Autonomic nervous system functions in children with breath-holding spells and effects of iron deficiency

Aim: To analyse the activity of the autonomic nervous system during breath-holding spells, we assessed the ECG changes, including ventricular repolarization parameters before and during the spell. We also analysed the effects of iron deficiency on these ECG parameters. Methods: The study group consisted of 37 children with breath-holding spells (30 cyanotic, 7 pallid) (mean age±SD: 12.9±10.8 mo). Twenty-six healthy children (mean age±SD: 14.4±8.6 mo) served as a control group. All patients and controls had standard 12-lead simultaneous surface ECG. All patients had ECG recordings during at least one severe breath-holding spell obtained by “event recorder”. Traces obtained by “event recorder” were analysed in terms of mean heart rate and the frequency and duration of asystole during the spell. Results: Respiratory sinus arrhythmia on standard ECGs and asystole frequency during spells were higher in patients with pallid breath-holding spells. Patients with iron deficiency had a lower frequency of respiratory sinus arrhythmia and prolonged asystole time during the spell. There was no difference in terms of ventricular repolarization parameters (QT/QTc intervals and QT/QTc dispersions) between patients and controls and between patient subgroups (cyanotic versus pallid).

Conclusion: These results confirmed the presence of autonomic dysregulation in children with breath-holding spells. Iron deficiency may have an impact on this autonomic dysregulation. Ventricular repolarization was unaffected in patients with breath-holding spells.     

Iron deficiency among apparently healthy children aged 6 to 24 months in Ibadan,Nigeria

Iron deficiency remains a global public health challenge, with a higher burden in children in the tropics. When it occurs early in life, it may have long-term effects on neurodevelopment. The aims of this study were to assess the iron status of children aged 6–24 months, to determine the prevalence of iron deficiency and its associated factors in Ibadan, Nigeria. The authors conducted a cross-sectional study between March and June 2014. A total of 202 apparently healthy children aged between 6 and 24 months attending 2 major immunization clinics in Ibadan were included. A questionnaire was used to collect information on sociodemographic characteristics, pregnancy and birth history, and nutritional history. Physical examination was carried out on all the subjects, and serum ferritin level was determined using an enzyme-linked immunosorbent assay (ELISA) technique. Iron deficiency was defined using a cutoff value of <30 µg/L. Fifty-nine children (29.2%) had iron deficiency. No clinical features were found to be significantly associated with iron deficiency. Iron deficiency was associated with breastfeeding (P = .020) and younger age (P = .015) in the study population. One hundred and forty-three (70.8%) of the study participants had anemia, and 39 (19.3%) had iron deficiency anemia. The prevalence of iron deficiency among apparently healthy children aged 6–24 months in Ibadan, Nigeria, is high. There is the need for a national policy on routine screening for iron deficiency and iron supplementation for infants and young children as recommended by the World Health Organization.     

Early deterioration of iron status among a cohort of Bolivian infants

Iron deficiency (ID) and iron deficiency anemia (IDA) are major contributors to infant and maternal morbidity worldwide. There is limited longitudinal data on iron status in young infants and on methods to adjust iron biomarkers for inflammation. We aimed to quantify the prevalence of inflammation‐adjusted ID, anemia, and IDA over the first year in a cohort of Bolivian infants and their mothers. Healthy mother‐infant dyads were recruited from two peri‐urban hospitals. Infants provided three blood draws (2, 6–8, and 12–18 months; N = 160); mothers provided two blood draws (1 and 6–8 months postpartum [plus third anemia measurement at 12–18 months]; N = 250). Blood was analyzed for hemoglobin, ferritin, soluble transferrin receptor, C‐reactive protein (CRP), and alpha(1)‐acid glycoprotein (AGP). Iron biomarkers were adjusted for inflammation using CRP and AGP; hemoglobin cutoffs were adjusted for altitude. Inflammation (elevated CRP or AGP) was 17% among toddlers 12–18 months of age. ID (inflammation‐adjusted ferritin) increased with age (<1%, 56%, and 79% at each blood draw), as did anemia and IDA (anemia: 70%, 76%, and 81%; IDA: <1%, 46%, and 68%). Maternal ID declined from the first to second assessment (39% vs. 27%). Inflammation‐adjusted ID prevalence was up to 15 percentage points higher than unadjusted estimates. The high prevalence of ID, anemia, and IDA in this cohort of Bolivian infants beginning at 6–8 months of age suggests that early interventions may be necessary in vulnerable populations.     

Measurement of reticulocyte hemoglobin content to diagnose iron deficiency in Saudi children

Iron deficiency and iron deficiency anemia are common conditions in children, especially in developing countries. It is often difficult for the pediatrician to know which indices should be used in the diagnosis of these conditions in children. Reticulocyte hemoglobin (Hb) content (CHr) has been shown to be an accurate indicator of anemia, however whether its use suits the situation in developing countries or not is unclear. The aim of this study was to evaluate the value and effectiveness of using CHr as a method to diagnose iron deficiency and iron deficiency anemia in Saudi children. The samples for the study were collected from 305 children suspected to have anemia. Complete blood count, transferrin saturation (Tfsat), ferritin, circulating transferrin receptor (TfR) and CHr were measured. Three groups were defined, iron deficiency (Tfsat <20%, Hb >11 g/dL; n=120), iron deficiency anemia (Tfsat <20%, Hb <11 g/dL; (n=73) and controls (Tfsat >20%; n=112). The anemic group had significantly lower macrocytic anemia (MCV), mean corpuscular hemoglobin (MCH) and CHr. All of the variables in the anemia group were significantly lower than those of the control group except for the ferritin level. Compared to the control group, the iron deficiency group also showed significantly lower values except for transferrin receptor and the ferritin levels. CHr levels of <26 pg correlated well with anemic states. CHr together with a complete blood count may provide an alternative to the traditional hematologic or biochemical panel for the diagnosis of iron deficiency and iron deficiency anemia in young children and is cost-effective in developing countries. A CHr cut-off level of 26 pg is considered to be a reasonable indicator of anemic states.     

Novel mutation in the TMPRSS6 gene with iron‐refractory iron deficiency anemia

Iron‐refractory iron deficiency anemia (IRIDA) is a rare autosomal recessive disease characterized by congenital hypochromic microcytic anemia, low transferrin saturation, low serum iron, normal–high serum ferritin, and increased hepcidin. This disease is caused by loss‐of‐function mutations in TMPRSS6 that lead to high hepcidin and result in severe anemia. We report our experience with an 11‐year‐old Japanese girl with hypochromic microcytic anemia, low serum iron, and high serum ferritin, with anemia that was refractory to the oral iron that was prescribed frequently from early childhood. Presence of high hepcidin suggested a diagnosis of IRIDA, which was eventually confirmed by identification of a novel homozygous mutation, p.Pro354Leu, in the TMPRSS6 gene. This case suggests that serum hepcidin should be routinely measured for differential diagnosis when patients with IDA are unresponsive to oral iron or have unusual clinical features.     

Diagnosing iron deficiency in cyanotic heart disease

Objective : To determine the incidence of iron deficiency in children with CCHD by noninvasive, inexpensive and easy laboratory methods.Methods : Forty four children with cyanotic congenital heart disease (CCHD), aged 6 to 48 months were included in this study. The patients were categorized as iron deficient (n:28) and iron sufficient group (n:16). Children with CCHD who had iron deficiency were treated with iron for 3 months.Result : Iron sufficient patients were followed during 3 months without giving iron preparation. Mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), red cell distribution width (RDW), serum iron (SI), total iron binding capacity (TIBC) and serum ferritin levels were measured in all patients at the beginning and at the end of the study.Conclusion : In children with CCHD, hemoglobin (Hb), hematocrit (Hct) and red blood cell (RBC) counts were not considered significant parameters in the diagnosis of iron deficiency. Determination of MCV, MCH, RDW values is relatively easy and inexpensive method requiring small amount of blood for the diagnosis of iron deficiency during the follow-up of patients with CCHD     

Microcytic anemia in children: parallel screening for iron deficiency and thalassemia provides a useful opportunity for thalassemia prevention in low- and middle-income countries

Abstract

Microcytic anemia in children is commonly attributed to iron deficiency without attempting to find the cause. Inadequate investigations to exclude hemoglobinopathies lead to missed opportunities for identification of thalassemia carriers. Here we aim to describe the relative contribution of iron deficiency and thalassemia to microcytic anemia in children. This hospital-based prospective study was conducted at the Colombo North Teaching Hospital, Ragama, Sri Lanka. All newly diagnosed patients with microcytic anemia were recruited and data were collected using an interviewer-administered questionnaire. Full blood count, blood film, serum ferritin, c-reactive protein, quantification of hemoglobin sub-types and α-globin genotype were performed using 4?ml of venous blood. A total of 104 children (Male- 60.5%) were recruited. Iron deficiency was the cause for anemia in 49% whilst 16% and 10% had α- and β-thalassemia trait respectively. Seven (6.7%) children had co-existing iron deficiency and thalassemia trait while two coinherited α- and β-thalassemia trait. Children with β-thalassemia trait had significantly higher red cell count and lower mean corpuscular volume compared to children with iron deficiency. However, none of the red cell parameters were significantly different between children with α-thalassemia trait and iron deficiency. Iron deficiency contributes only to half of children with microcytic anemia; one-fourth had thalassemia trait. Co-existence of iron deficiency and thalassemia trait or co-inheritance of α- and β-thalassemia trait were found in 9%. Parallel investigation of children with microcytic anemia to diagnose iron deficiency and thalassemia provides an opportunity to identify thalassemia carriers which is beneficial for thalassemia prevention.     

THE DIAGNOSIS OF IRON DEFICIENCY BY ERYTHROCYTE PROTOPORPHYRIN AND SERUM FERRITIN ANALYSES

ABSTRACT. Free erythrocyte protoporphyrin (FEP) and serum ferritin have been determined in 57 healthy children and in 25 children with varying degrees of iron deficiency. FEP was found to be inversely correlated to the concentration of hemoglobin (r=-0.80) as well as to serum ferritin (r=-0.64). Elevated FEP was found in children with hemoglobin less than 12.5 g/dl, or serum ferritin less than 8 μg/l. In a group of apparently hematologically normal children between the age of 10–14 years (hemoglobin≥ 12.5 g/dl), a 2-month-trial of iron medication resulted in an increase in hemoglobin and ferritin, and a decrease in FEP, indicating suboptimal supply of iron for hemoglobin synthesis before iron medication. In a patient with iron deficiency (FEP 15.3 μmole/l, hemoglobin 5.2 g/dl), iron therapy was followed by a rapid fall in FEP before any changes in hemoglobin, serum iron transferrin saturation and ferritin could be detected. The rapid fall in FEP during start of treatment in iron deficiency makes FEP a sensitive biochemical parameter on iron homeostasis in iron deficiency anemia.     

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.     

Iodine,selenium, and joints: Kashin-Beck disease

To evaluate the prognosis of breath holding spells (BHS) after iron treatment, 91 children (56 boys, 35 girls) aged between 6 months and 40 months (median, 17) were followed prospectively for a median of 45 months (range, 6-89). In 49 of the children, the frequency of BHS was less than 10 each month, in 22 it was 10-30 each month, and in 20 more than 30 each month. The spells were cyanotic in 60 children. All patients were evaluated initially and during follow up for haematological indices. Electroencephalographic and electrocardiographic abnormalities were also recorded. Sixty three patients were found to have iron deficiency anaemia and were treated with iron (6 mg/kg/day) for three months. Other patients were not given any treatment. After three months, there was a significant difference for correction of cyanotic spells between children who had been treated with iron and those who had not (84.1% v 21.4%). During further follow up, febrile convulsions occurred in 10 children (six were on iron treatment initially). It appears that treating iron deficiency anaemia is effective in reducing the frequency of BHS.     

Proton pump inhibitors use suppresses iron absorption in congenital dyserythropoietic anemia

Congenital dyserythropoietic anemia type I (CDA I) is associated, as other anemic noninflammatory states, with ineffective erythropoiesis and increased iron absorption, which may lead to complication of iron overload. The latter complication requires iron-chelating therapy, which may be associated with adverse effects and toxicity. Gastric acid production is known to be an important factor that facilitates non-heme iron absorption. The purpose of this study was to examine whether treatment with proton pump inhibitors (PPIs) can decrease iron absorption in patients with CDA I. Eight CDA I patients (4 boys) aged 12–18 years with mild iron overload (not yet requiring chelating therapy) received 20 mg/d omeprazole for 6 months. Blood samples were obtained for ferritin, C-reactive protein, hemoglobin, calcium, and magnesium at baseline, at the end of months intervention and 6 months after its cessation. The mean ferritin level decreased from 585 ± 180 ng/ml at baseline to 522 ± 172 ng/ml at the end of 6-month treatment and 660 ± 256 ng/ml 6 months after cessation of omeprazole treatment (p = 0.009). Omeprazole treatment caused a nonsignificant reduction in the mean iron level (iron 159 ± 42, 136 ± 54,167 ± 34 µg/dl, p = 0.302). However, mean hemoglobin level was mildly but significantly reduced (Hg 10.0 ± 0.8, 9.55 ± 1.0, 10.4 ± 10.7 g/dl, p = 0.002). No adverse effects were reported. Our investigation suggests that administration of PPI to patients with CDA I may reduce iron absorption and may lower iron overload and the need for chelation therapy.     

Anemia and markers of erythropoiesis in pediatric kidney transplant recipients compared to children with chronic renal failure

PTA and anemia of CKD share a similar pathogenesis. However, PTA may be disproportionate to the reduction in the GFR. Data relating to the mechanism of PTA are scarce. We evaluated the erythropoiesis parameters in pediatric kidney recipients compared to children with CKD. A total of 100 patients (54 post‐kidney TX, 46 with CKD) were enrolled in the single‐center cohort study. GFR was found to be significantly lower in the CKD group (49.7±22.4 vs 72.9±28.5 mL/min/1.73 m², P<.001); anemia was significantly more common in the TX patients (52% vs 41.3%, P<.001). Iron transferrin saturation and serum ferritin levels were lower in the CKD patients. In both groups, hemoglobin Z scores significantly correlated with GFR (R=.31, P=.07). This correlation was more prominent in the CKD group (R=.43, P=.008) compared to the TX group (R=.31, P=.04). Anemia was significantly more common in the TX patients than in the CKD patients despite a better GFR. The higher prevalence of anemia in the TX group could not be explained by an iron deficiency or reduced EPO production. We speculate that immunosuppressive therapy together with resistance to EPO may play a role in the pathogenesis of post‐transplantation anemia.     

Serum transferrin receptor levels in the evaluation of iron deficiency in the neonate

Iron deficiency anemia (IDA) is a major global problem. Early onset of iron deficiency in developing countries makes it imperative to identify iron deficiency in neonates. Most conventional laboratory parameters of iron status fail to distinguish neonates with iron deficient erythropoiesis. Serum transferrin receptor (STFR) levels are a recent sensitive measure of iron deficiency and the present study was carried out to evaluate the usefulness of cord serum transferrin receptors in identifying iron deficient erythropoiesis in neonates. A complete hemogram, red cell indices, iron profile: serum iron (SI), percent transferrin saturation (TS%) and serum ferritin (SF) was carried out in 100 full-term neonates and their mothers at parturition. Cord and maternal STFR levels were estimated using a sensitive enzyme-linked immunosorbent assay (ELISA) technique. Anemic women had a significantly lower SI, their TS% and high STFR levels suggesting that iron deficiency was responsible for the anemia. In the neonates of iron deficient mothers, cord SI, TS% and cord ferritin were not significantly different from those of neonates born to non-anemic mothers. Cord STFR level correlated well with hemoglobin (Hb) and laboratory parameters of iron status, and its level was significantly higher in neonates born to anemic mothers than in those bom to non-anemic mothers. It was the only laboratory parameter to differentiate between neonates bom to anemic and non-anemic mothers. Therefore, STFR is a sensitive index of iron status in neonates and identifies neonates with iron deficient erythropoiesis.     

Iron deficiency in proteinuric children with nephrotic syndrome: A cross-sectional pilot study

Massive proteinuria in nephrotic syndrome causes depletion of various proteins. Iron deficiency can occur due to urinary loss of iron, transferrin, and soluble transferrin receptors. We conducted this cross-sectional study of 52 children with proteinuric nephrotic syndrome, aged 1–12 years (mean 7.1 ± 2.7 years). Hemoglobin (Hb), RBC indices (MCV, MCH, MCHC), percentage of hypochromic RBCs (Hypo-He), reticulocyte hemoglobin content (Ret-He), and serum ferritin were examined. Seven (13%) patients had iron deficiency anemia and another 10 (19%) exhibited iron deficiency. A higher proportion of children with steroid-resistant disease had anemia than did steroid-sensitive children (P = 0.076). Thus, children with nephrotic syndrome may have iron deficiency (32.7%), which needs to be screened.     

Ferritin and iron levels in children with autistic disorder

Iron has an important role on cognitive, behavioral, and motor development. High prevalence of iron deficiency has been reported in autism. The aim of this study was to investigate iron status in a group of children with autistic disorder. The sample was composed of 116 children between 3 and 16 years with a diagnosis of autistic disorder according to DSM-IV criteria. Serum ferritin, iron, hemoglobin, hematocrit, mean corpuscular volume, and red cell distribution width values were measured. We found that 24.1% of subjects had iron deficiency, and 15.5% had anemia. There was a significant positive correlation between age and ferritin and hematological measures. Results of this study confirmed that iron deficiency and anemia are common in children with autistic disorder. Conclusion: These findings suggest that ferritin levels should be measured in subjects with autism as a part of routine investigation.     

Leukocyte DNA damage in children with iron deficiency anemia: effect of iron supplementation

Iron deficiency is frequently associated with anemia. Iron is a transition-metal ion, and it can induce free radical formation, which leads to formation of various lesions in DNA, proteins, and lipids. The aim of this study was to investigate baseline oxidative DNA damage and to clarify the role of the administration of a therapeutic dose of iron on DNA oxidation in children with iron deficiency anemia (IDA). Twenty-seven children with IDA and 20 healthy children were enrolled in the study. Leukocyte DNA damage (strand breaks and Fpg-sensitive sites) was assessed using comet assay before and after 12 weeks of daily iron administration. Before the iron administration, the frequency of DNA strand breaks in the children with IDA was found to be lower than those in the control group (P < 0.05), but there was not a significant difference for frequency of Fpg-sensitive sites. After 12 weeks of iron administration, the frequency of both DNA strand breaks and Fpg-sensitive sites were found to be increased (P < 0.01). No significant association was determined between DNA damage parameters and hemoglobin, hematocrit, serum iron, total iron binding capacity, and ferritin. In conclusion, basal level of DNA strand breaks is at a low level in children with IDA. After iron administration, DNA strand breaks and Fpg-sensitive sites, which represent oxidatively damaged DNA, increased. However, this increase was unrelated to serum level of iron and ferritin.     

Diagnostic Yield of Upper Gastrointestinal Endoscopy in the Evaluation of Iron Deficiency Anemia in Older Children and Adolescents

Iron deficiency anemia (IDA) is frequent in childhood. Inadequate nutrition and gastrointestinal malabsorption are the frequent causes of IDA in children. But reduced iron absorption and insidious blood loss from the gastrointestinal tract has been identified as the most frequent causes of IDA in older children and adolescents. Therefore the authors evaluated the frequency and etiologies of the upper gastrointestinal system pathologies causing IDA in older pediatric population. Patients with known hematological or chronic diseases, heavy menstrual flow, and obvious blood loss were excluded from the study. Forty-four children between the ages of 9.5 and 17.5 years and diagnosed with IDA were enrolled. They underwent upper gastrointestinal endoscopy and biopsy from esophagus, stomach, and duodenum. Mean age and hemoglobin (Hb) levels of study group (32 boys, and 12 girls) were 14.6 ± 2.0 years and 7.9 ± 1.8 g/dL, respectively. Only 1 patient had a positive serology testing with anti-tissue transglutaminase and small bowel biopsy correlating with celiac disease. Endoscopy revealed abnormal findings in 25 (56.8%) patients (21 endoscopic antral gastritis, 2 active duodenal ulcers, and 2 duodenal polyps). Helicobacter pylori (HP) infection was identified by using antral histopathological evaluation in 19 of 44 children (43.2%). In 2 of duodenal samples, one patient had celiac disease, and the other one was diagnosed as giardiasis. In conclusion, there are different etiologies resulting in IDA in older children and adolescents. When older children and adolescents are found to have iron deficiency, HP infection and other gastrointestinal pathologies should be ruled out before iron deficiency treatment.     

Iron supplementation in children with Celiac Disease

Objective : To evaluate the effect of iron supplementation, in addition to gluten free diet (GFD), on hematological profile of children with Celiac Disease (CD).Methods : Children diagnosed as CD as per modified ESPGAN criteria were prospectively evaluated for their hematological profile at the time of their enrolment and after consuming GFD for at least one year. The results were compared with age and sex matched controls. Evaluation of hematological profile included hemoglobin estimation, complete blood counts, peripheral blood smear examination, serum iron, total iron binding capacity (TIBC), and serum ferritin estimation. All the enrolled cases were given iron supplementation in addition to exclusion of gluten from their diet. Repeat intestinal biopsy was performed in all the cases after completing 1 year on GFD.Results : Twenty one children (mean age 6.67 years, range 4 2–11 years) diagnosed as CD who completed at least one year of regular follow up on GFD (mean 1.5 years, range 1 2–2 years) were analysed for their hematological profile at the time of enrolment and after consuming GFD and iron supplementation. At the time of enrolment all the children had hemoglobin level <11 gm%, 78% had microcytic hypochromic anemia and 22% had dimorphic anemia, with lower mean MCV, MCH and serum ferritin levels, and a significantly higher mean TIBC as compared to controls (p <0.001). In the follow up evaluation of these cases on GFD, mean hemoglobin levels were comparable with controls but the cases continued to have lower mean MCV, MCH serum ferritin levels (p <0.05) and higher mean TIBC (p <0.05). Seven children had mild anemia. Serum ferritin levels showed a negative correlation with the grade of villous atrophy and lamina propria infiltrate.Conclusion : Our results suggest that iron deficiency anemia (IDA) is commonly associated with CD and iron deficiency state continues for a longer time even after excluding gluten from the diet and iron supplementation. Apart from offering them GFD rich in iron, early detection and treatment of IDA and prophylactic iron folic acid supplementation will go a long way to optimize their mental and psychomotor functions.     

Breath holding spells in 91 children and response to treatment with iron.

To evaluate the prognosis of breath holding spells (BHS) after iron treatment, 91 children (56 boys, 35 girls) aged between 6 months and 40 months (median, 17) were followed prospectively for a median of 45 months (range, 6-89). In 49 of the children, the frequency of BHS was less than 10 each month, in 22 it was 10-30 each month, and in 20 more than 30 each month. The spells were cyanotic in 60 children. All patients were evaluated initially and during follow up for haematological indices. Electroencephalographic and electrocardiographic abnormalities were also recorded. Sixty three patients were found to have iron deficiency anaemia and were treated with iron (6 mg/kg/day) for three months. Other patients were not given any treatment. After three months, there was a significant difference for correction of cyanotic spells between children who had been treated with iron and those who had not (84.1% v 21.4%). During further follow up, febrile convulsions occurred in 10 children (six were on iron treatment initially). It appears that treating iron deficiency anaemia is effective in reducing the frequency of BHS.     

SEVERE THROMBOCYTOPENIA WITH IRON DEFICIENCY ANEMIA

Although severe thrombocytopenia has been reported among children with iron deficiency anemia, the presence of both anemia and thrombocytopenia can suggest serious or malignant bone marrow dysfunction, requiring further work-up. This paper reviews the management and outcomes of patients with the diagnosis of iron deficiency anemia presenting with severe thrombocytopenia. The authors present 4 pediatric patients with iron deficiency anemia and severe thrombocytopenia at initial presentation. Charts were reviewed after approval by the institutional review boards at both St. Jude Children's Research Hospital and LeBonheur Children's Medical Center in Memphis, Tennessee. All 4 patients’ hemoglobin concentrations and platelet counts normalized within 1 to 3 weeks of initiating iron supplementation, suggesting that in such patients iron supplementation can obviate the need for invasive diagnostic procedures.

In addition, these patients all had a platelet “overshoot” phenomenon during iron therapy prior to normalization of platelet counts, the mechanism of which is still unknown. The literature exploring the mechanism behind the current clinical findings is reviewed.