Study of Bronchial Inflammation in Adolescent Smokers With and Without Obesity

Obesity Clinical Trial

Official title:

Bronchial Inflammation in Adolescent Smokers With and Without Obesity

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00942019
• Other study ID #: KGU-88/08
• Status: Completed
• Phase: N/A
• First received: July 17, 2009
• Last updated: July 2, 2010
• Start date: October 2008
• Est. completion date: February 2010

Study information

• Verified date: July 2010
• Source: Johann Wolfgang Goethe University Hospitals
• Contact: n/a
• Is FDA regulated: No
• Health authority: Germany: Ethics Commission
• Study type: Observational

Clinical Trial 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 < 25)(4 patient groups). The aim of the study is to compare differences in lung function (VC, FEV1, VC/FEV1, 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 e.g. 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.

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 17.7 years) and 24 non-smoking (age 17.5 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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 110
• Est. completion date: February 2010
• Est. primary completion date: February 2010
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: Both
• Age group: 14 Years to 22 Years

Eligibility

Inclusion Criteria:

• informed consent

• age between 14 and 22 years

• smokers CO = 15 ppm

• non-smokers CO = 6 ppm

Exclusion Criteria:

• Asthma > GINA I°

• others chronic diseases or infections (e.x. HIV, tuberculosis, malignancy)

• pregnancy

• therapy with systemic corticosteroids

• permanent treatment with inhaled corticosteroids

• documented alcohol, substance, and/or drug abuse

• incapability to perform all study procedure

Study Design

Observational Model: Cohort, Time Perspective: Cross-Sectional

Related Conditions & MeSH terms

• Obesity
• Tobacco Smoking

Locations

Country	Name	City	State
Germany	Children's Hospital, Goethe-University	Frankfurt/Main

Sponsors (1)

Lead Sponsor	Collaborator
Johann Wolfgang Goethe University Hospitals

Country where clinical trial is conducted

Germany, 

References & Publications (8)

Carpagnano GE, Kharitonov SA, Foschino-Barbaro MP, Resta O, Gramiccioni E, Barnes PJ. Increased inflammatory markers in the exhaled breath condensate of cigarette smokers. Eur Respir J. 2003 Apr;21(4):589-93. — View Citation

Csoma Z, Kharitonov SA, Balint B, Bush A, Wilson NM, Barnes PJ. Increased leukotrienes in exhaled breath condensate in childhood asthma. Am J Respir Crit Care Med. 2002 Nov 15;166(10):1345-9. Epub 2002 Sep 5. — View Citation

Garey KW, Neuhauser MM, Robbins RA, Danziger LH, Rubinstein I. Markers of inflammation in exhaled breath condensate of young healthy smokers. Chest. 2004 Jan;125(1):22-6. — View Citation

Karimi K, Sarir H, Mortaz E, Smit JJ, Hosseini H, De Kimpe SJ, Nijkamp FP, Folkerts G. Toll-like receptor-4 mediates cigarette smoke-induced cytokine production by human macrophages. Respir Res. 2006 Apr 19;7:66. — View Citation

KiGGS Study of Robert Koch Institut

Kitz R, Rose MA, Borgmann A, Schubert R, Zielen S. Systemic and bronchial inflammation following LPS inhalation in asthmatic and healthy subjects. J Endotoxin Res. 2006;12(6):367-74. — View Citation

Kornmann O et al. Influence of second hand tobacco smoke exposure on inflammatory parameters in induced sputum Abstract ATS 2008

Sebastian A, Pehrson C, Larsson L. Elevated concentrations of endotoxin in indoor air due to cigarette smoking. J Environ Monit. 2006 May;8(5):519-22. Epub 2006 Mar 27. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Bronchial inflammatory in adolescents smokers with and without obesity		one day	No
Secondary	Association of bronchial inflammatory parameters in sputum and in the blood		one day	No