Iron Deficiency Anemia In Toddlers Research Articles

Fish-Based Complementary Feeding Practices Increasing Macro and Micro Nutrient Intake And Hemoglobin Levels in Anemia Toddlers

Iron deficiency anemia in toddlers can be prevented by introducing complementary foods alongside breastfeeding. Fish, rich in protein and iron, offers a valuable nutritional source for young children, but proper processing is crucial. This research investigated the impact of fish-based complementary food processing practices (known as MP-ASI in Indonesia) on the nutritional intake and hemoglobin levels of children under five in Tiro District, Pidie Regency. Using a quasi-experimental design, this study involved 40 toddlers from the stunting-prone area of Tiro District, Pidie Regency, along with their mothers as respondents. The toddlers, aged 12-36 months without severe illnesses, were included in the study. The intervention comprised educating and practicing complementary food processing. Before-and-after intervention comparisons showed significant improvements in energy, carbohydrate, protein, zinc, and iron intake levels. Additionally, there was a notable increase in the average hemoglobin (Hb) level, rising by 1.06 g/dl after one month of fish-based complementary food processing intervention. In summary, this intervention effectively enhanced the nutritional quality of children's intake and increased their hemoglobin levels, contributing to the prevention of iron deficiency anemia in toddlers.

Comparison of the effect of ferrous sulfate and ferrous gluconate on prophylaxis of iron deficiency in toddlers 6-24 months old: A randomized clinical trial

Iron deficiency anemia (IDA) is one of the most common anemias, especially in children 4-23 months. Therefore, prophylaxis is necessary to improve iron status as well as reduce IDA in Toddlers. The aim of this study was to compare the efficacy of daily supplementation with ferrous gluconate (FG) and ferrous sulfate (FS) on iron status in toddlers. A total of 120 healthy toddlers were divided randomly into 2 groups at the Amir-Kabir Hospital, Arak, Iran and received FS and FG from March 2020 to December 2020. Iron status was evaluated at baseline and after 6 months of supplementation. The statistical significance of the differences in iron status between FS and FG groups was calculated using Student's t-test and the Pearson' s Chi-square test for qualitative variables. SPSS software (version 16, Chicago, IL, USA) was used for statistical analysis. Comparison of iron status of FS and FG groups toddlers at baseline and after 6 months of supplementation showed that there was a significant difference in hemoglobin (Hb) (10.46 vs. 12.45, P = 0.001) and ferritin level (28.08 vs. 59.63, P = 0.001). Although prophylaxis with FG led to a higher Hb and ferritin levels, our study recommended that both FG and FS supplements were effective for prophylactic use in the prevention of IDA. However, FG was more effective than FS because FG group that received FG supplementation indicated a higher Hb and ferritin levels in comparison to the FS group that received FS supplementation.

Iron assessment to protect the developing brain

Iron deficiency (ID) before the age of 3 y can lead to long-term neurological deficits despite prompt diagnosis of ID anemia (IDA) by screening of hemoglobin concentrations followed by iron treatment. Furthermore, pre- or nonanemic ID alters neurobehavioral function and is 3 times more common than IDA in toddlers. Given the global prevalence of ID and the enormous societal cost of developmental disabilities across the life span, better methods are needed to detect the risk of inadequate concentrations of iron for brain development (i.e., brain tissue ID) before dysfunction occurs and to monitor its amelioration after diagnosis and treatment. The current screening and treatment strategy for IDA fails to achieve this goal for 3 reasons. First, anemia is the final state in iron depletion. Thus, the developing brain is already iron deficient when IDA is diagnosed owing to the prioritization of available iron to red blood cells over all other tissues during negative iron balance in development. Second, brain ID, independently of IDA, is responsible for long-term neurological deficits. Thus, starting iron treatment after the onset of IDA is less effective than prevention. Multiple studies in humans and animal models show that post hoc treatment strategies do not reliably prevent ID-induced neurological deficits. Third, most currently used indexes of ID are population statistical cutoffs for either hematologic or iron status but are not bioindicators of brain ID and brain dysfunction in children. Furthermore, their relation to brain iron status is not known. To protect the developing brain, there is a need to generate serum measures that index brain dysfunction in the preanemic stage of ID, assess the ability of standard iron indicators to detect ID-induced brain dysfunction, and evaluate the efficacy of early iron treatment in preventing ID-induced brain dysfunction.

Ferrotherapy Mistakes in Toddlers in Primary Health Care

Introduction. 20–30% of the world population suffers from iron deficiency anemia. Despite the availability of diagnostic and therapeutic options, the real medical practice in relation to iron deficiency anemia remains on a suboptimal level. As a result, over the past 20 years there is no significant improvement in the iron deficiency anemia frequency in young children. Objective. To analyze the existing care tactic for toddlers with iron deficiency anemia in a primary care setting and to identify the possible ferrotherapy mistakes. Methods. A retrospective study of 135 3-year-old children with anemia in primary health care. The inclusion criteria was: documented low hemoglobin level as recommended by WHO in at least two sequential complete blood tests. Results. Control complete blood count (CBC) was performed within 6 months of anemia detection in 70.4% cases. However, this control was performed during the optimal time only in 15.6% of cases. In 56.3% of cases the fact of ferrotherapy wasn’t documented. The onset of ferrotherapy after the first episode of low hemoglobin detection was in 19.3% of children. 29.6% of children received treatment with iron supplements in an adequate dose. Only in 11.9% of cases the dose of iron was lower than recommended. 30.4% of children had a relapse of iron deficiency anemia and up to 6% had multiple relapses. The average duration of iron deficiency anemia in children during the first three years of life was 6.4 months. Conclusion. In the majority of cases the therapy of the majority of iron deficiency anemia in toddlers was delayed. The biggest problem is the lack of adequate hemoglobin levels monitoring.

Cerebral Stroke Associated with Iron-Deficiency Anemia in Toddlers

Neurology| January 01 2008 Cerebral Stroke Associated with Iron-Deficiency Anemia in Toddlers AAP Grand Rounds (2008) 19 (1): 7. https://doi.org/10.1542/gr.19-1-7 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Cerebral Stroke Associated with Iron-Deficiency Anemia in Toddlers. AAP Grand Rounds January 2008; 19 (1): 7. https://doi.org/10.1542/gr.19-1-7 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search nav search search input Search input auto suggest search filter All PublicationsAll JournalsAAP Grand RoundsPediatricsHospital PediatricsPediatrics In ReviewNeoReviewsAAP NewsAll AAP Sites Search Advanced Search Topics: cerebrovascular accident, iron deficiency anemia, toddler, ischemic stroke Source: Maguire JL, de Veber G, Parkin PC. Association between iron-deficiency anemia and stroke in young children. Pediatrics. 2007;120(5):1053–1057; doi:10.1542/peds.2007-0502 The prevalence of iron-deficiency anemia (IDA) in children 12–38 months of age at the time of stroke and in age-matched healthy controls was compared in a case-control study conducted at the Hospital for Sick Children, Toronto, Canada. Case patients were selected from the Canadian Pediatric Ischemic Stroke Registry. Children who presented between January 1992 and December 2004 with arterial ischemic stroke (AIS) or sinovenous thrombosis (SVT) were considered for eligibility. Children with sickle cell disease, chronic systemic disease (excluding IDA), central nervous system disease or trauma, or indwelling catheters were excluded. For both case patients and control subjects, mean corpuscular volume (MCV), platelet count, and hemoglobin and serum ferritin levels were measured. IDA was defined as serum ferritin level of <12 g/L, MCV of... You do not currently have access to this content.

Iron Deficiency and Impaired Cognition in Toddlers

Iron deficiency in toddlers is associated with impaired cognition and is an underestimated and undertreated problem. The prevalence of iron deficiency anemia (IDA) during the first year of life has been dramatically reduced in developed countries, mainly due to the increase in breastfeeding and the use of iron-fortified feeding formulae. However, in US and UK children aged 1-2 years, recent studies have shown prevalence rates of >10% and 30% for IDA and iron deficiency, respectively. The daily iron intake in children aged 1-2 years is lower than in any other age group during life. IDA during the first 2 years of life is associated with impaired mental and psychomotor development and these deficits are long lasting, and perhaps irreversible, despite the correction of the anemia. Another compelling reason to prevent iron deficiency in children, especially in children aged 1-2 years, is the proven association of iron deficiency with increased lead absorption. Lead-associated cognitive deficits occur at blood lead levels <10 microg/L, a level once thought to be harmless. The current prevalence rates of iron deficiency and IDA in toddlers, especially among those in the lower socioeconomic groups, are unacceptably high. These young children are doubly at risk for neurodevelopmental impairment, both from the iron deficiency itself as well as from CNS damage caused by the associated increased lead absorption. The current screening and treatment recommendations for IDA in the US and in other developed countries appear to have been unsuccessful in preventing iron deficiency and IDA in a large number of toddlers. Similarly, the associated problem of impaired mental and psychomotor development has not been adequately recognized or addressed in the existing medical literature. The author recommends that, after breastfeeding or an iron-fortified formula is stopped, iron deficiency and IDA be prevented by routine daily supplemental doses of 10mg of elemental iron via iron-fortified vitamins, iron drops, or iron-fortified drinks.

Managing anemia in pediatric office practice: Part 1.

1. George B. Segel, MD* 2. Michael G. Hirsh, MD† 3. Stephen A. Feig, MD‡ 1. *Professor of Pediatrics and Chief of Hematology/Oncology 2. †Clinical Associate Professor of Pediatrics, Strong Children’s Hospital, University of Rochester, Rochester, NY 3. ‡Professor of Pediatrics and Chief of Hematology/Oncology, Mattel Children’s Hospital at UCLA, Los Angeles, CA After completing this article, readers should be able to: 1. Compare and contrast the pathogenesis of iron deficiency anemia in toddlers and older children. 2. Describe the genetic defects resulting in beta-thalassemia and hemoglobin E and differentiate between heterozygous and homozygous defects. 3. Outline the molecular basis for alpha-thalassemia syndromes, including silent carrier, alpha-thalassemia trait, hemoglobin H, and Bart’s hemoglobinopathy. 4. Describe the pathogenesis of spherocytes in herediatry spherocytosis and the reasons for the shortened red cell survival. 5. Characterize the risk of “aplastic crisis” in hereditary spherocytosis and the requisite monitoring and management. Children’s hematologic and oncologic problems often present initially to the pediatrician. This article provides direction for the diagnosis and office treatment of anemia and guidelines for follow-up and, where appropriate, referral to a subspecialist. Part 1 considers iron deficiency, beta- and alpha-thalassemia trait, and hereditary spherocytosis (Table 1⇓). Part 2 considers sickle cell syndromes, glucose-6-phosphate dehydrogenase (G6PD) deficiency, and transient erythroblastopenia. These topics were proposed by practicing pediatricians in our communities as those of particular concern in their office practices. View this table: Table 1. Red Blood Cell (RBC) Disorders The traditional measurements of hemoglobin concentration and hematocrit may not be sufficient to determine the presence of anemia of childhood. The “normal values” cited in clinical pathology laboratory reports are unlikely to apply to children. Tables of normal values for children of different ages have been published (Table 2⇓). In general, the hemoglobin is high at birth and falls during the initial 6 to 8 weeks of life to a physiologic nadir before it gradually increases to childhood levels. Patients who suffer from cyanotic congenital heart disease or chronic obstructive pulmonary disease may have values that are considerably higher than children who do not have these problems. These children, therefore, may be anemic when their hemoglobin and hematocrit values are within the normal range …