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

• Kuczia Pawel

  Department of Internal Medicine, Jagiellonian University Medical College

• Mastalerz Lucyna

  Department of Internal Medicine, Jagiellonian University Medical College

• Potaczek Daniel P.

  John Paul II Hospital Institute of Laboratory Medicine, Member of the German Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center (UGMLC), Philipps-Universität Marburg

• Cybulska Agnieszka

  Department of Internal Medicine, Jagiellonian University Medical College

• Zareba Lech

  Faculty of Mathematics and Natural Sciences, University of Rzeszow

• Bazan-Socha Stanislawa

  Department of Internal Medicine, Jagiellonian University Medical College

• Undas Anetta

  Department of Internal Medicine, Jagiellonian University Medical College John Paul II Hospital Institute of Cardiology, Jagiellonian University Medical College

書誌事項

タイトル別名

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

抄録

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.

収録刊行物

• Allergology International

  Allergology International 68 (4), 450-455, 2019

  一般社団法人日本アレルギー学会

キーワード

• Asthma
• Cardiovascular risk
• Coagulation
• Lipoprotein-associated phospholipase A₂
• Inflammation

詳細情報

• CRID: 1390001277374220800
• NII論文ID: 130007733153
• DOI: 10.1016/j.alit.2019.04.004
• ISSN: 14401592
• ISSN: 13238930
• Web Site: https://api.elsevier.com/content/article/PII:S1323893019300516?httpAccept=text/xml
• Web Site: https://api.elsevier.com/content/article/PII:S1323893019300516?httpAccept=text/plain
• Web Site: https://search.jamas.or.jp/link/ui/2020286615
• 本文言語コード: en
• データソース種別:
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  • Crossref
  • CiNii Articles
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