INTRODUCTION: The prevalence of iron deficiency and anemia in the setting of modern-day maintenance immunosuppression in pediatric heart transplant (HTx) recipients is unclear. The primary aim was to determine the prevalence of iron deficiency (serum ferritin < 30 ng/mL ± transferrin saturation < 20%) and anemia per World Health Organization diagnostic criteria and associated risk factors. METHODS: Single-center, cross-sectional analysis of 200 consecutive pediatric HTx recipients (<21 years old) from 2005 to 2021. Data were collected at 1-year post-HTx at the time of annual protocol biopsy. RESULTS: Median age at transplant was 3 years (IQR .5-12.2). The median ferritin level was 32 ng/mL with 46% having ferritin < 30 ng/mL. Median transferrin saturation (TSAT) was 22% with 47% having TSAT < 20%. Median hemoglobin was 11 g/dL with 54% having anemia. Multivariable analysis revealed lower absolute lymphocyte count, TSAT < 20%, and estimated glomerular filtration rate <75 mL/min/1.73 m2 were independently associated with anemia. Ferritin < 30 ng/mL in isolation was not associated with anemia. Ferritin < 30 ng/mL may aid in detecting absolute iron deficiency while TSAT < 20% may be useful in identifying patients with functional iron deficiency ± anemia in pediatric HTx recipients. CONCLUSION: Iron deficiency and anemia are highly prevalent in pediatric HTx recipients. Future studies are needed to assess the impact of iron deficiency, whether with or without anemia, on clinical outcomes in pediatric HTx recipients.
Anemia, Iron-Deficiency , Heart Transplantation , Humans , Heart Transplantation/adverse effects , Male , Female , Cross-Sectional Studies , Child , Prevalence , Child, Preschool , Follow-Up Studies , Risk Factors , Prognosis , Anemia, Iron-Deficiency/epidemiology , Anemia, Iron-Deficiency/diagnosis , Anemia, Iron-Deficiency/etiology , Postoperative Complications/epidemiology , Postoperative Complications/diagnosis , Postoperative Complications/etiology , Postoperative Complications/blood , Iron Deficiencies , Infant , Adolescent , Anemia/epidemiology , Anemia/etiology , Anemia/diagnosis , Transplant Recipients/statistics & numerical data , Graft Rejection/etiology , Graft Rejection/epidemiology , Graft Rejection/blood , Graft Rejection/diagnosis
BACKGROUND: Iron deficiency and iron deficiency anemia are common in pediatric inflammatory bowel disease and often require supplementation with iron. There is a paucity of literature regarding optimal iron formulation. The aim of this study is to compare outcomes in pediatric patients with inflammatory bowel disease receiving either iron sucrose or ferric carboxymaltose during inpatient hospitalizations. METHODS: This was a single-center retrospective study of pediatric patients with inflammatory bowel disease admitted for newly diagnosed disease or flare who received either iron sucrose or ferric carboxymaltose. Linear regression was used to assess differences in iron repletion. Longitudinal linear mixed-effects models and generalized estimating equations compared hematologic and iron outcomes 6 months post-iron repletion. RESULTS: Thirty patients received ferric carboxymaltose. Sixty-nine patients received iron sucrose. Baseline hemoglobin and iron deficits were similar in both groups. A larger percentage of iron deficit was repleted in the ferric carboxymaltose group (81.4%) compared with iron sucrose (25.9%) (P < 0.001) with fewer infusions. Cumulative doses of ferric carboxymaltose administered (18.7 mg/kg) were higher than iron sucrose (6.1 mg/kg) (P < 0.001). Hemoglobin increased more quickly with ferric carboxymaltose compared with iron sucrose (P = 0.04 and P = 0.02, respectively). Total iron binding capacity and red cell distribution width levels decreased more over time with ferric carboxymaltose vs iron sucrose (P < 0.01 and P = 0.01, respectively). No adverse effects were seen. CONCLUSIONS: Hematologic and iron parameters responded more quickly with fewer infusions in patients who received ferric carboxymaltose vs iron sucrose. Patients who received ferric carboxymaltose achieved a higher percentage of iron deficit repleted.
Inflammatory Bowel Diseases , Iron , Humans , Child , Ferric Oxide, Saccharated , Iron/therapeutic use , Retrospective Studies , Ferric Compounds/therapeutic use , Inflammatory Bowel Diseases/complications , Hemoglobins/metabolism
Inflammatory bowel disease (IBD) is treated with a variety of immunomodulating and immunosuppressive therapies; however, for the majority of cases, these therapies are not targeted for specific disease phenotypes. Monogenic IBD with causative genetic defect is the exception and represents a disease cohort where precision therapeutics can be applied. With the advent of rapid genetic sequencing platforms, these monogenic immunodeficiencies that cause inflammatory bowel disease are increasingly being identified. This subpopulation of IBD called very early onset inflammatory bowel disease (VEO-IBD) is defined by an age of onset of less than six years of age. Twenty percent of VEO-IBDs have an identifiable monogenic defect. The culprit genes are often involved in pro-inflammatory immune pathways, which represent potential avenues for targeted pharmacologic treatments. This review will provide an overview of the current state of disease-specific targeted therapies, as well as empiric treatment for undifferentiated causes of VEO-IBD.
