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Published on: May 31, 2021
Platelet-activating factor acetylhydrolase is a biomarker of severe anaphylaxis in children
Julia E M Upton1,2,3, Jennifer A Hoang4, Matilde Leon-Ponte5
1Department of Pediatrics, University of Toronto, Toronto, Ontario, Canada.
Insights
Reduced platelet-activating factor acetylhydrolase (PAF-AH) activity indicates severe pediatric anaphylaxis. PAF-AH levels do not change during acute reactions but are lower in children with anaphylaxis compared to healthy controls.
Area of Science:
- Pediatric Allergy and Immunology
- Biochemistry
- Clinical Medicine
Background:
- Predicting the severity of allergic reactions in children is challenging.
- The platelet-activating factor (PAF) pathway is implicated in severe anaphylaxis in adults.
- This study investigates the role of PAF pathway components in pediatric anaphylaxis.
Purpose of the Study:
- To prospectively assess the involvement of key platelet-activating factor pathway components in pediatric anaphylaxis.
- To identify potential biomarkers for severe anaphylaxis in children.
- To evaluate the relationship between PAF-AH activity and anaphylaxis severity.
Main Methods:
- Forty-six pediatric patients (<18 years) with acute anaphylaxis were enrolled.
- Anaphylaxis severity was graded, and serum markers, including platelet-activating factor acetylhydrolase (PAF-AH) activity, were measured.
- Measurements were compared between severe and mild-moderate anaphylaxis groups, and with healthy pediatric controls.
Main Results:
- 26% of children experienced severe anaphylaxis.
- Reduced PAF-AH activity was significantly associated with severe anaphylaxis (p < .05).
- Children requiring intensive care had markedly reduced PAF-AH activity compared to those requiring ward/ED care (p < .05).
Conclusions:
- Decreased serum PAF-AH activity serves as a biomarker for severe pediatric anaphylaxis.
- PAF-AH enzyme levels remain stable from basal levels during acute anaphylaxis.
- PAF-AH may play a role in modulating susceptibility to severe anaphylaxis in children.
Background:
There is limited ability to predict the severity of allergic reactions in children. Data derived predominantly from adults have implicated the platelet-activating factor pathway as a potential contributor to severe anaphylaxis. In this study, we sought to prospectively assess involvement of key components of the platelet-activating factor pathway in pediatric patients with anaphylaxis.
Methods:
Forty-six pediatric patients (<18 years) presenting with acute anaphylaxis were assessed. Anaphylaxis severity was graded and serum anaphylaxis markers were measured acutely and in 36 children who returned for follow-up >4 weeks after their acute presentation. These markers were compared with pediatric laboratory reference sera.
Results:
Severe anaphylaxis was experienced by 12/46 (26%) and mild-moderate anaphylaxis in 34/46 (74%) children. Platelet-activating factor acetylhydrolase (PAF-AH) activity was inversely associated with severe anaphylaxis: 9/12 children with severe anaphylaxis had reduced PAF-AH activity as compared with 14/34 with mild-moderate anaphylaxis (p < .05). Furthermore, 3/3 children who required intensive care had markedly reduced mean PAF-AH (nmol/ml/min) (13.73, 95%CI: 7.42-20.03) versus 20/23 who required ward/emergency department care (17.81, 95%CI: 16.80-18.83; p < .05). In children with anaphylaxis, PAF-AH during acute anaphylaxis was unchanged relative to the child's basal levels (mean, 17.26, 95%CI: 16.10-18.42 vs 17.50, 95%CI: 16.21-18.78, p = .63) and was lower than healthy pediatric controls (mean 19.21; 95%CI:18.21-20.21; p < .05).
Conclusion:
Decreased serum PAF-AH activity is a biomarker of severe anaphylaxis. Levels of this enzyme do not change from basal levels during acute anaphylaxis. Our results show that PAF-AH is a biomarker of anaphylaxis severity in children. This key regulatory enzyme may modulate susceptibility to severe anaphylaxis.
