Study of Interleukin-6 as an Indicator Biomarker in Perinatal Asphyxia
DOI:
https://doi.org/10.21276/apalm.2275Keywords:
IL-6, neonates, perinatal, asphyxia, 48 hoursAbstract
Background: Birth asphyxia, though not always a recognizable cause, is a well documented contributor to perinatal and neonatal mortality. Four million babies are born asphyxiated annually resulting into 20% of all neonatal deaths. Perinatal asphyxia is the fifth largest cause of under-5 deaths
Methods: Serum IL-6 levels were measured by ELISA in sera of thirty newborn babies ≥31 weeks of gestation with Apgar score <8 at 1 minute after birth with perinatal asphyxia (Study group) and 30 age and sex matched healthy controls (Control group), at birth (within 6 hours) and 48 hours after delivery.
Result: The mean levels of IL-6 in the study and control groups were 158.09±63.76 pg/ml and 41.57±71.23 pg/ml at birth and 187.96±30.31 pg/ml and 24.54±58.74 pg/ml at 48 hours respectively. Rise in levels of IL-6 in study group when compared with the control was statistically significant both at birth and at 48 hours. The median IL-6 levels in the study group and control group were 196.40 pg/ml and 4.17 pg/ml respectively at birth. The median IL-6 levels in the study group at birth were 47 fold higher than levels of control group. Median IL-6 levels both at birth and at 48 hours were statistically not significant among the mild, moderate and severely asphyxiated neonates. Amongst 30 healthy neonates, IL-6 levels were statistically not significant both at birth and at 48 hours.
Conclusion: IL-6 levels were significantly raised at birth and after 48 hours in asphyxiated neonates compared to gestational age and sex matched healthy neonates.
References
2. De Costello LAM, Manandhar DS. Perinatal asphyxia in less developed countries. Arch Dis Child Fetal Neonatal Ed 1994; 71:F1-3.
3. National Neonatal-Perinatal Database (2002–03). New Delhi, India: National Neonatology Forum and Indian Council of Medical Research.
4. Kliegman RM, Stanton BF, St. Geme JW, Schor NF, Berhman RE. Nelson Textbook of Pediatrics , 19th ed. Philadelphia: Elsevier Saunders; 2011.
5. Volpe JJ. Neurology of the Newborn, 3rd Ed. WB Saunders, Philadelphia, 1995:pp 876–884.
6. Kjellmer I, Hagberg H 1994 Perinatal brain damage, excitatory amino acids and oxygen derived free radicals. In: Geijn HPV and Copray FJA (eds). A Critical Appraisal of Fetal Surveillance. Elsevier, Amsterdam, pp 604–614.
7. Vannucci RC. Experimental biology of cerebral hypoxia-ischemia: relation to perinatal brain damage. Pediatr Res 1990;27:317–326.
8. Johnston MV. Neurotransmitters and vulnerability of the developing brain. Brain Dev 1995;17:301–306.
9. Boskabadi H, Afshari JT, Ghayour-Mobarhan M, Maamouri G, Shakeri MT, Sahebkar A, et al. Association between serum interleukin-6 levels and severity of perinatal asphyxia. Asian Biomed 2010;4:79-85
10. Xanthou M, Fotopoulos S, Mouchtouri A, Lipsou N, Zika I, Sarafidou J. Inflammatory mediators in perinatal asphyxia and infection. Acta Paediatr Suppl. 2002;91(438):92-7.
11. Slaats J, Oever J, Veerdonk FL, Netea MG. IL-1β/IL-6/CRP and IL-18/ferritin: Distinct Inflammatory Programs in Infections. PLoS Pathog 2016; 12(12): e1005973
12. Arntzen KJ, Lien E, Austgulen R. Maternal serum levels of interleukin-6 and clinical characteristics of normal delivery at term. ActaObstetGynecolScand 1997;76(1):55-60.
13. Sävman K, Blennow M, Gustafson K, Tarkowski E, Hagberg H. Cytokine response in cerebrospinal fluid after birth asphyxia. Pediatr Res 1998;43(6):746-51.
14. Chiesa C, Pellegrini G, Panero A, De Luca T, Assumma M, Signore F, Pacifico L. Umbilical cord interleukin-6 levels are elevated in term neonates with perinatal asphyxia. Eur J Clin Invest 2003;33(4):352-8.
15. Aly H, Khashabab MT, El-Ayoutyb M, El-Sayedb M, Hasanein BM. IL-1β, IL-6 and TNF-ï¡ and outcomes of neonatal hypoxic ischemic encephalopathy. Brain Development 2006; 28:178-82.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2019 Tajuddin Mohd, Iqbal R Kaur, Bineeta Kashyap, MMA Faridi, N P Singh
This work is licensed under a Creative Commons Attribution 4.0 International License.
Authors who publish with this journal agree to the following terms:
- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access at http://opcit.eprints.org/oacitation-biblio.html).
