Increased activity of lipoprotein-associated phospholipase A 2 in non-severe asthma.

BACKGROUND: Given 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.

METHODS: In 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.

RESULTS: In 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]).

CONCLUSIONS: Elevated 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.