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Published on: March 14, 2017
Poor efficacy of oral iron replacement therapy in pediatric patients with heart failure
Kriti Puri1,2, Joseph A Spinner2, Jacquelyn M Powers3
1Section of Critical Care Medicine, Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital, Houston, TX, USA.
Insights
Oral iron therapy is ineffective for most children with heart failure, failing to correct iron deficiency in over half of patients. This highlights a critical gap in pediatric cardiovascular care and iron management.
Area of Science:
- Pediatric Cardiology
- Hematology
- Nutritional Science
Background:
- Iron deficiency is linked to poorer outcomes in pediatric systolic heart failure.
- Oral iron is ineffective in adults with heart failure, but its efficacy in children is unknown.
Purpose of the Study:
- To determine the efficacy of oral iron therapy in replenishing iron stores in children with systolic heart failure.
- To test the hypothesis that oral iron would be ineffective in at least 50% of these patients.
Main Methods:
- Retrospective cohort study of 51 children (≤21 years) with systolic heart failure and iron deficiency.
- Iron deficiency defined by low serum iron, ferritin, high transferrin, or low transferrin saturation.
- Paired-samples Wilcoxon test used to compare iron studies pre- and post-therapy.
Main Results:
- 55% of children (11/20) remained iron deficient after oral iron therapy.
- Median oral iron dose was 2.9 mg/kg/day for 96 days.
- Common heart failure causes included cardiomyopathy and congenital heart disease.
Conclusions:
- This is the first study on oral iron efficacy in pediatric heart failure.
- Over half of the pediatric heart failure patients did not respond to oral iron, remaining iron deficient.
Introduction:
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.
Methods:
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.
Results:
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.
Conclusions:
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.
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