Iron Therapy In Children Research Articles

Hepcidin Levels in Response to Oral Iron Therapy in Children with Anemia

Hepcidin Levels in Response to Oral Iron Therapy in Children with Anemia

Mean Rise in Hemoglobin After Intravenous Iron Therapy in Children with Iron Deficiency Anemia

Introduction: Iron deficiency anemia (IDA) is a significant public health issue in Pakistan, affecting up to 63% of children, as revealed by the Pakistan National Nutritional Survey 2018. While oral iron remains the primary choice, challenges in compliance have led to the consideration of intravenous (IV) iron therapy, particularly iron sucrose. The study discusses the safety and efficacy of IV iron therapy in Pakistani children and aims to broaden our understanding of treating IDA in resource-constrained regions. Aims & Objectives: To determine the average hemoglobin (Hb) increase in iron-deficient-anemic children aged 01 to 12 years after treatment with intravenous iron sucrose. Place and Duration of Study: A quasi-experimental study was undertaken at Fauji Foundation Hospital in Rawalpindi, spanning from September 2021 to September 2022. Material & Methods: The study focused on a cohort of pediatric patients aged between 1 and 12 years, all of whom were diagnosed with iron deficiency anemia and had previously encountered ineffective outcomes with oral iron therapy. In this investigation, the patients received treatment involving intravenous iron sucrose. Subsequently, their progress was diligently monitored after a period of 8 weeks. Improvement in hemoglobin level was assessed at the end of treatment to evaluate its efficacy.Data processing and statistical analysis were carried out using SPSS version 23,p-value of <0.05 indicated statistical significance. Results: Out of 150 study cases, 96 (64.0 %) were male, while 54 (36.0 %) were female. The mean age of our study cases was 05 ± 2.3 years of these 150 study cases, 74 (49.3 %) belonged to rural areas, and 76 (50.7 %) belonged to urban areas. Poor socioeconomic status was noted in 97 (64.7 %), and 53 (35.3%) were middle-income. A family history of iron deficiency anaemia was recorded in 16 (10.7%). Iron deficiency due to dietary iron insufficiency was reported in 67 (44.7%), Total Parentral Nutrition (TPN) dependencywas seen in 61 (40.7%) and 22 (14.7%) had chronic gastritis. The mean baseline (pretreatment) haemoglobin level was 7.71 ± 0.63 g/dl, while the mean post-treatment haemoglobin level was 10.68 ± 0.60 g / dl (p = 0.001). Conclusion: After intravenous iron sucrose, we noted a significant rise in paediatric patients' hemoglobin levels, emphasizing its effectiveness and safety. Statistically, we found correlations with age, family history, and causes. Healthcare practitioners should consider injectable iron treatments for better results and reduced health issues in this group.

Intravenous iron therapy in pediatrics: who should get it and when is the right time?

Iron-deficiency anemia occurs most commonly in young children due to a low-iron diet and adolescent girls due to menstrual blood loss. However, children with gastrointestinal conditions such as intestinal failure, inflammatory bowel disease, celiac disease, and/or other chronic conditions, including chronic kidney disease and heart failure, also commonly have iron deficiency. Many patients with classic iron-deficiency anemia will improve with oral iron therapy. However, in children who have an incomplete response to oral iron, intravenous iron therapy is increasingly being used. Benefits of intravenous iron therapy include a rapid repletion of iron stores in addition to resolution of anemia, less gastrointestinal side effects, and relief for patients and families struggling with long-term iron supplementation. Indications for first-line therapy with intravenous iron in children with chronic conditions have also increased. Four intravenous iron formulations have approved indications in pediatrics, and many are increasingly used off-label in children as well. Here we discuss the indications and appropriate timing of intravenous iron therapy in children with a wide range of underlying etiologies.

Evaluation of serum hepcidin levels following oral iron therapy in children of iron deficiency anemia aged 2-12 years

Evaluation of serum hepcidin levels following oral iron therapy in children of iron deficiency anemia aged 2-12 years

Does iron therapy have a place in the management of all breath-holding spells?

Aim of this study was to analyze the effect of iron therapy in children with breath-holding spells, irrespective of their hemoglobin level. All of the children were evaluated in terms of age, sex, age at onset of the attack, attack frequency, type of breath-holding spell, family pedigree, laboratory values. All enrolled patients were given iron at the dose of 4 mg/kg/day as a single daily dose for 3 months. Patients were called for follow-up appointments 1 and 3 months after the initiation of treatment to record the frequency and severity of spells. The mean age of the patients was 12.50 ± 9.51 months. Patients were divided into two groups according to the hemoglobin level. The frequency of anemia in children with spells was recorded as 27%. Out of 100 patients treated with iron, 43% showed complete remission at the end of 1 month. At the end of the 3 months, percentage of complete responders increased to 80%. After three-month of iron treatment, 96.2% of the anemic and 73.97% of the non-anemic patients were spell-free. Eight children had mild adverse effects after iron therapy that did not require dose modification. This study confirmed that iron therapy reduces spell frequency regardless of anemia in all breath-holding spells. A three-month empiric iron therapy should be offered to all children with spells.

Role of iron in breath holding spells and effect of iron therapy in children

Background: Breath holding spells (BHS) are paroxysmal events resulting from painful stimulus or emotional event resulting in forceful crying, occur in children’s aged between 6 months to 6 years. To assess the role of iron in breath holding spells (BHS) and to assess the efficiency of iron therapy in reducing frequency of BHS.Methods: This was a prospective, interventional study conducted at GMC baramulla. A total of 70 patients between the ages of 6 months and 5 years with breath holding spells with iron deficiency and iron deficiency anemia were studied. After giving them iron therapy for 6 and 12 weeks, they were assessed for the improvement in their anemia and its impact on the frequency of breath holding spells.Results: Seventy children with breath holding spells were studied prospectively. Forty (57.15%) cases were males and 30 (42.85%) females. There was a statistically significant rise in the hemoglobin level, serum ferritin, serum iron with 6 and12 weeks of iron therapy (p<0.001). This rise in the hemoglobin level serum ferritin and serum iron was associated with a statistically significant fall in the frequency of breath holding spells with 6 and 12 weeks of iron therapy (p<0.001).Conclusions: iron supplement is effective in reducing the frequency of breath holding spells and thus iron has role in BHS.

Poor efficacy of oral iron replacement therapy in pediatric patients with heart failure.

Iron deficiency is associated with worse outcomes in children and adults with systolic heart failure. While oral iron replacement has been shown to be ineffective in adults with heart failure, its efficacy in children with heart failure is unknown. We hypothesised that oral iron would be ineffective in replenishing iron stores in ≥50% of children with heart failure. We performed a single-centre retrospective cohort study of patients aged ≤21 years with systolic heart failure and iron deficiency who received oral iron between 01/2013 and 04/2019. Iron deficiency was defined as ≥2 of the following: serum iron <50 mcg/dL, serum ferritin <20 ng/mL, transferrin >300 ng/mL, transferrin saturation <15%. Iron studies and haematologic indices pre- and post-iron therapy were compared using paired-samples Wilcoxon test. Fifty-one children with systolic heart failure and iron deficiency (median age 11 years, 49% female) met inclusion criteria. Heart failure aetiologies included cardiomyopathy (51%), congenital heart disease (37%), and history of heart transplantation with graft dysfunction (12%). Median dose of oral iron therapy was 2.9 mg/kg/day of elemental iron, prescribed for a median duration of 96 days. Follow-up iron testing was available for 20 patients, of whom 55% (11/20) remained iron deficient despite oral iron therapy. This is the first report on the efficacy of oral iron therapy in children with heart failure. Over half of the children with heart failure did not respond to oral iron and remained iron deficient.

Starting empirical iron therapy for children diagnosed clinically with anemia – a double-edged sword!

Starting empirical iron therapy for children diagnosed clinically with anemia – a double-edged sword!

Breath-holding Spells: Etiological Factors, Laboratory Findings, and Rates of Response to Iron Therapy

Aim: In this study, we aimed to investigate the etiological factors, electroencephalographic (EEG) findings, rates of response to iron therapy, and factors affecting response to iron therapy in children diagnosed with breath-holding spells (BHS). Methods: The study included 136 children aged 1 to 48 months who received iron therapy after a BHS diagnosis at our pediatric neurology clinic between November 2015 and No¬vember 2019. Patient medical records (physical examination, laboratory and EEG findings, medical history, and effectiveness of iron therapy) were reviewed retrospectively. Results: Of all patents, 81 (59.6%) exhibited partial response (partial remission) to iron therapy (50% decrease in BHS frequency), 52 (39%) responded completely (complete remission), and 2 were unresponsive. Comparison of the patients with complete and partial remission revealed a higher rate of complete remission in girls. In addition, patients with complete remission had higher levels of hemoglobin, MCV, and ferritin than those with partial remission. Complete remission rates were also higher in patients with normal EEG findings. Conclusion: BHS in childhood is a benign, recurring, and non-epileptic disorder and its differentiation from epilepsy is important. Children with BHS respond well to iron therapy, which can be recommended even if the serum iron and ferritin levels are normal.

Comparison of Efficacy of Oral and Intravenous Iron Replacement Therapy in Children with Systolic Heart Failure and Iron Deficiency

Purpose Iron deficiency (ID) is associated with increased risk of ventricular assist device implantation, transplant, or death in children with systolic heart failure (HF). Oral iron replacement is standard therapy for ID. However retrospective studies in children with HF estimate its efficacy at ∼50%. There are no data comparing the efficacy of oral and intravenous (IV) iron therapy in children with systolic HF. Methods In July 2019, we instituted a screening and treatment protocol for ID in children with systolic HF. We performed a retrospective analysis of patients who were screened with this protocol between 07/2019 and 10/2020. ID was defined as the presence of ≥2 of the following 4 criteria on serum iron testing: iron 300 ng/mL, transferrin saturation Results Forty patients with systolic HF (21 male, median age 4.5 years, 28 cardiomyopathy and 12 congenital heart disease) met inclusion criteria. Nine received oral iron while 31 received IV iron. Post-therapy iron studies were available for 6/9 of the oral iron cohort and 28/31 of the IV iron cohort. The oral and IV iron cohorts were similar in terms of demographics, etiology or chronicity of HF, renal dysfunction, and mechanical ventilation. Pre-treatment serum BNP was higher in the IV iron cohort (median 1092 vs 55, p = 0.028) compared to the oral iron cohort. At 3 months, iron therapy was effective in 50% (3/6) of the oral iron cohort, compared to 86% (24/28) of those on IV iron (p = 0.086). By 6 months, ID was effectively treated in 50% (3/6) of patients on oral iron, compared to 89% (25/28) of patients on IV iron (p = 0.053). Demographics, etiology or chronicity of HF, BNP, renal dysfunction, and mechanical ventilation were not associated with efficacy of iron therapy at 3 or 6 months. Conclusion IV iron tended to be more effective than oral iron in treating ID in children with systolic HF, despite the IV iron cohort having higher BNP levels and being presumably sicker. This is the first pediatric data on the topic, although statistical significance was limited by small sample size. Larger studies are needed to guide effective therapy for ID in children with systolic HF.

Response to Oral Iron Therapy in Children with Anemia of CKD

Response to Oral Iron Therapy in Children with Anemia of CKD

Low Dose Iron Therapy in Children with Iron Deficiency: DNA Damage and Oxidant Stress Markers.

Conflicting data are available regarding oral iron therapy in iron deficiency (ID), iron deficiency anemia (IDA) and its relation to DNA damage, oxidative stress and antioxidant markers. Our aim was assessment of DNA damage, oxidative stress and anti-oxidant markers in children with ID and IDA before and after low dose iron therapy. The study was conducted in two stages, first stage was assessment of DNA damage using comet assay, malondialdehyde (MDA) and anti-oxidant enzymes levels (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) & total antioxidant capacity (TAC) in thirty-nine children with IDA, forty-five children with ID without anemia and sixty healthy controls. Second stage was assessment of previous markers together with hematological response following oral therapy with 10mg/day ferric ammonium citrate for 8weeks. Before treatment, there was no significant difference between the three groups regarding MDA, GPx, SOD, CAT and TAC. A significant increase was detected in the DNA damage in the 2 groups compared to control (p < 0.005). Following iron therapy, hematological parameters was improved together with a significant increase in GPx (P = 0.04), SOD (p = 0.002), TAC (P = 0.001) and non-significant reduction in DNA damage in IDA group. There was a significant increase in SOD (p = 0.001) & TAC (p = 0.001) and significant decrease in DNA damage (p = 0.001) in ID group. Low dose iron therapy could be sufficient to improve antioxidant status and DNA damage together with correction of hematologic indices.

Barriers to and Facilitators of Iron Therapy in Children with Iron Deficiency Anemia

To characterize barriers to and facilitators of successful iron therapy in young children with iron deficiency anemia (IDA) from an in-depth parental perspective. Prospective, mixed methods study of children age 9months to 4years with a diagnosis of nutritional IDA by clinical history and laboratory criteria and their parents. Clinical data were obtained from the electronic health record. Semistructured interviews focused on knowledge of IDA, clinical effects, experience with iron therapies, and motivation were conducted with the parent who identified as the child's primary caregiver. Twenty patient-parent dyads completed the study; 80% (n=16) identified as Hispanic/Latino (white). Patients' median age was 23months (50% male); median initial hemoglobin concentration was 8.2g/dL and duration of oral iron therapy was 3months. Parents' median age was 29years (85% female); 8 interviews (40%) were conducted in Spanish. Barriers included difficulty in administering oral iron owing to side effects and poor taste. Facilitators included provision of specific instructions; support from healthcare providers and additional caregivers at home; motivation to benefit child's health, which was strengthened by strong emotional reactions (ie, stress, anxiety) to therapy and follow-up; and an appreciation of child's improvement with successful completion of therapy. Our findings support the need for interventions designed to promote oral iron adherence in children with IDA. Rather than focusing on knowledge content related to IDA, interventions should aim to increase parental motivation by emphasizing the health benefits of adhering to iron therapy and avoiding more invasive interventions.

Phosphorus Levels in Iron Deficient Children Treated with Ferric Carboxymaltose

INTRODUCTION Intravenous iron therapy in children with iron deficiency anemia (IDA) has previously been limited to those with severe or refractory anemia. However, increased availability of intravenous iron preparations with improved safety profiles has increased its utilization in both the adult and pediatric patient populations. Ferric carboxymaltose (FCM) was approved for adult patients by the Food and Drug Administration (FDA) in 2014 and has lower rates of severe allergic reactions. However, literature on adult patients has reported the development hypophosphatemia in up 50% of those receiving the drug. In early stages, hypophosphatemia can lead to abnormal bone mineral metabolism and hypercalciuria. Rickets and osteomalacia can result after prolonged hypophosphatemia. Severe, prolonged hypophosphatemia (&lt;1 mg/mL) is associated with neurologic, cardiopulmonary, muscular, and hematologic complications. Although not FDA approved for pediatric use, FCM is increasingly being utilized for IDA in children. Hypophosphatemia in children treated with FCM has not been formally evaluated or described. We sought to assess available phosphorus levels in children treated with FCM at a tertiary care center. METHODS This was a single center retrospective cohort study of all children who received FCM over the initial 2.5 year period for which the drug was added to our institution's formulary (November 1, 2016 through April 30, 2019). Pharmacy records of all FCM infusions administered over this period were obtained. Medical record numbers of all patients who received an infusion were then searched for any available phosphorus testing. Patients were included in the review if they had phosphorus laboratory results available from 1 to 6 weeks post-receipt of FCM and were less than 21 years of age at the time of infusion. Hypophosphatemia was defined as a phosphorus level below the lower limit of normal for age as delineated by our institution's central laboratory. Changes in phosphorus levels were calculated in those patients in whom pre-infusion phosphorus levels were also available within the 4 weeks prior to drug infusion. When multiple phosphorus levels were available within the post-infusion window, the lowest value was selected to calculate changes in levels. The electronic medical record (EMR) was reviewed in all patients in whom hypophosphatemia was identified to assess for administration of supplemental phosphorus, as well as other clinical factors that may affect phosphorus levels such as the administration of total parental nutrition (TPN) and/or renal medications (i.e. furosemide), as these are known risk factors for hypophosphatemia. RESULTS From November 1, 2016 through April 30, 2019, 1,081 infusions of FCM were administered in 656 patients. Post-infusion phosphorus testing was available in 165 patients in whom 247 infusions were administered (range 1 to 6). Patients' median age was 4.6 years (range 4 months to 20.6 years) and 56% (n=92) were female. Hypophosphatemia occurred after 36 (15%) infusions in 32 unique patients (19%). Six patients (19%) received potassium phosphorus supplementation (Table). In the 23 patients in whom phosphorus testing was available at 6 weeks, 15 (65%) continued to have phosphorus levels below the normal value for age. Of the entire cohort, pre- and post-infusion phosphorus levels were available relative to 197 infusions (80%) in 136 unique patients (82%). The median change in phosphorus was -0.6 mg/dL (IQR -0.1, -1.6). CONCLUSIONS The assessment of serum chemistries, including phosphorus, is not routinely performed in otherwise healthy children with iron deficiency. While over 650 children received over 1000 infusions of FCM during a 2.5 year period, only 165 patients had phosphorus testing available during the stated time frame of the infusion. In those in whom testing was available, and in which hypophosphatemia occurred, the majority were patients admitted to the hospital with co-morbid conditions or complex clinical care for which phosphorus levels may be affected. Our center has developed a clinical protocol to obtain baseline phosphorus levels in all children in whom intravenous FCM is being considered. Post FCM therapy, phosphorus monitoring is being performed to better identify those patients who may be at risk for hypophosphatemia and in whom phosphorus supplementation may be indicated. OffLabel Disclosure: Ferric carboxymaltose is FDA approved for treatment of iron deficiency in adults. This presentation will discuss the use of ferric carboxymaltose to treat iron deficiency in pediatric patients.

Comparison Of Pro-BNP Levels And Myocardial Performance Index Before And After Iron Treatment In Children With Congenital Cyanotic Heart Disease With Iron Deficiency Anemia

Introduction: Our aim was to compare NT-proBNP levels and cardiac functions after iron therapy in children with congenital cyanotic heart disease who had iron deficiency anemia.Materials and Methods: We included 40 children with pre-established cyanotic congenital heart disease and accompanying iron deficiency anemia, between the age of 6 months and 17 years, who were admitted to the outpatient clinic of Çukurova University Faculty of Medicine, Department of Pediatric Cardiology between September 2015 and March 2016. We recorded demographic data and performed following investigations: complete blood count, peripheral blood smear, reticulocyte count, measurement of serum iron levels, total iron-binding capacity, ferritin levels, transferrin saturation and NT-proBNP levels, and echocardiographic examination.Results: There was a statistically significant increase in following laboratory parameters after iron therapy: hemoglobin, hematocrit, MCV, MCHC, serum iron and ferritin, transferrin saturation and oxygen saturation. During the follow-up period, RDW and NT-proBNP levels were significantly decreased. In left ventricular tissue doppler; there was a significant difference in MPI measurements before and after treatment. There was no significant difference in other echocardiography findings. Conclusion: Iron therapy has improved cardiac functions in children with cyanotic congenital heart disease, and NT-proBNP levels can be used to evaluate the efficacy of treatment in the follow-up period.

Outcomes of long-term iron supplementation in pediatric restless legs syndrome/periodic limb movement disorder (RLS/PLMD)

ObjectivesRestless legs syndrome (RLS) and periodic limb movement disorder (PLMD) are thought to center around a genetically mediated sensitivity to iron insufficiency. Previous studies have shown the effectiveness of short-term iron therapy in children with low iron storage. Little is known, however, about long-term iron treatment in children with RLS and PLMD. Therefore, we performed this study to assess the long-term effect of iron therapy in children with RLS and PLMD. MethodsA retrospective chart review was performed for children who met the following criteria: A) diagnosed as having either RLS or PLMD, B) started on iron supplementation, C) followed up for >2 years in a sleep clinic. Baseline values for iron, ferritin, and periodic limb movement of sleep index (PLMS index) were defined in the three months leading up to the initiation of iron therapy. Values were also computed for follow-up periods of 3–6 months, 1–2 years, and >2 years. Serum iron and ferritin levels and PLMS index were compared between baseline and all subsequent follow-ups. ResultsIn total, 105 patients met inclusion criteria, of whom 64 were diagnosed with PLMD alone, seven with RLS alone, and 35 with both RLS and PLMD. The average age was 10.2 ± 5.3 years. Compared to the baseline (27.4 ± 12.1 ng/ml), the average ferritin values at 3–6 months (45.62 ± 21.2 ng/ml, p < 0.001, n = 34), 1–2 years (52.0 ± 48.3 ng/ml, p < 0.001, n = 63), and >2 years (54.7 ± 40.5 ng/ml, p < 0.001, n = 67) were all significantly increased. Inversely, compared to baseline (21 ± 27.0/h, n = 66), PLMS index values at 3–6 months (7.5 ± 9.5/h p < 0.05, n = 11), 1–2 years (6.9 ± 8.9/h, p < 0.001, n = 29), and >2 years (10 ± 14.5/h, p < 0.001, n = 31) were all significantly decreased. No significant change in serum iron levels was noted at any time point. ConclusionWhile retrospective in nature, this study demonstrates a sustained improvement in PLMS index and maintenance of adequate ferritin levels >2 years after iron therapy initiation in our RLS/PLMD cohort with a long-term follow-up. Iron therapy appears to lead to long-lasting improvements in children with RLS/PLMD.

Responsiveness to Parenteral Iron Therapy in Children with Oral Iron-Refractory Iron-Deficiency Anemia

Intravenous (IV) ferric iron (Fe)–carbohydrate complexes are used for treating Fe deficiency in children with iron-refractory iron-deficiency anemia (IRIDA). An optimal treatment has yet to be determined. There are relatively little publications on the responsiveness to IV iron therapy in children with IRIDA. Patients and Method: This study analyzed responses to IV iron sucrose therapy given to 11 children, ranging in age from 2 to 13 years (mean 4.8 years), with iron-deficiency anemia who were unresponsive to oral iron therapy. Results: The hemoglobin and ferritin values (mean) of the 11 children with IRIDA were 7.7 g/dL and 4.8 ng/mL at diagnosis. Both hemoglobin and ferritin levels increased to 9.5 g/dL, and 24 ng/mL, respectively, at 6 weeks after the first therapy. Although the level of hemoglobin was steady at 6 months after the first, and 6 weeks after the second therapy, the ferritin levels continued to increase up to 30 ng/mL and 47 ng/mL at 6 months after the first and 6 weeks after the second therapy, respectively. Conclusion: We recommend that IRIDA should be considered in patients presenting with iron-deficiency anemia of unknown cause that is unresponsive to oral iron therapy. Our results suggest that IV iron therapy should be administered only once in cases of IRIDA. Continued administration of IV iron would be of no benefit to increase hemoglobin levels. On the contrary, ferritin levels may continue to increase resulting in untoward effects of hyperferritinemia.

Serum hepcidin levels in Helicobacter pylori-infected children with iron-deficiency anemia: a case–control study

Recently, hepcidin, an antimicrobial-like peptide hormone, has evolved as the master regulator of systemic iron homeostasis. Hepcidin integrates signals from diverse physiological inputs, forming a key connection between iron trafficking and response to infection. In this study, we aimed to investigate whether Helicobacter pylori infection modulates serum hepcidin level and response to oral iron therapy in children with iron-deficiency anemia. This was a case-control study including 60 children with iron-deficiency anemia (IDA; 30 H. pylori infected and 30 H. pylori noninfected) and 30 healthy children with comparable age and gender as the control group. Iron parameters including serum iron, ferritin, transferrin, total iron binding capacity, and transferrin saturation and serum hepcidin levels were assessed initially and after 3months of oral iron therapy for IDA. Compared to the control group, serum hepcidin was significantly lower in H. pylori-noninfected children with IDA (P < 0.01) and significantly higher in H. pylori-infected children with IDA (P < 0.01). Hepcidin increased significantly in noninfected children with IDA after 3months of oral iron therapy (P < 0.01). On the other hand, H. pylori-infected children showed nonsignificant change in hepcidin level after oral iron therapy (P > 0.05). Although hepcidin showed significant positive correlations with serum ferritin, hemoglobin (Hb), iron, and transferrin saturation in noninfected children with IDA (P < 0.01), it showed significant negative correlations with serum ferritin, Hb, iron, and transferrin saturation in H. pylori-infected children with IDA (P < 0.05). H. pylori infection upregulates serum hepcidin levels and was associated with diminished response to oral iron therapy in children with iron-deficiency anemia.

Low Serum Lipocalin Levels in Patients With Iron Deficiency Anemia

In the recent literature, there are studies on the relationship between anemia and lipocalin, but there is no study regarding the relationship between lipocalin and iron deficiency anemia (IDA) up to date. In this study, we aimed to observe lipocalin levels at admission, and after iron therapy in children with IDA. We also compared our findings to those in healthy children. Sixty-one children admitted in our outpatient clinic were included in the study. Thirty of these children had IDA (study group) and the rest were healthy (control group). Thirty patients, meeting the IDA criteria, received oral ferrous sulfate of 4 mg/kg/d. As soon as the hemoglobin value reached >11 g/dL, half dose of oral ferrous sulfate therapy was continued for another month. Serum lipocalin levels before and after iron therapies were compared. Hematologic parameters and serum lipocalin levels were also compared between the 2 groups. Mean values of serum lipocalin were 31.01±14.46 and 74.77 ng/dL in patients with IDA at admission and at third month of therapy, respectively (P<0.0001). The same figure was 57.35±39.51 ng/dL in the control group. Before treatment, mean values of lipocalin levels in patients with IDA was significantly lower than the control group (P=0.001); however, such a difference was not detected after 3 months of therapy (P=0.102). We suggest that decreased serum lipocalin levels in our patients during iron insufficiency were caused by iron deficiency rather than anemia.

Iron Deficiency Anemia in Infants and Toddlers – Role of Milk and Constipation

Abstract 5171 Introduction: One of the most common nutritional deficiencies in the world is iron-deficiency anemia and young children are at high risk of developing it. In spite of fortification of foods in the United States, there is a high prevalence of anemia in infants and toddlers increasing their risk of neuro-developmental effects. Constipation is defined as delay or difficulty in defecation ≥ 2 weeks. Around one year of age, various changes are commonly implemented in a child9s diet including introduction of whole milk and solids. Children may then present with sub-clinical colitis, constipation and anemia secondary to blood loss in stool or develop anemia due to increased consumption of milk. The American Academy of Pediatrics (AAP) recommends screening for anemia at 1 year and 2 year visits. The only clue to intolerance to milk may be symptomatic constipation and treating the anemia and switching the type of milk often helps to resolve this problem. This study explores the relation between iron deficiency, constipation and milk. Methods: This is an ongoing prospective study, which has been extended from Cornell to different centers. Data presented here is only from the Cornell principal site. Children between 6 months and 30 months visiting the resident9s pediatric clinic and having routine blood work drawn as a part of their visit were included in the study. The National Health Sciences (NHS) Constipation questionnaire was administered to the parents of these children; ≥ 2 was considered Constipation. In addition, a detailed diet history of the child, and history of medicines and illness was taken and questions were asked about family history of anemia, constipation and allergies. If the mother was breast feeding, questions were asked about her dairy intake. Comparisons were made between children with and without constipation/iron deficiency. If the child had Hemoglobin (Hgb) Results: Two hundred five children, 92 females and 113 males between 8 and 30 months mean age 16. 7 months, are enrolled in the study. Seventy-two children (35 %) were constipated (score ≥2). Forty-two children (20. 5%) had Hgb Of the 42 children who had Hgb Compliance with Iron: Of the 39 children who were on Iron, 9 parents could not be reached via phone. Only 6 parents gave no Iron at all but another 12 did not give Iron properly resulting in 18/30 or 60% of infants/toddlers not receiving an adequate trial of replacement Iron. Among the side effects of Iron, one parent felt Iron caused rash on back and wanted multivitamin with Iron after finishing a month9s course, one child had discoloration of teeth, so the parent gave it with juice. Two parents with infants with apparent true milk protein allergy colitis said constipation improved with diet change and iron. Conclusions: The prevalence of mild anemia is high in infants and toddlers. There was no clear association of constipation and anemia. Compliance is one of the key factors for Iron replacement therapy and in view of how erratic compliance was, it is imperative to give proper instructions to the parent while prescribing Iron. Material to better indicate which foods were rich in iron and follow-up phone calls were included in the management to optimize iron intake of anemic children. We will include more patients, more closely monitor the change in the diet of the child, and monitor responses to Iron therapy in children with low Hgb. In addition, different practices at other involved centers e. g. Brooklyn hospital Center may allow comparison of the time of screening (9 months v/s 1 year) and testing with Hemoglobin/Hematocrit versus a full Complete Blood Count with indices. Disclosures: Bussel:Amgen: Equity Ownership, Membership on an entity9s Board of Directors or advisory committees, Research Funding; Cangene: Research Funding; GlaxoSmithKline: Equity Ownership, Membership on an entity9s Board of Directors or advisory committees, Research Funding; Genzyme: Research Funding; IgG of America: Research Funding; Immunomedics: Research Funding; Ligand: Membership on an entity9s Board of Directors or advisory committees, Research Funding; Eisai, Inc: Membership on an entity9s Board of Directors or advisory committees, Research Funding; Shinogi: Membership on an entity9s Board of Directors or advisory committees, Research Funding; Symphogen: Membership on an entity9s Board of Directors or advisory committees; Sysmex: Research Funding; Portola: Consultancy.