Ivona Markelić1, Iva Hlapčić2, Dunja Rogić3, Ivana Rako4, Miroslav Samaržija5, Sanja Popović-Grle5, Lada Rumora2, Andrea Vukić Dugac6. 1. University Hospital Centre Zagreb, Clinical Department for Pulmonary Diseases Jordanovac, Zagreb, Croatia. 2. University of Zagreb, Faculty of Pharmacy and Biochemistry, Department of Medical Biochemistry and Haematology, Zagreb, Croatia. 3. University of Zagreb, Faculty of Pharmacy and Biochemistry, Department of Medical Biochemistry and Haematology, Zagreb, Croatia; University Hospital Centre Zagreb, Clinical Institute of Laboratory Diagnostics, Zagreb, Croatia. 4. University Hospital Centre Zagreb, Clinical Institute of Laboratory Diagnostics, Zagreb, Croatia. 5. University Hospital Centre Zagreb, Clinical Department for Pulmonary Diseases Jordanovac, Zagreb, Croatia; University of Zagreb, School of Medicine, Zagreb, Croatia. 6. University Hospital Centre Zagreb, Clinical Department for Pulmonary Diseases Jordanovac, Zagreb, Croatia; University of Zagreb, School of Medicine, Zagreb, Croatia. Electronic address: avukic@kbc-zagreb.hr.
Abstract
BACKGROUND AND AIMS: Limited number of studies investigated lipid profile in chronic obstructive pulmonary disease (COPD) with inconsistent results. This study aimed to investigate lipid parameters in sera of patients with stable COPD and their associations with disease severity, smoking, comorbidities and therapy. METHODS AND RESULTS: The study included 137 COPD patients and 95 controls. Triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) were assessed. Non-HDL-C (NHC), atherogenic coefficient (AC), TG/HDL-C, atherogenic index of plasma (AIP), Castelli's risk index I and II (CRI-I, CRI-II), and monocyte to HDL ratio (MHR) were calculated. HDL-C and MHR were increased, while other lipid parameters and indices were decreased in COPD patients compared to healthy individuals. Smoking did not influence lipid parameters. However, lipid profile was altered only in more severe disease stages. AC, CRI-I and CRI-II showed positive association with lung function parameters in COPD patients, and negative with COPD multicomponent indices (ADO, BODCAT, BODEx, CODEx and DOSE). Combined model that included CRI-II, C-reactive protein, fibrinogen and white blood cells showed great diagnostic performances, and correctly classified 72% of study participants with an AUC of 0.800 (0.742-0.849), P < 0.001. Bronchodilator monotherapy and statins have opposite impact on TC, LDL-C and NHC, while TG, TG/HDL-C and AIP were increased in COPD patients with cardiovascular diseases. CONCLUSION: Lipid disbalance is present in COPD, and it seems to occur later as the disease progresses. Further studies are needed to illuminate the underlying mechanism of dyslipidaemia.
BACKGROUND AND AIMS: Limited number of studies investigated lipid profile in chronic obstructive pulmonary disease (COPD) with inconsistent results. This study aimed to investigate lipid parameters in sera of patients with stable COPD and their associations with disease severity, smoking, comorbidities and therapy. METHODS AND RESULTS: The study included 137 COPDpatients and 95 controls. Triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) were assessed. Non-HDL-C (NHC), atherogenic coefficient (AC), TG/HDL-C, atherogenic index of plasma (AIP), Castelli's risk index I and II (CRI-I, CRI-II), and monocyte to HDL ratio (MHR) were calculated. HDL-C and MHR were increased, while other lipid parameters and indices were decreased in COPDpatients compared to healthy individuals. Smoking did not influence lipid parameters. However, lipid profile was altered only in more severe disease stages. AC, CRI-I and CRI-II showed positive association with lung function parameters in COPDpatients, and negative with COPD multicomponent indices (ADO, BODCAT, BODEx, CODEx and DOSE). Combined model that included CRI-II, C-reactive protein, fibrinogen and white blood cells showed great diagnostic performances, and correctly classified 72% of study participants with an AUC of 0.800 (0.742-0.849), P < 0.001. Bronchodilator monotherapy and statins have opposite impact on TC, LDL-C and NHC, while TG, TG/HDL-C and AIP were increased in COPDpatients with cardiovascular diseases. CONCLUSION:Lipid disbalance is present in COPD, and it seems to occur later as the disease progresses. Further studies are needed to illuminate the underlying mechanism of dyslipidaemia.