Introduction : Hemoptysis is observed frequently in patients, although chest computed tomography (CT) shows no explainable lesion as the cause of hemoptysis. However, the clinical course of these patients has not been reported fully.

Methods : This study included patients who visited Seoul National University Hospital and Seoul National University Bundang Hospital to be treated for hemoptysis from January 2003 through October 2009 and who had no lesion causing hemoptysis in chest CT. We retrospectively analyzed their bronchoscopic and clinical findings.

Results : A total of 228 patients were included, and the mean follow-up duration was 781 days. All patients underwent bronchoscopy. The bronchoscopic findings of 191 patients (83.8%) were negative for hemoptysis and showed the possible causes of bleeding in 37 patients (16.2%). Forty-three of the 191 patients with negative bronchoscopic findings had oronasopharyngeal problems or were using anticoagulants. After excluding these 43 patients, hemoptysis recurred in 29 (19.6%) of the remaining patients. Thirteen of the patients whose bronchoscopic findings identified the possible causes of bleeding (35.1%) experienced recurrence. Only one patient (0.4%) was diagnosed with lung cancer by the initial bronchoscopy, and no patient developed malignancy during the follow-up period.

Conclusion : The recurrence rate was higher in the patients with positive findings than in the patients with negative findings on bronchoscopy. Although about 20% of patients with negative bronchoscopy findings experienced recurrence, the clinical course of those in whom recurrent bleeding occurred was usually benign.

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For outpatients with pneumonia, guidelines recommend empiric antibiotics and some suggest macrolides are preferred agents. We hypothesized that both guideline-concordant antibiotics and macrolides would be associated with reduced mortality.

Methods : All outpatients with pneumonia assessed at 7 Emergency Departments in Edmonton, Alberta, Canada were enrolled in a population-based registry that included clinical-radiographic data, Pneumonia Severity Index (PSI) and treatments. Guideline-concordant regimens included macrolides and respiratory fluoroquinolones; other regimens were “discordant”. Main outcome was 30-day all-cause mortality.

Results : The study included 2973 outpatients; mean age 51 years, 47% female, most had mild pneumonia (73% PSI Class I–II). Over 30-days, 38 (1%) patients died, 228 (8%) were hospitalized, and 253 (9%) reached the endpoint of death or hospitalization. Most (2845 [96%]) patients received guideline-concordant antibiotics. Compared to patients receiving discordant antibiotics, those receiving guideline-concordant antibiotics were less likely to die within 30-days (8 [6%] versus 30 [1%], adjusted OR 0.23, 95% CI 0.09–0.59,p = 0.002). Within the guideline-concordant subgroup, compared to the 947 (33%) patients treated with fluoroquinolones, those receiving macrolides [1847 (64%)] were less likely to die (25 [3%] versus 4 [0.2%], adjusted OR 0.28, 95% CI 0.09–0.86,p = 0.03).

Conclusions : In outpatients with pneumonia, treatment with guideline-concordant antibiotics and macrolides were both associated with mortality reduction.

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There are only a few studies assessing the relationship between adherence rate to ICS, as assessed by electronic monitoring, and the level of asthma control in childhood. The present study was carried out to examine the relationship between adherence to beclomethasone diproprionate (BDP) as well as other factors related to poor asthma control.

In this prospective cohort study, 102 steroid naïve randomly selected subjects with persistent asthma, aged 5–14 years were prescribed 500–750 μg daily of BDP-CFC and followed during one year. Adherence to BDP was measured electronically in the 4th, 8th and 12th months of study. The level of asthma control was classified as either controlled or uncontrolled instead of the current three categories recommended by the Global Initiative for Asthma (GINA). Mean adherence rate was higher in patients with controlled asthma during follow-up, but went down from 60.4% in the 4th month to 49.8% in the 12th month (p = 0.038). Conversely, among patients with uncontrolled asthma, the mean adherence rate decreased from 43.8% to 31.2% (p = 0.001). Multivariate analysis showed that the level of asthma control was independently associated to the adherence rate in all follow-up visits (p-values equal or lower than 0.005).

The level of asthma control was directly proportional to adherence rate. Our results suggest that a BDP daily dose by 300 μg seems to be enough to attain control over mild and moderate persistent asthma, including exercise induced asthma.

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Asthma and COPD are two chronic inflammatory disorders of the airway characterized by airflow limitation. While many similarities exist between these two diseases, they are pathologically distinct due to the involvement of different inflammatory cells; predominantly neutrophils, CD8 lymphocytes in COPD and eosinophils and CD4 lymphocytes in asthma.

Cigarette smoking is associated with accelerated decline of lung function, increased mortality, and worsening of symptoms in both asthma and COPD. Furthermore, exposure to cigarette smoke can alter the inflammatory mechanisms in asthma to become similar to that seen in COPD with increasing CD8 cells and neutrophils and may therefore alter the response to therapy. Cigarette smoke exposure has been associated with a poor response to inhaled corticosteroids which are recommended as first line anti-inflammatory medications in asthma and as an add-on therapy in patients with severe COPD with history of exacerbations. While the main proposed mechanism for this altered response is the reduction of the histone deacetylase 2 (HDAC2) enzyme system, other possible mechanisms include the overexpression of GR-β, activation of p38 MAPK pathway and increased production of inflammatory cytokines such as IL-2, 4, 8, TNF-α and NF-Kß.

Few clinical trials suggest that leukotriene modifiers may be an alternative to corticosteroids in smokers with asthma but there are currently no drugs which effectively reduce the progression of inflammation in smokers with COPD.

However, several HDAC2 enhancers including low dose theophylline and other potential anti-inflammatory therapies including PDE4 inhibitors and p38 MAPK inhibitors are being evaluated.

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