Viewing Study NCT00942019



Ignite Creation Date: 2024-05-05 @ 9:43 PM
Last Modification Date: 2024-10-26 @ 10:08 AM
Study NCT ID: NCT00942019
Status: COMPLETED
Last Update Posted: 2010-07-05
First Post: 2009-07-17

Brief Title: Study of Bronchial Inflammation in Adolescent Smokers With and Without Obesity
Sponsor: Johann Wolfgang Goethe University Hospital
Organization: Johann Wolfgang Goethe University Hospital

Study Overview

Official Title: Bronchial Inflammation in Adolescent Smokers With and Without Obesity
Status: COMPLETED
Status Verified Date: 2010-07
Last Known Status: None
Delayed Posting: No
If Stopped, Why?: Not Stopped
Has Expanded Access: False
If Expanded Access, NCT#: N/A
Has Expanded Access, NCT# Status: N/A
Acronym: None
Brief Summary: The investigators want to assess differences in lung function and bronchial inflammation of young smokers and non-smokers with BMI 30 and without obesity BMI 254 patient groups The aim of the study is to compare differences in lung function VC FEV1 VCFEV1 metacholine challenge and bronchial inflammation in relation with smoking history and levels of exhaled CO For the latter the investigators will analyze the levels of IL-8 IL-6 TNF alpha and INF gamma and mRNA of LBP TLR2 and TLR4 in sputum Further inflammatory markers eg low CRP and inflammatory cytokines levels in the blood will be investigated The aim is to describe a early stage of chronic obstructive pulmonary disease caused by cigarette smoke in juvenile smokers and the relationship between bronchial inflammation and obesity in adolescents
Detailed Description: Tobacco smoke is the crucial factor at the beginning and in the course of the bronchial inflammation leading to COPD It has been shown that cigarette smoke in vitro leads to a MAP kinase and NF-κB-dependent increase of pro-inflammatory cytokines and inhibits bacteria-induced expression of β-defensins Several studies revealed an increase of inflammatory cytokines like IL-8 and TNF in the sputum of smokers Further studies demonstrated an up regulation of LTB4 and LBP possibly due to the LPS derived from tobacco smoke Hasday et al could show that up to 15 ng per cigarette LPS is released In principle the cigarette smoke exposure liked a mild LPS inhalation In separate work we could show that LPS inhalation in healthy non-smokers to an increase of CRP and LBP concentrations in the serum lead In another study of adolescents 24 smokers age 177 years and 24 non-smoking age 175 years were compared The CO in smokers was significantly increased and the NO concentrations decreased At the same time there was a significantly greater bronchial hyperreagibility in the smoker group

According to a recent study in Germany KiGGS study already 31 of the adolescents boys and 32 of the girls do smoke The social status is of great importance Boys and girls from families with a low social status smoke more frequently than those from families with middle-and especially with higher social status Similarly obesity is linked to the social status with overweight occurring more often in families with a lower social status

A visceral obesity is closely associated with the risk of type-2-diabetes as well as other aspects of the metabolic syndrome However the existing insulin resistance is of fundamental importance Due to increased visceral fat depots and subsequently increased release of proinflammatory proteins various complications do occur

Study Oversight

Has Oversight DMC: None
Is a FDA Regulated Drug?: None
Is a FDA Regulated Device?: None
Is an Unapproved Device?: None
Is a PPSD?: None
Is a US Export?: None
Is an FDA AA801 Violation?: None