• Turk J Med Sci · Apr 2020

    Correlation of serum fatty acid binding protein-4 and interleukin-6 with airflow limitation and quality of life in stable and acute exacerbation of COPD

    • Mohammad Reza Aslani, Zeynab Ghazaei, and Hassan Ghobadi.
    • Lung Inflammatory Diseases Research Centre, Faculty of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran
    • Turk J Med Sci. 2020 Apr 9; 50 (2): 337345337-345.

    Background/AimThe serum fatty acid binding protein 4 (FABP-4) level increases in chronic inflammatory diseases. The present study aimed to examine serum FABP-4 and interleukin (IL)-6 levels in patients with stable and acute exacerbation of chronic obstructive pulmonary disease (COPD) and the correlation of these markers with airflow limitation.Materials And MethodssWe measured serum FABP-4 and IL-6 levels in 60 COPD patients [30 stable COPD (SCOPD), and 30 acute exacerbation of COPD (AECOPD)], and 30 healthy subjects and compared them with airflow limitation according to the COPD stage in the Global Initiative for Chronic Obstructive Pulmonary Disease (GOLD) criteria, peripheral O2 saturation (SpO2), and COPD Assessment Test (CAT) score. We also tested the association between serum FABP-4 levels and some characteristics of study parameters.ResultsBoth serum FABP-4 and IL-6 levels increased with increasing severity of GOLD grades in SCOPD (P < 0.01 for both) and AECOPD groups (P < 0.001 and P < 0.01, respectively). It also increased in patients with AECOPD group compared with SCOPD group in GOLD grades I-II (P < 0.01) and GOLD grades III-IV (P < 0.05). In addition, there was a significant positive correlation between serum FABP-4 level with IL-6, CAT score, and smoking history and inversely with FEV1 and SpO2.ConclusionThe study revealed that serum FABP-4 level was elevated with increasing GOLD grades in COPD patients, markedly in acute exacerbation phase. The increase was associated with elevated serum levels of IL-6 and severity of hypoxia. Thus, it seems that FABP-4 may be involved in the pathogenesis of COPD.This work is licensed under a Creative Commons Attribution 4.0 International License.

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