Iron Status In Children Research Articles

Abnormal iron status is independently associated with reduced oscillometric lung function in schoolchildren.

Associations between anemia and allergic diseases have been reported, but the relationship of iron deficiency with airway dysfunction in children remains unclear. We aimed to investigate the relationship between abnormal iron parameters and lung function in schoolchildren. Four hundred and forty-five children (10-12years-old) from 11 elementary schools in were enrolled. The relationships of different iron parameters (hemoglobin, serum iron, transferrin saturation, and serum ferritin) with lung function evaluated by impulse oscillometry (airways resistanceat 5Hz [Rrs5], 10Hz [Rrs10], and the difference of Rrs5 and Rrs20 Hz [Rrs5-20]), and with exhaled nitric oxide (FeNO) were evaluated after adjustment for confounders including height, sex, and body mass index z-score, and for additional covariates that could affect airway function. Total airway dysfunction represented by Rrs5 was reduced in participants with low serum iron level (aβ: -0.13, 95% CI: -0.23 to -0.03, p=0.040) after adjustment for key confounders, but did not correlate with other iron profiles. Reduced oscillometric lung function recorded as Rrs5-20 was related with low serum iron and high serum ferritin, but the results were inconsistent after multiple comparisons. Associations were not observed with serum hemoglobin. Decreased serum iron level was related with airway dysfunction represented as oscillomteric Rrs5. Our results suggest a relationship of reduced lung function with abnormal iron status in children.

Vitamin D and iron status in children with food allergy

BackgroundChildren with food allergy are at specific risk for nutritional deficiencies. ObjectiveTo retrospectively determine prevalence of vitamin D and iron deficiencies in children with or without food allergy (FA). MethodsWe compared the markers of vitamin D and iron status of 0 to 17-year-olds with cow’s milk allergy (CMA) (n = 77), those with other FAs (n = 70), and those with atopy without FA (n = 87) at an academic pediatric allergy practice. Multiple linear regression analyses were performed to determine the impact of CMA and other FAs on vitamin D levels and iron markers. ResultsVitamin D deficiency was detected in one-fourth and insufficiency in one-third of children with CMA and other FAs and in those with atopic diseases but no FA, respectively. Vitamin D levels were associated with vitamin D supplementation and consumption of breast milk, cow’s milk, infant formula, or plant-based milk beverage, but not with CMA or other FAs. Older children with FA who did not consume any cow’s milk or alternative milk beverage were at highest risk for vitamin D insufficiency. Children with CMA have a higher rate of iron deficiency anemia (8%) than children with other FAs (1%) or those with no FA (5%, P < .001); however, suboptimal levels of transferrin saturation and iron were detected in up to one-third of children with CMA or other FAs. ConclusionVitamin D deficiency and insufficiency is common in children with atopy overall, but children with CMA are at higher risk for iron deficiency anemia. Intensive nutritional counseling and nutrient intake monitoring, specifically for vitamin D and iron in those avoiding cow’s milk, are necessary to optimize nutritional status.

Evaluation of Iron Status in Children with Autism Spectral Disorder: A Case-control Study

Introduction: Iron is an important factor in neural development. Iron Deficiency (ID) and Iron Deficiency Anaemia (IDA) anaemia is highly prevalent in patients of autism. There are a very small number of studies to show association between iron profile and autism. Aim: To investigate factors affecting iron status such as hemoglobin (%), serum iron, ferritin, and Total Iron Binding Capacity (TIBC) level in children with Autism Spectral Disorder (ASD) and healthy control. Materials and Methods: It was a case-control study done from April 2018 to April 2019. Total 100 participants were recruited of which 50 autistic patients were taken as cases, and 50 healthy subjects were taken as control. Childhood Autism Rating Scale (CARS) was used to evaluate the severity of autistic symptoms. Cut-off value of serum ferritin was &lt;10 ng/mL for preschoolers (&lt;6 years) and &lt;12 ng/mL for school-aged (&gt;6 years) children to evaluate ID. Anaemia was defined as haemoglobin &lt;11.0 g/dL for preschoolers and &lt;12.0 g/dL for school-aged categorical variables and were compared by using chi-square test. Normally distributed parametric variables were compared between groups by using independent samples t-test. Serum ferritin, iron, TIBC values were compared between severe, mild-moderate and control groups with ANOVA. The p-value &lt;0.05 was accepted to be statistically significant. Results: Mean serum levels of ferritin iron TIBC were significantly reduced in ASD patients (p&lt;0.001). The level of haemoglobin was also lower in ASD patients but it was not significant. Risk of ID and IDA was higher than normal subjects (RR for ID 1.74). Level of serum ferritin, iron and TIBC was lowest in severe autism as compared to mild-moderate autism and control groups. Conclusion: These findings suggest iron and ferritin levels should be measured in autistic patients as a baseline investigation and it may be used as a screening test for ASD.

Association between vitamin D3 deficiency and iron status in children between six months to five years

Association between vitamin D3 deficiency and iron status in children between six months to five years

Serum hepcidin concentrations in relation to iron status in children with type 1 diabetes

Chronic low-grade inflammation in type 1 diabetes (T1D) might increase hepcidin synthesis, possibly resulting in functional iron deficiency (FID). We hypothesized that in T1D children with FID, hepcidin concentrations are increased compared to those with normal iron status and those with absolute iron deficiency (AID). We evaluated hepcidin concentrations in T1D children in relation to iron status, and investigated whether hepcidin is useful in assessing FID. A cross-sectional study was conducted. FID was defined as elevated zinc protoporphyrin/heme ratio and/or red blood cell distribution width, and AID as low serum ferritin concentration. Post-hoc analyses with different definitions of FID were performed, using transferrin saturation and reticulocyte hemoglobin content. Serum hepcidin concentrations were measured using mass-spectrometry. The IRODIAB-study is registered at www.trialregister.nl (NTR4642). This study included 215 T1D children with a median age of 13.7 years (Q1–Q3: 10.1–16.3). The median (Q1–Q3) hepcidin concentration in patients with normal iron status was 1.8 nmol/l (0.9–3.3), in AID-patients, 0.4 nmol/l (0.4–0.4) and in FID-patients, 1.6 nmol/l (0.7–3.5). Hepcidin concentrations in FID-patients were significantly higher than in AID-patients (p < 0.001). Irrespective of FID-definition used, hepcidin concentrations did not differ between FID-patients and patients with normal iron status. This might be explained by the influence of various factors on hepcidin concentrations, and/or by differences in response of iron parameters over time. Single hepcidin measurements do not seem useful in assessing FID in T1D children. Multiple hepcidin measurements over time in future studies, however, might prove to be more useful in assessing FID in children with T1D.

Study the iron status in children with febrile seizures: a hospital based cross sectional study

Background: Febrile seizures are most common among childhood seizures, accounts to 2% to 5% in children below 5 years of age. Iron deficiency can cause many neurological deficits and may lower the seizure threshold. The present study was conducted to determine the iron status in children with febrile seizures.Methods: The present cross-sectional study was conducted in the Department of Pediatrics, HIMS, Dehradun, over a period of 12 month from January 2018 to December 2018. A total of 105 children of age group 6 month to 5 years, coming to pediatrics department were included in the study. Total study subjects were divided into two groups, Group I (febrile seizure) and Group II (other than febrile seizure). A consecutive sampling method was done for selection of study subjects.Results: In Group I (febrile seizure), the number of males were 71.7% while females were 28.3% with male: female ratio of 2.5:1. In Group I (febrile seizure), 61.7% of subjects had deficient iron level while 38.3% of subjects had normal serum iron level. Our study shows significantly low mean serum ferritin and mean serum iron level in subjects with febrile seizures.Conclusions: We concluded that iron deficiency is more common in febrile seizures and there is a positive association between serum iron level and febrile seizures.

Vitamin A and iron status of children before and after treatment of uncomplicated severe acute malnutrition.

Treatment of children with uncomplicated severe acute malnutrition (SAM) is based on ready-to-use therapeutic foods (RUTF) and aims for quick regain of lost body tissues while providing sufficient micronutrients to restore diminished body stores. Little evidence exists on the success of the treatment to establish normal micronutrient status. We aimed to assess the changes in vitamin A and iron status of children treated for SAM with RUTF, and explore the effect of a reduced RUTF dose. We collected blood samples from children 6-59 months old with SAM included in a randomised trial at admission to and discharge from treatment and analysed haemoglobin (Hb) and serum concentrations of retinol binding protein (RBP), ferritin (SF), soluble transferrin receptor (sTfR), C-reactive protein (CRP) and α1-acid glycoprotein (AGP). SF, sTfR and RBP were adjusted for inflammation (CRP and AGP) prior to analysis using internal regression coefficients. Vitamin A deficiency (VAD) was defined as RBP<0.7μmol/l, anaemia as Hb<110g/l, storage iron deficiency (sID) as SF<12μg/l, tissue iron deficiency (tID) as sTfR>8.3mg/l and iron deficiency anaemia (IDA) as both anaemia and sID. Linear and logistic mixed models were fitted including research team and study site as random effects and adjusting for sex, age and outcome at admission. Children included in the study (n=801) were on average 13 months of age at admission to treatment and the median treatment duration was 56 days [IQR: 35; 91] in both arms. Vitamin A and iron status markers did not differ between trial arms at admission or at discharge. Only Hb was 1.7g/l lower (95% CI -0.3, 3.7; p=0.088) in the reduced dose arm compared to the standard dose, at recovery. Mean concentrations of all biomarkers improved from admission to discharge: Hb increased by 12% or 11.6g/l (95% CI 10.2, 13.0), RBP increased by 13% or 0.12μmol/l (95% CI 0.09, 0.15), SF increased by 36% or 4.4μg/l (95% CI 3.1, 5.7) and sTfR decreased by 16% or 1.5mg/l (95% CI 1.0, 1.9). However, at discharge, micronutrient deficiencies were still common, as 9% had VAD, 55% had anaemia, 35% had sID, 41% had tID and 21% had IDA. Reduced dose of RUTF did not result in poorer vitamin A and iron status of children. Only haemoglobin seemed slightly lower at recovery among children treated with the reduced dose. While improvement was observed, the vitamin A and iron status remained sub-optimal among children treated successfully for SAM with RUTF. There is a need to reconsider RUTF fortification levels or test other potential strategies in order to fully restore the micronutrient status of children treated for SAM.

Is a Gluten-Free Diet Enough to Maintain Correct Micronutrients Status in Young Patients with Celiac Disease?

The current study assesses whether the use of a gluten-free diet (GFD) is sufficient for maintaining correct iron status in children with celiac disease (CD). The study included 101 children. The celiac group (n = 68) included children with CD, with long (> 6 months) (n = 47) or recent (< 6 months) (n = 21) adherence to a GFD. The control group (n = 43) included healthy children. Dietary assessment was performed by a food frequency questionnaire and a 3-day food record. Celiac children had lower iron intake than controls, especially at the beginning of GFD (p < 0.01). The group CD-GFD >6 months showed a higher intake of cobalamin, meat derivatives and fish compared to that of CD-GFD <6 months (all, p < 0.05). The control group showed a higher consumption of folate, iron, magnesium, selenium and meat derivatives than that of children CD-GFD >6 months (all, p < 0.05). Control children also showed a higher consumption of folate and iron compared to that of children CD-GFD <6 months (both, p < 0.05). The diet of celiac children was nutritionally less balanced than that of the control. Participation of dietitians is necessary in the management of CD to guide the GFD as well as assess the inclusion of iron supplementation and other micronutrients that may be deficient.

Rheology and Acceptance of Pap (Zea mays) Enriched with Jatropha carcus Leaves to Improve Iron Status in Children

This study was carried out to determine the Rheology and acceptance of Pap (Zea mays) enriched with Jatropha carcus leaves to improve iron status in Children. The blends of pap slurry and Jatropha curcas leaves was made at substitution level of 70:30 respectively. However, the sample formulation was coded as sample A for 100% pap, B for 100% Jatropha curcas leaves and sample C for 70% pap and 30% Jatropha curcas leaves. Sensory evaluation was conducted on the gruel made from the samples to test acceptability. All samples were subjected to laboratory analysis for proximate, mineral, anti-nutrients, viscocity and functional properties using standard method and thereafter, the results obtained were further subjected to statistical analysis using SPSS. The result showed that the proximate composition of the samples ranged from 11.82 to 43.31% for moisture, fibre 2.71 to 10.20%, protein 3.24 to 6.28%, carbohydrate 41.61 to 61.55% and energy 250.10 to 401.50 kcal. The minerals were also ranged from 4.62 to 10.04 mg/100 g for iron, magnesium 62.55 to 112.01 mg/100 g, zinc 0.03 to 0.67 mg/100 g and calcium 44.21 to 110.28 mg/100 g. The anti-nutrients were found to be tannin 0.03 to 2.67 mg/100 g, phytate 0.34 to 1.11 mg/100 g, oxalate 0.91 to 2.64 mg/100 g, and saponin 0.00 to 1.24 mg/100 g. The study however showed that the functional properties of 100% pap and the pap fortified with Jatropha carcus leaves were water absorption capacity 65.78 and 52.68%, oil absorption capacity 140.20 and 120.00%, and foaming capacity 22.45 and 28.01% respectively. The panelist preferred the 100% pap than the pap enriched with Jatropha curcas leaves. This study has revealed an increase in iron, magnesium and zinc which shows that fortification of pap with Jatropha curcas leaves will enhance the iron status of the populace.

Iron status of children with attention deficit/hyperactivity disorder: A systematic review

Iron status of children with attention deficit/hyperactivity disorder: A systematic review

Comment on Ferritin as a functional biomarker of iron status in children and young adults

Comment on <i>Ferritin as a functional biomarker of iron status in children and young adults</i>

A Randomized Feeding Trial of Iron-Biofortified Beans on School Children in Mexico.

Iron deficiency is a major public health problem worldwide, with the highest burden among children. The objective of this randomized efficacy feeding trial was to determine the effects of consuming iron-biofortified beans (Fe-Beans) on the iron status in children, compared to control beans (Control-Beans). A cluster-randomized trial of biofortified beans (Phaseolus vulgaris L.), bred to enhance iron content, was conducted over 6 months. The participants were school-aged children (n = 574; 5–12 years), attending 20 rural public boarding schools in the Mexican state of Oaxaca. Double-blind randomization was conducted at the school level; 20 schools were randomized to receive either Fe-Beans (n = 10 schools, n = 304 students) or Control-Beans (n = 10 schools, n = 366 students). School administrators, children, and research and laboratory staff were blinded to the intervention group. Iron status (hemoglobin (Hb), serum ferritin (SF), soluble transferrin receptor (sTfR), total body iron (TBI), inflammatory biomarkers C-reactive protein (CRP) and α-1-acid glycoprotein (AGP)), and anthropometric indices for individuals were evaluated at the enrollment and at the end of the trial. The hemoglobin concentrations were adjusted for altitude, and anemia was defined in accordance with age-specific World Health Organization (WHO) criteria (i.e., Hb <115 g/L for <12 years and Hb <120 g/L for ≥12 years). Serum ferritin concentrations were adjusted for inflammation using BRINDA methods, and iron deficiency was defined as serum ferritin at less than 15.0 µg/L. Total body iron was calculated using Cook’s equation. Mixed models were used to examine the effects of Fe-Beans on hematological outcomes, compared to Control-Beans, adjusting for the baseline indicator, with school as a random effect. An analysis was conducted in 10 schools (n = 269 students) in the Fe-Beans group and in 10 schools (n = 305 students) in the Control-Beans group that completed the follow-up. At baseline, 17.8% of the children were anemic and 11.3% were iron deficient (15.9%, BRINDA-adjusted). A total of 6.3% of children had elevated CRP (>5.0 mg/L), and 11.6% had elevated AGP (>1.0 g/L) concentrations at baseline. During the 104 days when feeding was monitored, the total mean individual iron intake from the study beans (Fe-bean group) was 504 mg (IQR: 352, 616) over 68 mean feeding days, and 295 mg (IQR: 197, 341) over 67 mean feeding days in the control group (p < 0.01). During the cluster-randomized efficacy trial, indicators of iron status, including hemoglobin, serum ferritin, soluble transferrin receptor, and total body iron concentrations improved from the baseline to endline (6 months) in both the intervention and control groups. However, Fe-Beans did not significantly improve the iron status indicators, compared to Control-Beans. Similarly, there were no significant effects of Fe-Beans on dichotomous outcomes, including anemia and iron deficiency, compared to Control-Beans. In this 6-month cluster-randomized efficacy trial of iron-biofortified beans in school children in Mexico, indicators of iron status improved in both the intervention and control groups. However, there were no significant effects of Fe-Beans on iron biomarkers, compared to Control-Beans. This trial was registered at clinicaltrials.gov as NCT03835377.

Malaria causes long-term effects on markers of iron status in children: a critical assessment of existing clinical and epidemiological tools

BackgroundMost epidemiological studies on the interplay between iron deficiency and malaria risk classify individuals as iron-deficient or iron-replete based on inflammation-dependent iron markers and adjustment for inflammation by using C-reactive protein (CRP) or α-1-acid glycoprotein (AGP). The validity of this approach and the usefulness of fibroblast growth factor 23 (FGF23) as a proposed inflammation-independent iron marker were tested.MethodsConventional iron markers and FGF23 were measured in children with acute falciparum malaria and after 1, 2, 4, and 6 weeks. Children, who were transfused or received iron supplementation in the follow-up period, were excluded, and iron stores were considered to be stable throughout. Ferritin levels 6 weeks after admission were used as a reference for admission iron status and compared with iron markers at different time points.ResultsThere were long-term perturbations in iron markers during convalescence from acute malaria. None of the tested iron parameters, including FGF23, were independent of inflammation. CRP and AGP normalized faster than ferritin after malaria episodes.ConclusionMalaria may bias epidemiological studies based on inflammation-dependent iron markers. Better markers of iron status during and after inflammation are needed in order to test strategies for iron supplementation in populations at risk of malaria.

Serum Hepcidin Level as a Marker of Iron Status in Children with Cystic Fibrosis.

Introduction Iron deficiency is common in patients with cystic fibrosis. Conventional iron status markers are often abnormal in patients with CF, reflecting inflammation and/or infection, rather than actual iron stores. The aim was to evaluate serum hepcidin levels against selected iron status markers, assuming that hepcidin may be a more sensitive indicator of iron management in patients with active inflammation, such as those with CF. Material and Methods 46 children with cystic fibrosis and 31 healthy controls were enrolled. Hepcidin concentration was evaluated, along with the following other blood assays: full blood count, Fe, ferritin, transferrin, TIBC, liver markers, and CRP. Results Higher ferritin and CRP levels as well as lower TIBC levels significantly predicted hepcidin levels in the study group, control group, and the entire sample. There was no significant difference in hepcidin levels between the patients and controls. Children with exacerbations had significantly higher hepcidin levels than those with stable disease. These findings support the serum hepcidin level as useful in assessing iron status in children with cystic fibrosis. It may also be useful in early detection and monitoring of treatment of exacerbations.

Study on association of iron status in children with simple febrile seizure and without seizures

Background: Considering the age prevalence of iron deficiency anaemia and febrile convulsion which are the same, the role of iron in the metabolism of neurotransmitters (such as GABA and serotonin) and some enzymes (such as monoaminoxidase and aldehideoxidase), the function of hemoglobin in conveying oxygen to the brain and since fever can exacerbate symptoms that result from anaemia, a relationship between iron deficiency anaemia and febrile convulsions is probable. Thus, the present study was conducted to determine the iron profile in children with simple febrile seizures and febrile children without seizures and also to find out the association between iron levels and simple febrile seizures.Methods: A cross sectional comparative study was conducted among the infants and children aged between 6 months to 6 years with complaints of fever with/ without seizures attending Pediatrics OPD, Sri Siddartha Medical College, Tumkur during the period between 2016 to 2018. Purposive sampling of equal number of children in two study groups were made. Demographic data, seizure details, nature of febrile illness, family history of epilepsy /febrile seizures, temperature at admission and nutritional status were recorded. For laboratory assessment, 2 ml venous blood was drawn and sent for estimation of complete blood count with peripheral smear. Statistical analysis was done using SPSS version 16.Results: Among 112 study participants, 60.7% were anaemic. The indicators of iron deficiency anaemia like Hb%, MCH, TIBC and S. ferritin were associated with febrile seizures and were statistically significant.Conclusions: Anaemia prevalence in infants and young children is high and was significantly associated with febrile seizures.

Serum zinc, copper and iron status of children with coeliac disease on three months of gluten-free diet with or without four weeks of zinc supplements: a randomised controlled trial.

Data about the effect of zinc supplementation with gluten-free diet on normalisation of plasma zinc, copper and iron in patients with coeliac disease are scanty. We evaluated the effect of zinc supplementation on serum zinc, copper and iron levels in patients with coeliac disease, by randomising 71 children newly diagnosed with coeliac disease into two groups: Group A = gluten-free diet (GFD); and Group B = gluten-free diet with zinc supplements (GFD +Zn). The rise in iron and zinc was significantly higher in the latter, but the mean rise of copper levels was slightly higher in the former, but the difference was not significant.

Anaemia control and the interpretation of biochemical tests for iron status in children

BackgroundAnaemia is one of the world’s most prevalent child health problems. Its control in Africa and other developing nations has been hindered by uncertainty regarding its cause. Anaemia control has been particularly problematic in regions where the non-iron deficiency causes of anaemia, are projected to be substantial. The implementation of effective interventions to reduce the anaemia prevalence, requires improved documentation on iron status and other causes of anaemia for target populations.MethodsThis cross-sectional study enrolled n = 184 children, aged 6–8 years from Kwazulu-Natal, South Africa. Tests of haemoglobin, serum ferritin, soluble transferrin receptor and C-reactive protein were performed. These conventional measures of iron status were used to calculate body iron and to categorize the children into different groups of anaemia profiles.ResultsAnaemia prevalence was high, 43/184 (23.4%). Iron deficiency anaemia contributed 7/43 (16.3%) to the anaemia prevalence compared to non-iron deficiency anaemia 34/43 (79.1%) and mixed anaemia 2/43 (4.7%). In total 47/184 (25.5%) of the sampled children had either iron deficiency or anaemia. Information about the presence of inflammation was used to adjust serum ferritin concentrations, resulting in improved diagnosis of iron deficiency.ConclusionAppropriate investigations for iron status and inflammation/infection screening, need to be integral in the evaluation of anaemia and its causes before anaemia control interventions are implemented. Interventions that target the multifactorial nature of anaemia in school-aged children need to be strengthened. Additionally, regular screening of anaemia in school-aged children from disadvantaged communities is recommended.

Delaying Iron Therapy by 28 Days Is Associated with Improved Long‐Term Iron Status and Equivalent Hemoglobin in Children with Severe Malaria and Iron Deficiency

BackgroundIron therapy started concurrently with antimalarial treatment in children with severe malaria and iron deficiency may not be well absorbed due to inflammation‐induced impairment of iron absorption and trapping of iron in reticuloendothelial stores under the influence of the hepatic protein hepcidin. Malaria‐induced increases in hepcidin concentration normalize after approximately 4 weeks.ObjectiveWe aimed: 1) To determine if iron therapy started concurrently with vs. 28 days after antimalarial treatment is associated with improvements in long‐term hemoglobin and iron status in children with severe malaria and iron deficiency; and 2) To establish how delayed iron affects long‐term iron and inflammatory markers in children with severe malarial anemia (SMA) vs. cerebral malaria (CM).MethodsWe enrolled Ugandan children with severe malaria (CM, n=77; SMA, n=79) and healthy community children (CC, n=83) aged 6–18 mos into a 12‐mo iron therapy study in Kampala, Uganda. Children with zinc protoporphyrin (ZPP) ≥ 80 μmol/mol heme were randomized to start a 3‐month‐course of oral iron therapy (2 mg/kg/day as ferrous sulfate) concurrently with antimalarial treatment on Day 0 (immediate group, I) or 28 days after antimalarial treatment (delayed group, D). We compared markers of iron status [hemoglobin (Hb), ferritin, soluble transferrin receptor (sTfR), hepcidin] and inflammation [C‐reactive protein (CRP)] at 6 and 12 mos follow up between the treatment groups and also among the study groups using ANOVA.ResultsAll children with severe malaria and 35/83 CC had elevated ZPP. There was no interaction between study group and treatment group for any biomarker at 6 or 12 months. At both time points, children in the I and D groups had equivalent hemoglobin, but children in the D group had significantly lower adjusted geometric mean ZPP (95% CI) concentrations [I vs. D: 6 mos: 86.7 (79.1, 95.1) vs. 75.8 (68.8, 83.4) μmol/mol heme, p=0.02; 12 mos: 84.3 (78.0, 91.0) vs. 72.7 (67.3, 78.6), p&lt;0.01]. Children in the D group also had lower mean sTFR (95% CI) concentrations at 6 months [I vs. D: 6.0 (5.4, 6.7) vs. 5.1 (4.6, 5.7) mg/L, p=0.01) and higher mean hepcidin (95% CI) concentrations at 12 months [I vs. D 10.1 (8.3, 12.2) vs. 14.5 (11.8, 17.8) ng/mL, p&lt;0.01]. At 6 and 12 months, children with SMA had significantly lower hemoglobin concentrations than children in the CM or CC group (pooled group effect 6 mos p=0.03; 12 mos p=0.02), higher ferritin (pooled group effect 6 &amp; 12 mos p&lt;0.001), and marginally higher CRP concentrations (pooled group effect 6 mos p=0.07; 12 mos p=0.08).ConclusionsDelaying iron by 28 days in children with severe malaria may improve long‐term iron status, while causing no change in hemoglobin concentrations as compared to immediate iron. The aberrations to iron metabolism in children with SMA appear to be persistent and associated with chronic inflammation, while those in children with CM are acute and rapidly reversible.Support or Funding InformationFunded by 1U01HD064698 from NIH/NICHD

The impact of H63D HFE gene carriage on hemoglobin and iron status in children.

The molecular mechanism that regulates iron homeostasis is based on a network of signals, which reflect on the iron requirements of the body. Hereditary hemochromatosis is a heterogenic metabolic syndrome which is due to unchecked transfer of iron into the bloodstream and its toxic effects on parenchymatous organs. It is caused by the mutation of genes that encode proteins that help hepcidin to monitor serum iron. These proteins include the human hemochromatosis protein -HFE, transferrin-receptor 2, hemojuvelin in rare instances, and ferroportin. HFE-related hemochromatosis is the most frequent form of the disease. Interestingly, the low penetrance of polymorphic HFE genes results in rare clinical presentation of the disease, predominantly in middle-aged males. Taking into account the wide dispersion of HFE mutation in our population and also its unknown role in heterozygotes, we analyzed the impact of H63D HFE carriage in the developmental age, with respect to gender, on the iron status and hemoglobin concentration of carriers in comparison to those of wild-type HFE gene (12.7 ± 3.07 years, 42 boys and 41 girls). H63D carriers presented higher blood iron, transferrin saturation, and ferritin concentration than wild-type probands (p < 0.05.) Interestingly, male H63D carriers showed higher hemoglobin concentration than the unburdened children. Moreover, in the H63D carrier group, a positive correlation between iron and hemoglobin was noted. In conclusion, this study demonstrates that changes in iron metabolism occur at a young age in HFE heterozygotes.

Assessing the Relationship of Vitamin D with Iron Status in Children with Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) is a chronic intestinal condition with severalnutrition‐related comorbidities including anemia and vitamin D deficiency. Vitamin D has recently been linked to iron metabolism through down‐regulatory effects on hepcidin and hepcidin‐stimulatorypro‐inflammatory cytokines. It has been proposed that vitamin D may increase bioavailable iron for erythropoiesis and hemoglobin synthesis. We aimed to investigate the association of inflammation, anemia and iron biomarkers with vitamin D levels in pediatric IBD. We obtained cross‐sectional data from N=69 IBD patients aged 5 to &lt;19y, in which iron biomarkers [reticulocyte hemoglobincontent (CHr), ferritin, soluble transferrin receptor (sTfR)], plasma25‐hydroxyvitamin D (25(OH)D), inflammatory biomarkers [C‐reactive protein(CRP), α1 acid glycoprotein (AGP), hepcidin] and hemoglobin (Hb) were collected. Multivariable logistic and linear models were used to examine the associations of vitamin D with inflammation, anemia and iron status. The prevalence of iron deficiency using ferritin &lt; 15 μg/L or sTfR &gt; 8.3mg/L was 65%, anemia was 36%, vitamin D deficiency was 38%, vitamin D insufficiency was 76% and 49% of subjects were inflamed (elevated CRP/AGP). 25(OH)D was positively associated with log(AGP), controlling for age, sex, race, Medicaid, BAZ, disease duration, RBP, and ferritin, (β(SE)=0.02(0.01), P=0.01), and inversely associated with log(hepcidin) (β(SE)=−0.02(0.01), P=0.05), controlling for the same covariates. When categorized by insufficiency/sufficiency, 25(OH)D &lt; 30 ng/mL was associated with a 0.90 g/dL reduction in Hb concentration, compared to 25(OH)D ≥ 30 ng/mL, controlling for age, sex, race, medicaid, BAZ, disease duration, RBP, and ferritin (β(SE)=−0.90 (0.45), P=0.05). This association was most pronounced among those without elevations in inflammatory markers (β(SE)=−1.46(0.53), P=0.01). The association between vitamin D insufficiency and anemia was not significant overall, but when stratified by race, vitamin D insufficient African Americans had 20 times higher odds of anemia compared to vitamin D insufficient non‐African Americans (OR=20.18, 95% CI: 1.80, 226.5). In conclusion, Vitamin D insufficiency was associated with reduced hemoglobin concentrations in this population of children with IBD. Vitamin D may improve iron status by decreasing hepcidin, but the effect of inflammation status remains unclear. In non‐inflamed children with IBD, 25(OH) D and hemoglobin concentrations should be monitored. Among AAs with IBD, vitamin D status was related to anemia and merits further investigation.