Startseite The role of the deficiency of vitamin B12 and folic acid on homocysteinemia in children with Turner syndrome
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The role of the deficiency of vitamin B12 and folic acid on homocysteinemia in children with Turner syndrome

  • Eman R. Youness , Shaimaa A. Hashem , Khaled Hamed , Azzah A. Khedr , Eatemad Nabil Abdulhalim , Shimaa Mostafa Kamel und Hala T. El-Bassyouni ORCID logo EMAIL logo
Veröffentlicht/Copyright: 20. Dezember 2022

Abstract

Objectives

Premature atherosclerosis and ischemic heart disease represent a major cause of comorbidities among children with Turner syndrome. The identification of non-traditional risk aspects is crucial for the early identification and management of such comorbidities through establishing effective preventive measures. The aim of the study is to explore the role of the deficiency of vitamin B12, folic acid and homocysteine in children with Turner syndrome.

Methods

The study included 78 children with Turner syndrome and 67 healthy age and sex matched children. Karyotype was implemented for all patients. The serum levels of vitamin B12, folic acid and serum homocysteine were assessed. The prevalence of the deficiency of vitamin B12 and folic acid was estimated to study its correlation to hyperhomocysteinemia in Turner syndrome children.

Results

The karyotype analysis showed 45,X (monosomy X) in the 78 patients. Vitamin B12 and folic acid were significantly decreased in children with Turner syndrome in 65–73% of the patients, respectively, while the serum level of homocysteine significantly increased to 48.7% compared to healthy controls. Homocysteine level negatively correlated with vitamin B12 and folic acid. The deficiency of vitamin B12 and folic acid increased the risk of hyperhomocysteinemia in children with Turner syndrome (OR 2.49 and 2.36, respectively).

Conclusions

This report highlights that hyperhomocyste-inemia in children with Turner syndrome may be related to the deficiency vitamin B12 and folic acid.


Corresponding author: Hala T. El-Bassyouni, Clinical Genetics Department, Human Genetics and Genome Research Division, National Research Centre, Giza, Egypt, E-mail:

  1. Research funding: The authors declare that no funds, grants or other support were received during the preparation of this manuscript.

  2. Author Contributions: All authors contributed to the study conception and design. Analyses was performed by [Eman R. Youness], [Shaimaa A. Hashem] and [Azzah A. Khedr]. Material preparation, data collection was performed by [Khaled Hamed], [Eatemad Nabil Abdulhalim] and [Shimaa Mostafa Kamel]. The first draft of the manuscript was written by [Hala T. El-Bassyouni] and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

  3. Competing Interests: The authors have no relevant financial or non-financial interests to disclose.

  4. Informed consent: Informed consent was obtained from all individuals included in this study.

  5. Ethics approval: This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of Al-Azhar University (No: IRP 201912320).

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Received: 2022-09-22
Accepted: 2022-11-30
Published Online: 2022-12-20
Published in Print: 2023-02-23

© 2022 Walter de Gruyter GmbH, Berlin/Boston

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