Volume 6, Issue 1 (Journal of Clinical and Basic Research (JCBR) 2022)                   jcbr 2022, 6(1): 28-31 | Back to browse issues page

XML Print

Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Singaravelu A, Rajan Vasantharajan S, Raveendra R, Nancy A. Evaluation of Plasma Levels of Folic Acid and Homocysteine in Babies Born With Various Types of Neural Tube Defects: A Single Center Study in South India. jcbr. 2022; 6 (1) :28-31
URL: http://jcbr.goums.ac.ir/article-1-350-en.html
1- Department of Anatomy, PSP Medical College, Dr. M.G.R. University, Tamil Nadu, Chennai, India
2- Department of Obstetrics & Gynecology, St.Peter’s Medical College Hospital & Research Institute, Hosur, Tamil Nadu, India
3- Department of Anatomy, Phulo Jhano Medical College, Dumka, Jharkhand, India
4- Sri Balaji Vidyapeeth , ancyjean2010@gmail.com
Abstract:   (279 Views)
Background and objectives: Neural tube defects (NTDs) are common congenital anomalies caused by genetic, environmental, or nutritional factors. Normal plasma folic acid levels in the fetus are required for proper development of the neural tube. Plasma folic acid level has an inverse relationship with homocysteine level. This study aimed to determine plasma folic acid and homocysteine levels in babies born with NTDs and healthy controls.
Methods: The study included 30 clinically diagnosed NTD cases and 30 healthy age- and sex-matched control subjects. Plasma levels of folic acid and homocysteine were measured using a direct chemiluminescence method. Data were compared using the independent t-test. Statistical analysis of data was performed using GraphPad InStat 3.0 at significance of 0.05
Results: The mean plasma level of folic acid in NTD cases (5.1±4.9 mol/l) was significantly lower than that in healthy controls (19.5±2.1 mol/l) (p<0.05). The mean plasma level of homocysteine in NTD cases (14.3 ± 2.4 ng/ml) was significantly higher than that in healthy controls (4.9±1.8 ng/ml)(p<0.05). The mean plasma level of folic acid was 20.1±1.5 µmol/l, 8.5 ±2.9 µmol/l, and 1.9 ±0.4 µmol/l in mild, moderate, and severe cases of NTD, respectively. The mean plasma level of homocysteine was 10.7±3.4 ng/ml, 15.4±1.2 ng/ml, and 18.5±0.8 ng/ml in mild, moderate, and severe cases of NTD, respectively.
Conclusion: Low level of folic acid and high level of homocysteine are directly associated with the development of neural tube abnormalities. Moreover, the severity of the NTD is inversely related to plasma level of folic acid and directly related to plasma level of homocysteine.
Full-Text [PDF 324 kb]   (118 Downloads) |   |   Full-Text (HTML)  (71 Views)  
Article Type: Research | Subject: Biochemistry
Received: 2022/02/12 | Accepted: 2022/04/4 | Published: 2022/04/17

1. Keith L. Moore P. The Developing Human, Clinically oriented anatomy, 8th edition. 387-92. [View at Publisher] [Google Scholar]
2. Anil C, Siju S. Incidence of neural tube defects in the least-developed area of India: A population-based study. The Lancet 2005; 366: 930-31. [View at Publisher] [DOI] [Google Scholar]
3. Hema G, Piyush G. Neural Tube Defects and Folic Acid. Indian pediatrics. 2004; 41:577-586. [Google Scholar]
4. Alfarra HY, Alfarra SR, Sadiq MF. Neural tube defects between folate metabolism and genetics. Indian Journal of Human Genetics. 2011 Sep;17(3):126. [DOI] [PMID] [PMCID] [Google Scholar]
5. Norturp H, Volcik KA. Spina bifida and other Neural tube defects. Cur Probl Pediatr, Nov-Dec 2000;30(10):313-32. [View at Publisher] [DOI] [PMID] [Google Scholar]
6. Patterson AD, Hildeshcim J, Fornace AJ. Neural tube development requires the co-operation of p53 and Gadd45a associated pathways. Birth Defects Res A Clin Mol Teratol. Feb 2006;76(2):129-32 [View at Publisher] [DOI] [PMID] [Google Scholar]
7. Felkner M, Suarez L, Canfield M A. Maternal serum homocysteine and risk for neural tube defects in Texas-Mexico border population. Birth Defects Res A Clin Mol Teratol. Jun2009; 85(6):574-81. [View at Publisher] [DOI] [PMID] [Google Scholar]
8. Van der put N M, Van straiten H W, Trijbels F J. Folate, homocysteine and neural tube defects: an overview. Exp Biol Med Apr2001;226(4)243-70. [View at Publisher] [DOI] [PMID] [Google Scholar]
9. Patrizia D M, Anna M, Elisa M. Folate pathway gene alterations in patients with neural tube defects. American Journal of Medical Genetics. Nov2000; 95(3): 216-23. [View at Publisher] [DOI] [Google Scholar]
10. Ames BN. Micronutrient deficiencies: a major cause of DNA damage. Annals of the New York Academy of Sciences. 1999 Oct;889(1):87-106. [View at Publisher] [Google Scholar]
11. Nowaczyk MJ, Ramsay JA, Mohide P, Tomkins DJ. Multiple congenital anomalies in a fetus with 45, X/46, X, r (X)(p11. 22q12) mosaicism. American journal of medical genetics. 1998 May 26;77(4):306-9. [View at Publisher] [DOI] [Google Scholar]
12. Mills JL, Scott JM, Kirke PN, McPartlins JM, Conley MR, Weir DG, Molloy AM, Lee YJ. Homocysteine and neural tube defects. The Journal of nutrition. 1996 Mar 1;126(suppl_3):756S-60S. [View at Publisher] [PubMed] [Google Scholar]
13. García-Fragoso L, García-García I, Cadilla CL. The Role of Folic Acid in the Prevention of Neural Tube Defects. In: Narasimhan KL, editor. Neural Tube Defects - Role of Folate, Prevention Strategies and Genetics [Internet]. London: IntechOpen; 2012 [cited 2022 Feb 10]. Available from: https://www.intechopen.com/chapters [DOI]

Add your comments about this article : Your username or Email:

Send email to the article author

Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

© 2022 CC BY-NC 4.0 | Journal of Clinical and Basic Research

Designed & Developed by : Yektaweb

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0).