Zinc Deficiency In Infants Research Articles

Consider Zinc Deficiency in Infants with Periorificial Lesions

Background: Zinc is an essential trace element required for proper bodily function. Its deficiency can lead to various manifestations, including dermatological issues. There are two forms of zinc deficiency: hereditary and acquired. Case Report: We present two cases. The first case involved a child with a family history of two brothers who passed away at the age of 1 year, exhibiting a similar symptomatology. The second case involved a patient with hereditary epidermolysis bullosa and malnutrition. Both cases presented with erosive erythematous lesions around the mouth and extremities, which were unresponsive to symptomatic treatments. Additionally, they experienced diarrhea. A definitive diagnosis was made by measuring the levels of zinc in their blood, which were found to be low. Treatment with oral zinc sulfate was prescribed. The first patient showed rapid improvement with the treatment, but experienced recurrence when it was discontinued and subsequently improved again upon reinstatement. Unfortunately, the second infant passed away due to complications from an infection. Conclusion: The presence of periorificial and extremity lesions in infants should raise suspicion of zinc deficiency. Measuring zinc levels in the blood can help confirm the diagnosis and guide appropriate treatment

A dynamic model for predicting growth in zinc-deficient stunted infants given supplemental zinc

Zinc deficiency limits infant growth and increases susceptibility to infections, which further compromises growth. Zinc supplementation improves the growth of zinc-deficient stunted infants, but the amount, frequency, and duration of zinc supplementation required to restore growth in an individual child is unknown. A dynamic model of zinc metabolism that predicts changes in weight and length of zinc-deficient, stunted infants with dietary zinc would be useful to define effective zinc supplementation regimens. The aims of this study were to develop a dynamic model for zinc metabolism in stunted, zinc-deficient infants and to use that model to predict the growth response when those infants are given zinc supplements. A model of zinc metabolism was developed using data on zinc kinetics, tissue zinc, and growth requirements for healthy 9-mo-old infants. The kinetic model was converted to a dynamic model by replacing the rate constants for zinc absorption and excretion with functions for these processes that change with zinc intake. Predictions of the dynamic model, parameterized for zinc-deficient, stunted infants, were compared with the results of 5 published zinc intervention trials. The model was then used to predict the results for zinc supplementation regimes that varied in the amount, frequency, and duration of zinc dosing. Model predictions agreed with published changes in plasma zinc after zinc supplementation. Predictions of weight and length agreed with 2 studies, but overpredicted values from a third study in which other nutrient deficiencies may have been growth limiting; the model predicted that zinc absorption was impaired in that study. The model suggests that frequent, smaller doses (5-10 mg Zn/d) are more effective for increasing growth in stunted, zinc-deficient 9-mo-old infants than are larger, less-frequent doses. The dose amount affects the duration of dosing necessary to restore and maintain plasma zinc concentration and growth.

Infants and elderlies are susceptible to zinc deficiency.

The importance of zinc for human health has been recognized since the early 1960s, but today there is little concern about zinc deficiency in developed countries. In this study, we measured the zinc concentration in hair from 28,424 Japanese subjects (18,812 females and 9,612 males) and found that 1,754 subjects (6.17%) had zinc concentrations lower than 2 standard deviations (86.3 ppm) below the control reference range, which qualifies as zinc deficiency. In particular, a considerable proportion of elderlies and children (20% or more) were found to have marginal to severe zinc deficiency. A zinc concentration of 9.7 ppm was the lowest observed in a 51-year-old woman; this concentration was approximately 1/13 of the mean reference level. The prevalence of zinc deficiency in adults increased with aging to a maximum of 19.7% by the 8th decade of life, and decreased to 3.4% above 90-year-old. The proportion of zinc deficiency in infants 0–4 years was 36.5% in males and 47.3% in females; these percentages were higher than the maximum prevalence in elderly subjects. These findings suggest that infants and elderlies are prone to zinc deficiency and that intervention of zinc deficiency is necessary for normal human development, health and longevity.

Maternal zinc status is associated with breast milk zinc concentration and zinc status in breastfed infants aged 4-6 months.

Breast milk provides adequate nutrients during the first 6 months of life. However, there are some reports of zinc deficiency in breastfed infants. This study was conducted to determine the prevalence of zinc deficiency in infants aged 4-6 months and the associated factors. Healthy infants aged 4-6 months and their mothers were enrolled. They were classified by feeding types as breastfed (BF), formula-fed (FF), and mixed groups (MF). Data collection included demographic data, perinatal data, given diets, and anthropometric measurement. Blood from infants and lactating mothers, and breast milk samples were collected to assess plasma and breast milk zinc concentrations. From 158 infants, the prevalence of zinc deficiency (plasma level below 10.7 mol/L) was 7.6%, and according to feeding groups 14.9%, 5.3%, and 2.9% in the BF, the FF, and the MF groups, respectively. Breastfed infants with zinc deficiency had significantly lower maternal zinc concentrations compared with those without zinc deficiency. There was a higher proportion of maternal zinc deficiency in zinc-deficient infants than those without zinc deficiency (66.7% vs 16.2%, p=0.02). There was a positive correlation between zinc concentrations in breast milk and plasma zinc concentrations of infants (r=0.62, p=0.01) and plasma zinc concentrations of lactating mothers (r=0.56, p=0.016). Using the regression analysis, infant zinc status was associated with maternal plasma zinc concentrations among breastfed infants. The results of this study suggest that breastfed infants aged 4-6 months may have a risk of zinc deficiency and that risk is associated with maternal zinc status and breast milk zinc concentrations.

Overview of Inherited Zinc Deficiency in Infants and Children.

Zinc nutrition is of special practical importance in infants and children. Poor zinc absorption causes zinc deficiency, which leads to a broad range of consequences such as alopecia, diarrhea, skin lesions, taste disorders, loss of appetite, impaired immune function and neuropsychiatric changes and growth retardation, thus potentially threatening life in infants and children. In addition to dietary zinc deficiency, inherited zinc deficiency, which rarely occurs, is found during the infant stage and early childhood. Recent molecular genetic studies have identified responsible genes for two inherited zinc deficiency disorders, acrodermatitis enteropathica (AE) and transient neonatal zinc deficiency (TNZD), clarifying the pathological mechanisms. Both of these zinc deficiencies are caused by mutations of zinc transporters, although the mechanisms are completely different. AE is an autosomal recessive disorder caused by mutations of the ZIP4 gene, consequently resulting in defective absorption of zinc in the small intestine. In contrast, TNZD is a disorder caused by mutations of the ZnT2 gene, which results in low zinc breast milk in the mother, consequently causing zinc deficiency in the breast-fed infant. In both cases, zinc deficiency symptoms are ameliorated by a daily oral zinc supplementation for the patients. Zinc is definitely one of the key factors for the healthy growth of infants and children, and thus zinc nutrition should receive much attention.

Scientific Opinion on the substantiation of a health claim related to zinc and normal growth pursuant to Article 14 of Regulation (EC) No 1924/2006

Following an application from Specialised Nutrition Europe (formerly IDACE), submitted pursuant to Article 14 of Regulation (EC) No 1924/2006 via the Competent Authority of France, the EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA) was asked to deliver an opinion on the scientific substantiation of a health claim related to zinc and normal growth. The food constituent, zinc, which is the subject of the health claim, is sufficiently characterised. Normal growth is a beneficial physiological effect for infants and young children. The Panel considers that the role of zinc in normal growth is well established. Growth retardation is one of the clinical manifestations of severe zinc deficiency. Zinc supplementation has been reported to stimulate growth and development in zinc-deficient infants and young children. The Panel concludes that a cause and effect relationship has been established between the dietary intake of zinc and normal growth. The following wording reflects the scientific evidence: “zinc contributes to normal growth”. The target population is infants and children up to three years of age.

Zinc deficiency in infants and children: a review of its complex and synergistic interactions

Zinc deficiency is estimated to contribute to over half a million deaths per year in infants and children under 5 years of age. This paper reviews the features of mild-to-moderate zinc deficiency, which include growth faltering, deficits in immune function and altered integrity and function of the gastro-intestinal tract. Sub-clinical features include oxidative stress and a pro-inflammatory state. The homeostatic response to low dietary zinc intake by increasing absorption is limited, especially if the source of zinc is of poor bioavailability, and conservation of endogenous intestinal losses is a critical component of adaptation. Owing to low zinc intakes, older breastfed infants, especially those of low birthweight, are predictably at risk of zinc deficiency if complementary food choices are unfortified and/or low in zinc. Host factors such as young age, poor intra-uterine zinc accretion owing to poor maternal status and/or prematurity, and gastro-intestinal dysfunction also potently predispose to zinc deficiency. Environmental enteropathy, which is prevalent in low-resource settings, may substantially impair zinc absorption and/or increase endogenous losses, and thus lead to relatively high zinc requirements. Emerging evidence highlights common features between chronic inflammation and zinc deficiency, and each may exacerbate the other. More investigations of zinc homeostasis in populations in low-resource settings are needed to better quantify absorption capacity and losses. Effective preventive strategies must address potentially higher zinc requirements as well as the underlying context that perpetuates a vicious cycle of zinc deficiency and multiple adverse outcomes.

High frequency of symptomatic zinc deficiency in infants in northern ethiopia.

Background. Zinc deficiency occurs in infants when its demand exceeds its supply. It presents with cutaneous signs which, in severe cases, are associated with diarrhea, alopecia, and irritability. Genetic and acquired forms of zinc deficiency have been reported and often overlap clinical features. Malnutrition, prematurity, malabsorption syndromes, and burns may cause an increased demand for zinc. Methods. Cases of acquired transient infantile zinc deficiency (TIZD) observed during a period of 3 years at Ayder Referral Hospital of Mekelle, Northern Ethiopia, are reported here. Since no sophisticated tests were available at our center, the diagnosis was based on the clinical signs and prompt response to oral zinc supplementation. Results. We observed 18 cases of TIZD at our center. All patients were full-term and breastfeeding infants with no relevant associated diseases. Conclusions. In this region, a high incidence of this condition is observed. We could not rule out whether heterozygosity for the genetic mutation was present or that the disease was caused by a nutritional deficiency in the mothers or more probably because both the factors coexisted together. However, further studies are necessary to better understand the causes of the increased incidence of this disease in Northern Ethiopia.

Effect of zinc supplementation between 1 and 6 mo of life on growth and morbidity of Bangladeshi infants in urban slums

Evidence for an effect of zinc supplementation on growth and morbidity in very young infants in developing countries is scarce and inconsistent. We assessed the effect of zinc supplementation on growth and morbidity in poor Bangladeshi infants aged 4-24 wk. Infants from Dhaka slums were enrolled at 4 wk of age and randomly assigned to receive 5 mg elemental Zn/d (n = 152) or placebo (n = 149) until 24 wk of age. They were followed weekly for information on compliance and morbidity; anthropometric measurements were performed monthly. Serum zinc was assessed at baseline and at 24 wk of age. At 24 wk of age, serum zinc concentrations were higher in the zinc than in the placebo group (13.3 +/- 3.8 and 10.7 +/- 2.9 micro mol/L, respectively; P < 0.001). Significantly greater weight gains were observed in the zinc than in the placebo group for 43 infants who were zinc deficient (< 9.18 micro mol/L) at baseline (3.15 +/- 0.77 and 2.66 +/- 0.80 kg, respectively; P < 0.04). In the other infants, no significant differences were observed in mean weight and length gains during the study period. Zinc-deficient infants showed a reduced risk of incidence of acute lower respiratory infection after zinc supplementation (relative risk: 0.30; 95% CI: 0.10, 0.92); among the non-zinc-deficient infants there were no significant differences between treatment groups. Zinc-deficient Bangladeshi infants showed improvements in growth rate and a reduced incidence of acute lower respiratory infection after zinc supplementation. In infants with serum zinc concentrations > 9.18 micro mol/L, supplementation improved only biochemical zinc status.

Evaluation of zinc metabolism with use of stable-isotope techniques: implications for the assessment of zinc status

Zinc stable isotopes can be applied to the identification of populations at risk for zinc deficiency and to moni-toring the effects of zinc intervention studies designed to improve zinc nutriture. Techniques using these isotopes can provide information on how effectively the intestine is absorbing exogenous dietary zinc and conserving endogenous zinc. They can also yield estimates of the quantity of readily exchangeable zinc in the body. Data derived from stable-isotope studies can provide extensive information on zinc status and the bioavailability of dietary zinc, allowing researchers to relate zinc intake to physiologic and pathologic conditions. Application of these techniques in longitudinal studies can provide quantitative data on the effectiveness of prevention programs such as simple community measures aimed at reducing dietary phytate and zinc fortification and supplementation programs. Further, judicious application of zinc stable-isotope techniques could make an important contribution to progress toward the eradication of zinc deficiency in infants and young children in the developing world. Am J Clin Nutr 1998(suppl);68:410S–3S.

Abnormal zinc content in human milk. Risk for development of nutritional zinc deficiency in infants.

An abnormally low concentration of zinc in mother's milk has been associated with clinical nutritional zinc deficiency in premature and term newborns. Defective mammary gland secretion of zinc was suggested as the causative factor. We investigated whether low milk zinc concentration might be reflected in an abnormality of the distribution of zinc between casein, whey, and fat components of the milk, in a reduction in the levels of milk citrate, a zinc-binding ligand, or in abnormal levels of copper and iron. Milk from mothers of four low-birth-weight infants was identified as being deficient in zinc content for the lactational stage. One infant had clinical signs of nutritional zinc deficiency. For two of the three infants with subclinical deficiencies in whom balance study data were available, the apparent zinc balance was negative (-5.7 and -6.0 mumol/kg per day). These milks were examined for content and distribution of zinc, copper, and iron, and citrate concentration. Although total zinc concentration (4.5 to 17.2 mumol/L) was below the 95% prediction interval (15.2 to 59.7 mumol/L) for the lactational stage, the distribution of zinc was normal between milk components. Levels of citrate (1.46 to 5.13 mmol/L) were also within normal limits, as were levels of copper (0.27 to 0.85 mumol/L and iron (0.41 to 1.13 mumol/L). We concluded that there was no indirect evidence of a secretory abnormality in milk zinc deficiency, but speculated that there might instead be an abnormality of zinc uptake by the mammary gland from the plasma.

Studies of marginal zinc deprivation in rhesus monkeys: VI. Influence on the immunohematology of infants in the first year

Rhesus monkey infants fed a marginally zinc-deficient diet (4 ppm) from conception through 12 mo of postnatal life were monitored for changes in hematological, biochemical, and immunological parameters. These zinc-deprived (ZD) infants were compared to control infants whose mothers were fed a zinc-replete (100 ppm) diet either ad libitum (AL) or pair-fed (PF) throughout gestation and lactation. Blast transformation of peripheral blood lymphocytes to phytohemagglutinin (PHA-P), concanavalin A (Con A), and pokeweed mitogen (PWM), was dramatically depressed in the zinc-deficient (ZD) group. Similarly, ZD infants had reduced polymorphonuclear leukocyte function as measured by chemotaxis to endotoxin-activated plasma and phagocytosis of Candida albicans. Levels of serum IgM were significantly altered in zinc-deficient infants compared to controls. Serum concentrations of IgG and IgA were similar in zinc-deficient and control infants. ZD infants also manifested a hypochromic microcytic anemia at one month of age, reduced activity of the zinc metalloenzyme alkaline phosphatase, and lower activity of SGPT.

Studies of marginal zinc deprivation in rhesus monkeys. IV. Growth of infants in the first year

Growth was evaluated in rhesus monkey infants that were the offspring of females given a marginally zinc-deficient diet (4 µg/g zinc) from the beginning of pregnancy and through 12 months of postnatal life. These zinc-deficient (ZD) infants were compared to controls whose mothers were fed a complete diet, either ad libitum or pair-fed to zinc-deficient dams, throughout gestation and lactation. Male ZD infants had evidence of growth retardation at birth. In contrast, growth retardation in female ZD infants was not observed until 1 month of age. From 3 to 9 months of age (late lactation and subsequent to weaning) ZD infants attained weights similar to those of the control group. However, analysis of crown-rump and femur length indicated that ZD infants' growth was less than optimal throughout the entire 1st yr of observation. In addition, skinfold thickness was markedly higher in ZD than in control infants in the postweaning period. In the juvenile period (9–12 months of age) both male and female ZD animals fell behind controls in body weight. ZD juveniles were also hypogeusic, as determined by a quinine acceptance test. Low weight ZD infants had reduced somatic growth as reflected in sitting height, long bone growth, head circumference, and limb circumference. Regression analysis indicated that impaired growth rates from 9 to 12 months were associated with both lower food intake and reduced food use efficiency. Plasma zinc concentration was, in general, inversely related to weight gain in both groups during the 1st yr.

Zinc Absorption From Human Milk: Need for Zinc Supplementation-Reply

In Reply .—We read with interest the letter by Drs Gupta and Gupta. We agree that zinc nutrition of the neonate should still be of concern and that zinc requirements may need to be reevaluated; however, we take issue with some of the statements provided. That two single cases of zinc deficiency in infants have been reported is surely not sufficient evidence to contradict the statement that zinc deficiency is rare in breast-fed infants. Although we are aware of two additional cases, 1,2 all four of these infants were born prematurely. It is well known that premature infants will have lower stores of trace elements such as zinc, copper, and iron 3 and consequently have higher requirements than full-term infants. We agree that pooled mature breast milk may provide inadequate amounts of zinc to compensate for this increased demand. There are several reasons why it is often recommended that the

Zinc Deficiency in a Premature Infant Fed Exclusively Human Milk

The most notable changes of severe zinc deficiency are diarrhea, growth failure, delayed sexual maturation, alopecia, dermatitis, anorexia, mood changes, and frequent infections.1While severe zinc deficiency is rare in infancy, milder forms of zinc deficiency may be more common.2Because breast milk seems to enhance zinc absorption, it is often referred to as the most appropriate formula for prevention of zinc deficiency in infants.3However, a recent report of symptomatic zinc deficiency in a breast-fed premature infant would seem to question this concept.4Herein we report the development of zinc deficiency in another breast-fed premature infant and discuss possible factors that contributed to its occurrence. Report of a Case.—The patient was the second child born of a 27-year-old woman. The pregnancy was uncomplicated until the 26th week, when premature onset of labor resulted in delivery of the 710-g infant. The neonatal course was complicated