Association between iron and zinc deficiency and retinopathy of premature: A Narrative Review

Retinopathy of premature (ROP) is known as the abnormal growth of retinal blood vessels in premature infants, occurring mainly due to the exposure to high levels of oxygen. Improper growth of retinal vessels because of ischemia-reperfusion causes oxidative damage and inflammation, and this condition is exacerbated by the abnormal proliferation of new vessels (neovascularization).

Zinc and iron, as the most abundant trace metals in the retina, control the redox-oxidation state in the retina; they also act as cofactors for many enzymes, including antioxidant enzymes. The deficiency of these two elements is common in preterm neonates and is considered one of the pathogens of ROP.

Adequate zinc and iron levels inhibited not only inhibit oxidative damage and inflammation caused by hypoxia but also vascular endothelial growth factor (VEGF) expression. In support of this mechanism, the results of the study showed that premature infants receiving high doses of zinc and adequate doses of iron significantly reduce the ROP process.

Oxidative damage and inflammation due to vascular ischemia in the retina are a major cause of ROP in infants, which may be due to zinc and iron deficiency. Therefore, monitoring serum zinc and iron levels and normalizing them may play an important preventive role in the development of retinopathy of prematurity.