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1. Introduction
Zinc (Zn) is an essential nutrient, present in all body tissues and fluids. The biologic role ofZn is now recognized in structure and function of proteins, including more than 300 enzymes,transcription factors, hormonal receptor sites, and biologic membranes. Zn is a criticalmicronutrient for normal growth, haematopoiesis, immune function and neurologic developmentduring infancy. Infants have a relatively high requirement of Zn per unit body weight during asensitive period of rapid growth and development [1]. About 30 years ago, clinicians first notedthat human zinc deficiency secondary to acrodermatitis enteropathica, an inborn error ofmetabolism that causes reduced intestinal absorption of zinc, is associated with impaired growth,increased susceptibility to infections, and other functional abnormalities[2]. Functionally Znparticipates in cell division and growth, intestinal electrolyte absorption, neurotransmission,immune response, thymus activity, and vision [3–5]. Human Zn deficiency was described sincethe early 1960s, but it was not until 1990, when Zn became to be a micronutrient of majorinterest until the current date due to the important function of Zn in the immune system integrity[6] hence its deficiency may have grave consequences in human [7]. Clinical manifestations ofZn deficiency become evident only with severe deficiency; dermatitis, diarrhea, neurologicaldisorders, growth failure, infections and delayed tissue healing following injuries are the mostfrequent clinical consequences of zinc deficiency.The global prevalence of Zn deficiency is unknown unfortunately, due to perceived highcosts and logistical challenges, as well as the existence of a limited number of valid biomarkers,few nationally representative surveys have been conducted in low-income countries to assesspopulation Zn status and the risk of Zn deficiency using the aforementioned recommendedindicators [8].The diagnosis of Zn deficiency currently requires some evidence of a physiologicalresponse to a therapeutic trial of Zn, hence a substantial investment of time and resources isnecessary to establish the diagnosis, and large-scale population studies are still limited.
In early life, Zn deficiency during pregnancy may affect normal embryonic and fetal growthin experimental animals, and the length of gestation may also be affected. There is an evidencethat trace element deficiencies such as Zn, copper and magnesium during pregnancy play animportant role on pregnancy outcome [9]. As with many other nutrients, preterm neonates do nothave functional reserves or body stores of available Zn, except neonates born at term, who maybe able to draw on the hepatic Zn accumulated during the entire gestational period [10]. Pretermand low birth weight babies may have impaired Zn status due to low body stores, limitedcapacity to absorb and retain micronutrients coupled with increased endogenous lossesassociated with organ immaturity, high nutrient demand to support catch-up growth, andinadequate intakes because exclusive breastfeeding does not compensate for increased demanddue to prematurity also environmental injuries, frequent use of antibiotics, significantly increasethe risk of Zn deficiency. In addition, preterm birth reduces the duration of pregnancy and thusthe amount of hepatic stores available during periods of reduced Zn intake. Preterm infants havehigh Zn deficit and dietary requirements as 60% fetal Zn is acquired during third trimester ofpregnancy. It seems clear that very preterm infants, who have poor Zn stores and great need forgrowth, are at particular risk of Zn deficiency, as shown by Ram Kumar et al. [11]. Zn intake hasbeen associated with improving growth outcomes in both term and preterm infants over the first12 months [12, 13], also study indicates that higher dietary Zn may be required to meet the dailyreq
