Authored by Khajik Sirob Yaqob
Introduction
Zinc is the second most abundant trace mineral after iron, and is important in the protein metabolism and synthesis, in DNA metabolism, and in stabilization of cell membrane [1].It is essential for functions of various cellular metabolisms, and it acts as a cofactor for more than two hundred enzymes [1]. Also, zinc has its crucial role during periods of growth and tissue proliferation (immune system, wound healing, skin, and GIT integrity). Furthermore, zinc has its own vital physiologic role in immune function, sexual maturation and normal growth [1].
Animal products including human milk are considered the best dietary source of zinc. In addition, whole grains and legumes contain moderate amount of zinc. Globally, poor bioavailability of zinc secondary to phytic acid, which inhibits zinc absorption from its sources, is considered more important factor than low intake in many cases of zinc deficiency [1].
A syndrome called Zinc Deficiency Dwarfism was first described in a group of children in the Middle East with low level of zinc in their hair, poor appetite, diminished taste acuity, hypogonadism, and short stature [1]. In developing countries, zinc supplementation can reduce morbidity and mortality among children from diarrhea and pneumonia, and zinc can enhance growth [1]. Prevalence of zinc deficiency is highly noticed in populations with high rates of stunting. Other contributing factors that can lead to zinc deficiency include inadequate zinc intake in complementary feeding or general diet, sever infection, lack of zinc in total parenteral nutrition and in premature infants fed human milk without fortification [1].
Clinical Manifestation of Zinc Insufficiency
In mild cases, poor appetite, growth faltering and immune impairment. Moderate-severe symptoms and signs include, delayed sexual maturation, rough skin and enlarged liver and spleen; whereas, manifestation as mood changes, growth and immune impairment, diarrhea, alopecia, photophobia, night blindness, scaling dermatitis, and acral and periorificial erythematous appear in severe zinc deficiency [1].Diagnosis of zinc deficiency Is challenging and mainly clinical. In mild zinc deficiency, plasma zinc level is often normal although zinc level is frequently used; levels in moderate to severe deficiency are characteristically less than 60μg/dl. Nevertheless, the response to a trial of zinc supplementation with outcomes such as improved linear growth or weight gain, enhanced appetite, and improved immune function, is the principles for identification of zinc insufficiency [1]. As zinc has no pharmacologic effect on these functions, a positive response to supplementation is considered evidence of preexisting deficiency. Therefore, clinically an empirical trial of zinc supplementation (1μg/kg/day) is a safe and a sensible approach in situations in which zinc deficiency is considered probable.
A specific condition called acrodermatitis enteropathica occurs when there is sever zinc deficiency in which plasma zinc level is markedly reduced and serum alkaline phosphatase activity is low [1]. Clinically, this condition is characterized by acute oral and perianal dermatitis, alopecia, and failure to thrive as a result of lack of intestinal zinc absorption [1]. This is occurring 2-4 weeks after infants have been weaned from breast milk.
Such condition is an autosomal recessive disorder, and it is relatively uncommon due to lack in the secretion of zinc from the mammary gland resulting in abnormally low milk zinc concentration [1]. Hence, this occurs in breast fed infants especially premature present with standard signs of zinc deficiency including growth failure, diarrhea, and dermatitis. Treatment is with high dose of zinc with successful continuous breast feeding.
Zinc is nontoxic element, certain features such as nausea, vomiting, abdominal pain, headache, vertigo and seizures might appear as a result of excessive intake of zinc [1].
Moreover, the main dietary sources of zinc are meat, shellfish, wholegrain, legumes and cheese. In developing countries, due to malnutrition, zinc deficiency is quite common [1].
Zinc dwarfism, hypogonadism, dermatitis and T-cell immunodeficiency are signs of chronic zinc deficiency which often associated with lack of iron micronutrient [1].
People with certain conditions such as Crohn’s disease, short bowel syndrome, and sprue are more prone to zinc deficiency as a result of malabsorption of zinc and increased zinc losses in the urine [2,3]. In contrast, persons with mild human zinc deficiency states, the obvious features and laboratory/functional abnormalities of mild zinc deficiency are varied. Such variety is not altogether astonishing in view of the biochemistry of zinc and the ubiquity of this metal in biology with its contribution in an extraordinarily wide range of essential metabolic processes. Impaired growth velocity is a main clinical feature of mild zinc insufficiency and can be corrected with zinc supplementation [4,5]. Pregnancy outcome [6] and the function of the immune system [7] are evident cases that clinically respond to zinc supplementation.
Zinc is widely used in people with common cold. However, the clinical consequence of zinc lozenges in dropping the duration of flue is still unclear [8].
In patients fed intravenously with no addition of enough zinc to the infusates [9] and in cases of the autosomal recessively inherited disease such as acrodermatitis enteropathica, sever zinc deficiency is documented [10]. Because of association of zinc micronutrient in so many core areas of metabolism, the features of zinc deficiency are basic and nonspecific, including growth retardation, alopecia, diarrhea, delayed sexual maturation and impotence, eye and skin lesions, and impaired appetite. Therefore, clinical features and laboratory criteria are not always reliable. As a result, certain potentially useful laboratory indicators such as alkaline phosphatase activity can be used clinically to validate reliable, sensitive clinical or functional indicators of zinc status in the body.
Zinc and Neurodevelopment
In addition to studies on the clinical impacts of low-dose zinc supplements on individuals with pneumonia, diarrhea [11] and on nonspecific laboratory functional tests of zinc status such as tests of neuro- cognitive function [12] or immune status [13], research results including the effects of zinc supplementation on physical growth velocity in children are helpful to assess the dietary zinc intake for many causes. 1st, approved clinical evidence of zinc supplements on growth velocity (linear growth and weight) in children with variable degrees of growth delay has been documented [14,15]. 2nd, because an adequate figure of these studies has been done in North America, growth is appropriate as a functional/clinical indicator of zinc requirement in North American children [5,16-18]. Finally, database involved in these studies are adequate to use for cohort analysis.Average Zinc Consumption from Human Milk During the First 12 Months of Feeding
In order to match the zinc intake of the infant in early weeks (Figure) the adequate intake is set at 2.0 mg/day (2.5mg/L × 0.78L/ day). Interestingly, similar clinical results have been obtained concerning weight gain and body length or height at ages foursix months when evaluated by zinc intake from human milk and complementary foods at this age [19]. Consequently, a helpful connection between zinc content of human milk at five months and improvement in the weight-for age Z scores for the five to seven months interval have been documented [20]. However, that growthlimiting zinc deficiency can occur in infants mainly fed human milk after the age of four months [21].
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