Acute and chronic inflammatory responses induced by smoking in individuals being susceptible and non-susceptible for development of COPD: from specific disease phenotyping towards novel made therapy (study 1).

Acute and chronic inflammatory responses induced by smoking in individuals being susceptible and non-susceptible for development of COPD: from specific disease phenotyping towards novel made therapy (study 1). - Acute smoking in COPD

Status

Active, not recruiting

Phases

Unknown

Study type

Observational

Source

NL-OMON

Registry ID

NL-OMON31923

Enrollment

120

Registered

2008-12-15

Start date

2008-07-01

Completion date

Unknown

Last updated

2024-05-06

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

chronic ibstructive brochitis( COPD) emphysema

Interventions

None listed

Eligibility

Age

18 Years to 99 Years

Inclusion criteria

Inclusion criteria: • Age 18-75 years • Age, pack years, FEV1/FVC and FEV1% predicted must fit in one of the 5 groups of table 4.1 • Able to stop smoking for 10 days and start smoking 3-4 cigarettes within 1 hour • Physically and mentally able to undergo the total study protocol • Written informed consent

Exclusion criteria

Exclusion criteria: • Participation in another study • Alpha-1-antitrypsin deficiency • Selected grade 1-3 co-morbidity listed in the ACE-27 • Active pulmonary infection like tuberculosis, pneumonia, flue, tracheobronchitis • Active extra-pulmonary infection like hepatitis A-C, cystitis, gastro-enteritis etc • Pulmonary diseases like sarcoidosis, IPF, silicosis, hypersensitivity pneumonitis • Life threatening diseases like carcinoma, AIDS (including HIV+), acute leukaemia etc • Medication that may affect the results of the study: NSAID*s, immunosuppressive agents like prednisolon, metotrexate, azathioprine,Sintrom tablets

Design outcomes

Primary

Measure	Time frame
• Local inflammation before and after cigarette smoking assessed by exhaled breath condensate, microprobe sampling and bronchial biopsies. • Systemic inflammation before and after cigarette smoking assessed by the expression of established and newly developed markers on innate immune cells associated with pre-activation. • Extensive clinical characterisation including life style factors, lung function, CT scanning of the lung. • Corticosteroid responsiveness of epithelial cells in vitro. • Distribution of candidate genes (SNPs) for COPD between the 5 different groups and associations with the inflammatory responses on acute smoking.	—

Measure

Time frame

• Local inflammation before and after cigarette smoking assessed by exhaled breath condensate, microprobe sampling and bronchial biopsies. • Systemic inflammation before and after cigarette smoking assessed by the expression of established and newly developed markers on innate immune cells associated with pre-activation. • Extensive clinical characterisation including life style factors, lung function, CT scanning of the lung. • Corticosteroid responsiveness of epithelial cells in vitro. • Distribution of candidate genes (SNPs) for COPD between the 5 different groups and associations with the inflammatory responses on acute smoking.

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Secondary

Measure	Time frame
n.a.	—

Countries

Netherlands

Outcome results