Endothelial dysfunction and pentraxin-3 in clinically stable adult asthma patients.

BACKGROUND AND OBJECTIVE: Asthma is associated with low-grade systemic inflammation, prothrombotic state, and premature atherosclerosis. Objective: To evaluate the relationships between asthma, inflammatory biomarkers, and parameters of endothelial dysfunction. METHODS: In 92 adult, clinically stable asthmatics and 62 well-matched controls we analyzed flow-mediated dilatation (FMD) of the brachial artery and intima-media thickness (IMT) of the common carotid artery using ultrasonography. We also measured blood levels of selected inflammatory and asthma specific biomarkers, including interleukin (IL)-4, IL-5, IL-6, IL-10, IL-12(p70), IL-17A, IL-23, interferon γ, as well as a disintegrin and metalloproteinase domain-containing protein 33 (ADAM-33), together with endothelial damage laboratory markers: circulating pentraxin-3 and plasma activity of von Willebrand factor (vWF). We analyzed relationships of studied variables with asthma severity, lung function abnormalities, lung computer tomography (CT) indices of airway remodeling, and transthoracic echocardiography parameters. RESULTS: Asthmatics had higher IL-6, IL-10, and ADAM-33. They were also characterized by 23% lower FMD% and 15% thicker IMT, as compared to controls (p<0.001, both). In asthma vWF was related to age (β=0.28 [95%CI: 0.15 to 0.41]) and remained in an inverse relationship with FEV1 (β=-0.2 [95%CI: -0.05 to -0.35]). Surprisingly, a negative correlation was revealed between vWF and pentraxin-3 (β=-0.17 [95%CI: -0.3 to -0.04]). Pentraxin-3 remained in positive associations with CT airway remodeling indices. CONCLUSIONS: Asthma is characterized by endothelial dysfunction that was related to the airway obstruction. The biological role of pentraxin-3 is unknown, although our data suggests its protective role against endothelial damage and atherosclerosis.