Determinants of smoke induced lung damage and relationship with metabolic syndrome
Bagmane, Dinesh (2008) Determinants of smoke induced lung damage and relationship with metabolic syndrome. University of Southampton, School of Medicine, Doctoral Thesis , 246pp.
Smoking is the major risk factor for COPD. Smoking also has systemic effects and is considered as one of the risk factors for metabolic syndrome (MeS). It is unclear whether it is smoking per se or the systemic effects of COPD that cause metabolic syndrome in smokers.
Smokers with and without COPD and non-smoking controls were studied by pulmonary function testing, skin prick tests, body composition, fasting glucose, CRP, and lipids analysis to diagnose MeS. This showed a gradual increase in prevalence of MeS, but with only difference between non-smokers on one hand and smokers with or without COPD on the other being significant. This suggested that smoking, rather than the systemic effect of COPD, was the cause of MeS.
All smokers were then grouped and smokers and non-smokers compared in respect of lung function, inflammatory markers (CRP, a series of inflammatory cytokines), insulin resistance, and body composition. Smokers had increased central obesity and total body fat, which is in contrast to the common belief that smoking reduces weight. Male smokers demonstrated increased abdominal fat, while females showed an increase in total body fat. FEV1 was reduced when comparing all smokers with MeS and those without MeS, and there was a greater reduction in males who had a greater prevalence of MeS, but had better quality of life even though they smoked more. However, whilst smokers with MeS had higher levels of insulin resistance, as measured by Homeostasis Model Assessment (HOMA-R), none of the plasma inflammatory markers, except for IL-12, was raised, suggesting that these indices of inflammation were not the reason for MeS.
Smoking is associated with a gradual decline in lung function in smokers with and without COPD. A previously recruited cohort of smokers with and without COPD and healthy non-smoking subjects were followed up over a period of 5 years. Amongst a whole series of measurements, including HRCT, measures of lung density/emphysema, only sputum neutrophilia (both absolute and percentage counts) predicted the annual decline in FEV1.
In summary, this study suggests that there is an increased prevalence of MeS in smokers associated with insulin resistance caused by smoking but it fails to show an association between MeS and COPD. Smoking is also associated with central obesity and increased body fat, contributing to a reduction in FEV1. Sputum neutrophilia, but not smoking pack years or lung HRCT measurements, predicts the annual FEV1 decline in smokers.
|Item Type:||Thesis (Doctoral)|
|Subjects:||R Medicine > RB Pathology
Q Science > QP Physiology
|Divisions:||University Structure - Pre August 2011 > School of Medicine > Infection, Inflammation and Repair
|Date Deposited:||16 Mar 2010|
|Last Modified:||08 Jun 2012 12:33|
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