Increased activity of lipoprotein-associated phospholipase A2 in non-severe asthma

BackgroundGiven increased risk of cardiovascular events in asthma we hypothesized that lipoprotein-associated phospholipase A₂ (Lp-PLA₂), an enzyme involved in atherosclerosis, is associated with proinflammatory and prothrombotic blood alterations in this disease.MethodsIn 164 adult asthmatics (63 with severe asthma) we measured plasma Lp-PLA₂ activity using the PLAC test. We determined its relations to inflammation and prothrombotic blood alterations.ResultsIn asthma, Lp-PLA₂ was inversely related to the age (β = ?0.1 [?0.18 to ?0.02]) and was lower in women (n = 122 [74%], 205 [182–242] vs. 243 [203–262] nmol/min/ml, p = 0.001). Interestingly, Lp-PLA₂ correlated negatively with the asthma severity score (β = ?0.15 [?0.23 to ?0.07]), being 10.3% higher in those with non-severe (mild or moderate) asthma (n = 101, 62%) as compared to the severe disease subtype (224 [191–261] vs. 203 [181–229], p = 0.006 after adjustment for potential confounders). Lp-PLA₂ activity was positively related to the levels of low-density lipoprotein (β = 0.1 [0.02–0.18]), triglycerides (β = 0.11 [0.03–0.19]) and glucose (β = 0.1 [0.02–0.18]) and inversely to the tumor necrosis factor α (β = ?0.27 [?0.35 to ?0.2]), high sensitivity C-reactive protein (β = ?0.1 [?0.19 to ?0.02]) and fibrinogen (β = ?0.12 [?0.21 to ?0.03]), as well as prothrombin (β = ?0.16 [?0.24 to ?0.08]), and parameters describing thrombin generation potential, such as endogenous thrombin potential (β = ?0.14 [?0.21 to ?0.06]) and peak thrombin generated (β = ?0.2 [?0.28 to ?0.12]).ConclusionsElevated Lp-PLA₂ activity in non-severe asthmatics suggests increased atherosclerotic risk in this group. Lower Lp-PLA₂ activity accompanied by its inverse relationship to inflammatory or prothrombotic blood biomarkers observed in turn in severe asthmatics might be related to the pathogenesis of more severe asthma phenotype.