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Atopy and Frequency of Exacerbation in Chronic Obstructive Pulmonary Disease Patients

M

Mansoura University Hospital

Status

Enrolling

Conditions

Chronic Obstructive Pulmonary Disease

Treatments

Diagnostic Test: Skin prick test

Study type

Observational

Funder types

Other

Identifiers

NCT06518473
R.24.06.2680

Details and patient eligibility

About

Chronic Obstructive Pulmonary Disease (COPD) is a heterogeneous lung condition characterized by chronic respiratory symptoms (dyspnea, cough, sputum production and/or exacerbations) due to abnormalities of airways (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction.

The presence of non-fully reversible airflow obstruction (FEV1/FVC < 0.7 post-bronchodilation) measured by spirometry confirms the diagnosis of COPD

Full description

Chronic Obstructive Pulmonary Disease(COPD) is a heterogeneous lung condition characterized by chronic respiratory symptoms (dyspnea, cough, sputum production and/or exacerbations) due to abnormalities of airways (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction.

The presence of non-fully reversible airflow obstruction (FEV1/FVC < 0.7 post-bronchodilation) measured by spirometry confirms the diagnosis of COPD Inflammation of the bronchial wall is characterized by the presence of neutrophils and macrophages and by increased concentrations of IL-8 and Th1 cytokines, as well as by a proteinase /antiproteinase imbalance, and this could explain the poorer response to inhaled corticosteroids (ICs) seen in COPD.

Asthma may also be a risk factor for the development of chronic airflow obstruction and COPD and Epidemiological Study of Airway Obstructive Disease, adults diagnosed of asthma were found to have a 12-fold higher risk of acquiring COPD over time compared to those without asthma, after adjusting for smoking.

Although both COPD and asthma are associated with chronic inflammation of the respiratory tract, there are differences in the inflammatory cells and mediators involved in the two diseases, some patients with COPD have an inflammatory pattern with increased eosinophils cells, similar to that of asthma.

When there is diagnostic of Asthma and COPD overlap (ACO) uncertainty, an elevated total serum immunoglobulin E (IgE; >100 international units/mL), elevated peripheral blood eosinophil count (>300 cells/microL), and evidence of allergic disease (eg, skin testing or immunoassays for perennial allergen sensitivity) may point a clinician to asthma or Asthma - COPD overlap (ACO). Elevated sputum eosinophil counts, if available, are more common in asthma or ACO than COPD The Dutch hypothesis suggests that atopy and bronchial hyper-responsiveness , which are important markers of asthma, can be involved in the pathogenesis of COPD, although there is no clear evidence regarding the frequency of atopy (including asthma), Allergic rhinitis (AR), eczema, or increased IgE levels in patients with COPD, because most studies have involved small samples and limited evaluation of atopy.

Enrollment

50 estimated patients

Sex

All

Ages

40 to 70 years old

Volunteers

No Healthy Volunteers

Inclusion criteria

  • Adults aged 40-70 years diagnosed with COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2024 criteria

Exclusion criteria

  • Patients with known allergic diseases before enrollment
  • Patients with associated other chronic respiratory disorders
  • Patients with significant comorbidities that could influence respiratory function.
  • Recent respiratory infections or use of systemic corticosteroids within the last month before enrollment.

Trial design

50 participants in 1 patient group

Chronic obstructive pulmonary disease patients
Description:
Adults aged 40-70 years diagnosed with COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2024 criteria
Treatment:
Diagnostic Test: Skin prick test

Trial contacts and locations

1

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Central trial contact

Mohamed AbdElmoniem, lecturer; Taha Abdelgawad, Professor

Data sourced from clinicaltrials.gov

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