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Biomedical subjects

P-R Burgel

Publications and source records attributed to P-R Burgel.

8 recordsLinked to original sources
PubMed2006

[Antibiotics for acute exacerbations of chronic obstructive pulmonary disease (COPD)].

OBJECTIVE: This study had for aim to evaluate the rationale and indications for antibiotic treatment in acute exacerbations of COPD and to identify potential differences among various antibiotics available for the treatment of exacerbations in France. METHODS: A search was performed in Medline and for references quoted in identified articles from 1995 to 2005. Open or blind randomized studies involving antibiotics available in France were reviewed. RESULTS: About 50% of all exacerbations are related to bacterial infection. Haemophilus influenzae, Moraxella catarrhalis and Streptococcus pneumoniae are the main pathogens responsible for bacterial exacerbations. Pseudomonas aeruginosa and enterobacter spp are frequently found in patients with severe functional impairment. Increased purulence of sputum is associated with bacterial infection. Patients with severe functional impairment benefit the most from antibiotic treatment. Although new molecules have larger antibiotic spectrum and better pharmacological properties, the evidence supporting their use compared to standard therapy remains scarce. CONCLUSIONS: Additional studies are needed to better identify the subset of patients benefiting from antibiotics and to determine whether new molecules produce significant improvement on relevant outcomes such as exacerbation free interval compared to standard therapy.

Acute Disease↗
PubMed2005

[Asthma 2005].

Explore the source record for details and available documents.

Asthma↗
PubMed2004

Roles of epidermal growth factor receptor activation in epithelial cell repair and mucin production in airway epithelium.

The epithelial cells lining the airways serve protective functions. The "barrier function" of the epithelium protects the individual from damage by inhaled irritants. The epithelium produces mucins which become hydrated and form a viscoelastic gel which spreads over the epithelial surface. In healthy individuals inhaled foreign materials become entrapped in the mucus and are cleared by mucociliary transport and by coughing. In many chronic inflammatory airway diseases, however, excessive mucus is produced and is inadequately cleared, leading to mucous obstruction and infection. At present there is no specific treatment for hypersecretion. However, the discovery that an epidermal growth factor receptor (EGFR) cascade is involved in mucin production by a wide variety of stimuli suggests that blockade may provide specific treatment for hypersecretory diseases. EGFR pathways have also been implicated in the repair of damaged airway epithelium. The roles of EGFR in airway epithelial cell hypersecretion and epithelial damage and repair are reviewed and future potential treatments are suggested.

Bronchi↗
PubMed2004

Intranasal steroids decrease eosinophils but not mucin expression in nasal polyps.

Increased mucin expression is a feature of nasal polyposis. Corticosteroids reduce polyp size and symptoms, but their effect on mucin production remains unknown. In this study, the effects of intranasal corticosteroids on MUC5AC mucin expression, nasal resistance, eosinophil and neutrophil infiltration, epidermal growth factor receptor (EGFR), interleukin (IL)-8, and tumour necrosis factor (TNF)-alpha expression was assessed in nasal polyps. In nine subjects, one nasal polyp was removed surgically before treatment and another was removed after 8 weeks of intranasal fluticasone (400 microg.day(-1)). Tissues were processed for in situ hybridisation and immunohistochemical staining. Described effects of fluticasone on nasal polyps (reduction in nasal resistance and in eosinophil infiltration) were evaluated. Morphometric analysis was performed to assess the effect of fluticasone on epithelial-, MUC5AC-, EGFR- and IL-8-stained areas, TNF-alpha-stained cells, and neutrophil numbers. Treatment with fluticasone decreased nasal resistance and intra-epithelial eosinophils. The MUC5AC-stained area in the epithelium was unchanged by treatment; MUC5AC mRNA expression was unaffected by treatment. EGFR-stained area, intra-epithelial neutrophil numbers, IL-8 and TNF-alpha expression were also unchanged by therapy. Intranasal fluticasone was effective in decreasing nasal airflow resistance and intra-epithelial eosinophils but had no effect on mucin or epidermal growth factor receptor expression or on neutrophil recruitment.

Administration, Intranasal↗