements were performed. Correlation coefficients (r) evaluated the association between oxidative stress markers and independent variables (plethysmographic data and physical activity score).

Results: Non-COPD (48±6 years) and COPD (49±5 years) groups had similar tobacco consumption patterns, that is, 27±14 PY versus 30±19 PY, respectively. Compared to the Non-COPD group, the COPD group had significantly lower levels of GSH and PSH, that is, mean±SE were 40±6 versus 25±5 µg/mL and 54±10 versus 26±5 µg/g of hemoglobin, respectively. However, MDA level and FeNO values were similar. In the COPD group, none of the oxidative stress markers was significantly correlated with plethysmographic data or physical activity score. In the Non-COPD group, GSH was significantly correlated with physical activity score (r = 0.47) and PSH was significantly correlated with total lung capacity (TLC) (r=-0.50), residual volume (r = 0.41), and physical activity score (r = 0.62). FeNO was significantly correlated with TLC of the COPD group (r=-0.48).

Conclusion: Compared to the Non-COPD group, the COPD group had a marked decrease in blood antioxidant markers (GSH and PSH) but similar blood oxidant (MDA) or lung (FeNO) burden.

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