Volume 7, Issue 2 (9-2021)                   CJP 2021, 7(2): 0 | Back to browse issues page


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Rasoulinejad S A, Akbari A. Association between iron and zinc deficiency and retinopathy of premature: A Narrative Review. CJP 2021; 7 (2) :566-575
URL: http://caspianjp.ir/article-1-153-en.html
Department of Physiology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran , A.akbari@shirazu.ac.ir
Abstract:   (3459 Views)
Context: Retinopathy of prematurity (ROP) is known as the abnormal growth of retinal blood vessels in premature and very low birth weight (VLBW) infants that can be caused by exposure to high oxygen pressure through oxidative damage and inflammation.
Evidence Acquisition: In this review, the keywords zinc deficiency, iron deficiency, and retinopathy of premature was first searched in databases including Scopus, Google Scholar, and PubMed. There were no time limitations for the search. Full-text articles in the English language were included in this study. Searching with these keywords did not yield any results. In the next step, preterm neonate, preterm infant and VLBW infants were added to the keywords.
Findings: The results showed that iron and zinc deficiencies are very common in premature and VLBW infants. VLBW and preterm birth are also risk factors for ROP. In addition, the use of zinc and iron supplements in low birth weight and premature infants is also commonly necessary to maintain normal growth and development.
Conclusion: It can be concluded that premature infants receiving high doses of zinc and adequate doses of iron inhibited not only inhibit oxidative damage and inflammation caused by hypoxia but also vascular endothelial growth factor (VEGF) expression. In support of this mechanism, our results showed that premature infants receiving high doses of zinc and adequate doses of iron significantly reduce the ROP process. Therefore, monitoring serum zinc and iron levels and normalizing them may play an important preventive role in the development of ROP.
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Type of Study: Applicable | Subject: Special

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