Journals / Turkish Journal of Pediatrics / 2018 / Cilt: 60 - Sayı: 5

Plasma lipoxin A4 levels in childhood chronic spontaneous urticaria

Pages
527–534
DOI
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⚡ TL;DR(Too Long; Didn't Read)

Additionally, the median plasma LXA4 levels in the ASST-positivepatients were significantly reduced compared to the ASST-negative ones (45.8[36.7–67.6] versus 63.8 [58.3–78.9] ng/ml, respectively, p <0.05).Our results showed that diminished LXA4 biosynthesis may be a critical partof CSU pathogenesis in children, especially in patients with an autoimmunecomponent.

📌 3 Key Takeaways

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Objective & Hypothesis:Chronic spontaneous urticaria (CSU) is an idiopathic inflammatory disorder.Despite great research progress, the pathogenesis of the disease is still notfully understood.
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Key Findings & Data:In this study, we aimed to investigate the possible role of LXA4in the pathogenesis of CSU.Forty-two children with CSU and 25 healthy children were enrolled in thestudy.
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Conclusion & Impact:Additionally, the median plasma LXA4 levels in the ASST-positivepatients were significantly reduced compared to the ASST-negative ones (45.8[36.7–67.6] versus 63.8 [58.3–78.9] ng/ml, respectively, p <0.05).Our results showed that diminished LXA4 biosynthesis may be a critical partof CSU pathogenesis in children, especially in patients with an autoimmunecomponent.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Chronic spontaneous urticaria (CSU) is an idiopathic inflammatory disorder.Despite great research progress, the pathogenesis of the disease is still notfully understood. Lipoxins (LXs) are autacoid lipid metabolites that are thefirst discovered members of a new genus named called “specialized proresolvingmediators”. In this study, we aimed to investigate the possible role of LXA4in the pathogenesis of CSU.Forty-two children with CSU and 25 healthy children were enrolled in thestudy. The demographic and clinical features of patients were evaluated,autologous serum skin tests (ASSTs), and routine laboratory assessmentswere performed. Disease activity was determined using the urticaria activityscore. An enzyme-linked immunosorbent assay was used to evaluate LXA4plasma levels.The median value of plasma LXA4 was found to be 60.8 ng/ml (interquartilerange, 48.1–71.8) in CSU patients and 137.4 ng/ml (121.4–150.8) in thecontrol group. The difference between the groups was statistically significant(p<0.001). Additionally, the median plasma LXA4 levels in the ASST-positivepatients were significantly reduced compared to the ASST-negative ones (45.8[36.7–67.6] versus 63.8 [58.3–78.9] ng/ml, respectively, p <0.05).Our results showed that diminished LXA4 biosynthesis may be a critical partof CSU pathogenesis in children, especially in patients with an autoimmunecomponent.

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Cite This Article

DİLEK, F., ÖZÇEKER, D., GÜLER, E. M., ÖZKAYA, E., YAZICI, M., TAMAY, Z., KOÇYİĞİT, A., GÜLER, N. (2018). Plasma lipoxin A4 levels in childhood chronic spontaneous urticaria. Turkish Journal of Pediatrics, Cilt: 60 - Sayı: 5, 527–534. https://ajindex.com/articles/412123

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References (12)

  1. Kaplan AP, Greaves M. Pathogenesis of chronic urticaria. Clin Exp Allergy 2009; 39: 777-787
  2. Zuberbier T, Aberer W, Asero R, et al.; European Academy of Allergy and Clinical Immunology; Global Allergy and Asthma European Network; European Dermatology Forum; World Allergy Organization. The EAACI/GA(2) LEN/EDF/WAO Guideline for the definition, classification, diagnosis, and management of urticaria: the 2013 revision and update. Allergy 2014; 69: 868-887
  3. Powell RJ, Leech SC, Till S, Huber PA, Nasser SM, Clark AT; British Society for Allergy and Clinical Immunology. BSACI guideline for the management of chronic urticaria and angioedema. Clin Exp Allergy 2015; 45: 547-565
  4. Jain S. Pathogenesis of chronic urticaria: an overview. Dermatol Res Pract 2014; 2014: 674709
  5. Xu Y, Chen G. Mast cell and autoimmune diseases. Mediators Inflamm 2015; 2015: 246126
  6. Levy BD, Vachier I, Serhan CN. Resolution of inflammation in asthma. Clin Chest Med 2012; 33: 559-570
  7. Romano M, Cianci E, Simiele F, Recchiuti A. Lipoxins and aspirin-triggered lipoxins in resolution of inflammation. Eur J Pharmacol 2015; 760: 49-63
  8. Serhan CN. Novel lipid mediators and resolution mechanisms in acute inflammation: to resolve or not? Am J Pathol 2010; 177: 1576-1591
  9. Levy BD, Vachier I, Serhan CN. Resolution of inflammation in asthma. Clin Chest Med 2012; 33: 559-570
  10. Serhan CN. Resolution phase of inflammation: novel endogenous anti-inflammatory and proresolving lipid mediators and pathways. Annu Rev Immunol 2007; 25: 101-137
  11. Higgins G, Ringholz F, Buchanan P, McNally P, Urbach V. Physiological impact of abnormal lipoxin A4 production on cystic fibrosis airway epithelium and therapeutic potential. Biomed Res Int 2015; 2015: 781087
  12. Maderna P, Godson C. Lipoxins: resolutionary road. Br J Pharmacol 2009; 158: 947-959.