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The Lipid Profile and Biochemical Parameters of COPD Patients in Relation to Smoking Status

Abstract

Tobacco consumption is the most incriminated and studied risk factor for Chronic obstructive pulmonary disease (COPD), but other factors such as air pollution, are also linked to this disease. One of the known aspects of this chronic lung disease is that its occurrence is mainly due to the chronic inflammation of the airways. Lipid metabolism seems to be affected by smoking, with studies showing a correlation between this habit and high levels of triglycerides and low levels of high-density lipoprotein cholesterol (HDL-CHOL). Uric acid concentration is thought to reflect the antioxidative capacity of the body because it is the most abundant aqueous antioxidant. The aim of this study was to investigate the lipid profile and biochemical parameters of COPD patients in relation to smoking status. The present study was conducted between 2020 and 2021 in the Clinical Hospital of Pneumology in Iasi, Romania. Patients diagnosed with COPD (n = 52) were included and divided in three groups depending on their smoking status: non-smokers, smokers and ex-smokers. The obtained results show low correlations between COPD stages and serum uric acid concentrations (r = 0.4; ˂ 0.05), smoking status (smoker/non-smoker/ex-smoker) and total serum cholesterol values (r = 0.45; ˂ 0.05), but also between serum urea concentrations and the number of packs-years for the smoker/ex-smoker groups (r = 0.45, ˂ 0.05). Smoking was associated with changes in the lipid profile of smokers and ex-smokers, along with increased low-density lipoprotein cholesterol (LDL-CHOL) and low serum uric acid values.

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References
1.
Sliwinska-Mosson M, Mihulka E, Milnerowicz H . [Assessment of lipid profile in non-smoking and smoking young health persons]. Przegl Lek. 2015; 71(11):585-7. View

2.
Frati A, Iniestra F, Ariza C . Acute effect of cigarette smoking on glucose tolerance and other cardiovascular risk factors. Diabetes Care. 1996; 19(2):112-8. DOI: 10.2337/diacare.19.2.112. View

3.
Lee S, Seo J, Kim S, Jeong J, Nam B, Lee J . The changes of blood glucose control and lipid profiles after short-term smoking cessation in healthy males. Psychiatry Investig. 2011; 8(2):149-54. PMC: 3149110. DOI: 10.4306/pi.2011.8.2.149. View

4.
Esteve E, Ricart W, Fernandez-Real J . Dyslipidemia and inflammation: an evolutionary conserved mechanism. Clin Nutr. 2005; 24(1):16-31. DOI: 10.1016/j.clnu.2004.08.004. View

5.
Vujic T, Nagorni O, Maric G, Popovic L, Jankovic J . Metabolic syndrome in patients with chronic obstructive pulmonary disease: frequency and relationship with systemic inflammation. Hippokratia. 2017; 20(2):110-114. PMC: 5388510. View