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Published on: May 5, 2018
Influence of CD36 deficiency on heart disease in children
Masayuki Teraguchi1, Yumiko Ikemoto, Gen Unishi
1Department of Pediatrics, Kansai Medical University, Osaka, Japan. teraguch@takii.kmu.ac.jp
Insights
CD36 deficiency is as common in children with heart disease as in healthy individuals. However, some children with CD36 deficiency may experience myocardial damage under certain conditions.
Area of Science:
- Cardiology
- Immunology
- Genetics
Background:
- The physiological role of CD36 molecule in pediatric heart disease remains under-investigated.
- CD36 deficiency is a condition affecting platelet and monocyte function.
Purpose of the Study:
- To investigate the prevalence and role of CD36 deficiency in pediatric heart disease.
- To determine if CD36 deficiency is associated with specific types of heart conditions or increased susceptibility to myocardial damage.
Main Methods:
- Flow cytometry was used to measure CD36 antigen expression in platelets and monocytes.
- 189 pediatric patients with various heart diseases were analyzed.
- CD36 deficiency was classified into Type I and Type II.
Main Results:
- CD36 deficiency was identified in 7.9% of pediatric heart disease patients.
- Prevalence varied across heart disease types: congenital heart disease (7.6%), myocardial disease (20.0%), Kawasaki disease (4.9%), and arrhythmia (6.7%).
- Three patients with myocardial disease and CD36 deficiency experienced transient myocardial damage, potentially linked to fatty acid metabolism issues.
Conclusions:
- The frequency of CD36 deficiency in childhood heart disease is similar to that in healthy populations.
- CD36 deficiency may predispose individuals to myocardial damage under specific adverse conditions like infections or steroid therapy.
Background:
The physiological role of the CD36 molecule in pediatric heart disease has not been fully investigated.
Methods And Results:
The CD36 antigen in platelets and monocytes was measured by flow cytometry in 189 patients with various heart diseases; 15 (7.9%) had a diagnosis of CD36 deficiency (type I: 2[1 boy, 1 girl], type II: 13 [6 boys, 7 girls]). The prevalence in each heart disease was as follows: group A (congenital heart disease) 7.6% (9/118, type II: 9 [6 boys, 3 girls]); group B (myocardial disease) 20.0% (3/15, I: 1 girl, II: 2[1 boy, 1 girl]), group C (Kawasaki disease) 4.9% (2/41, II: 2 [1 boy, 1 girl]), group D (arrhythmia): 6.7% (1/15, I: 1 boy). Three patients in group B had transient myocardial damage, which was thought to be related to abnormal myocardial long-chain fatty acid metabolism.
Conclusion:
The frequency of CD36 deficiency in childhood heart disease was almost identical to that of healthy individuals. Some patients with CD36 deficiency may be susceptible to myocardial damage in the presence of disadvantageous conditions, such as serious infections or massive steroid therapy.
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