Mechanisms of iron deficiency formation and modern approach to administration of oral iron forms

AbstractOral iron promotes intestinal tumourigenesis in animal models. In humans, expression of iron transport proteins are altered in colorectal cancer. This study examined whether the route of iron therapy alters iron transport and tumour growth. Colorectal adenocarcinoma patients with pre-operative iron deficiency anaemia received oral ferrous sulphate (n = 15), or intravenous ferric carboxymaltose (n = 15). Paired (normal and tumour tissues) samples were compared for expression of iron loading, iron transporters, proliferation, apoptosis and Wnt signalling using immunohistochemistry and RT-PCR. Iron loading was increased in tumour and distributed to the stroma in intravenous treatment and to the epithelium in oral treatment. Protein and mRNA expression of proliferation and iron transporters were increased in tumours compared to normal tissues but there were no significant differences between the treatment groups. However, intravenous iron treatment reduced ferritin mRNA levels in tumours and replenished body iron stores. Iron distribution to non-epithelial cells in intravenous iron suggests that iron is less bioavailable to tumour cells. Therefore, intravenous iron may be a better option in the treatment of colorectal cancer patients with iron deficiency anaemia due to its efficiency in replenishing iron levels while its effect on proliferation and iron metabolism is similar to that of oral iron treatment.

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PSY4 A SYSTEMATIC LITERATURE REVIEW AND INDIRECT COMPARISON OF IRON ISOMALTOSIDE AND FERRIC CARBOXYMALTOSE IN IRON DEFICIENCY ANAEMIA AFTER FAILURE OR INTOLERANCE OF ORAL IRON TREATMENT

Value in Health ◽

10.1016/j.jval.2019.04.1829 ◽

2019 ◽

Vol 22 ◽

pp. S374

Author(s):

R. Pollock ◽

G. Muduma

Keyword(s):

Iron Deficiency ◽

Literature Review ◽

Systematic Literature Review ◽

Iron Deficiency Anaemia ◽

Indirect Comparison ◽

Oral Iron ◽

Ferric Carboxymaltose ◽

Deficiency Anaemia ◽

Iron Treatment

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IRON ABSORPTION AND RESPONSE TO ORAL IRON THERAPY IN IRON DEFICIENCY ANEMIA ASSOCIATED TO ASYMPTOMATIC GIARDIASIS.

Pediatric Research ◽

10.1203/00006450-199306000-00039 ◽

1993 ◽

Vol 33 (6) ◽

pp. 661-661

Author(s):

Helena U Suzuki ◽

Mauro B Morais ◽

Jose N Corral ◽

Ulisses Fagundes-Neto ◽

Nelson L Machado

Keyword(s):

Iron Deficiency ◽

Iron Deficiency Anemia ◽

Iron Absorption ◽

Oral Iron ◽

Iron Therapy ◽

Deficiency Anemia ◽

Oral Iron Therapy

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

Cardiology in the Young ◽

10.1017/s1047951121004066 ◽

2021 ◽

pp. 1-8

Author(s):

Kriti Puri ◽

Joseph A. Spinner ◽

Jacquelyn M. Powers ◽

Susan W. Denfield ◽

Hari P. Tunuguntla ◽

...

Keyword(s):

Heart Failure ◽

Iron Deficiency ◽

Transferrin Saturation ◽

Systolic Heart Failure ◽

Oral Iron ◽

Wilcoxon Test ◽

Iron Therapy ◽

Oral Iron Therapy ◽

Iron Deficient ◽

Iron Replacement

Abstract 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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The Treatment of Iron-deficiency Anemia—Palatable but Ineffective Iron Medication

PEDIATRICS ◽

10.1542/peds.31.6.1041 ◽

1963 ◽

Vol 31 (6) ◽

pp. 1041-1044

Author(s):

LOUIS K DIAMOND ◽

J. LAWRENCE NAIMAN ◽

DONALD M. ALLEN ◽

FRANK A. OSKI,

Keyword(s):

Iron Deficiency ◽

Iron Deficiency Anemia ◽

Ferrous Sulfate ◽

Oral Iron ◽

Gastrointestinal Absorption ◽

Deficiency Anemia ◽

Therapeutic Effects ◽

Rapid Rise ◽

Carbohydrate Complex ◽

Therapeutic Results

Experience with a new oral iron-carbohydrate complex (Jefron) in the treatment of iron-deficiency anemia shows that the therapeutic results are inferior to those obtainable with ferrous sulfate. Many children showed no response after months of treatment with this drug and when subsequently placed on ferrous sulfate therapy showed a rapid rise in hemoglobin to normal levels. Preliminary studies suggest that poor gastrointestinal absorption may be a factor in the inadequate therapeutic effects.

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Intravenous versus Oral iron for Iron-Deficiency Anemia in Pregnancy (IVIDA): A Randomized Controlled Trial

American Journal of Perinatology ◽

10.1055/s-0041-1740003 ◽

2021 ◽

Author(s):

Adam K. Lewkowitz ◽

Molly J. Stout ◽

Emily Cooke ◽

Seon C. Deoni ◽

Viren D'Sa ◽

...

Keyword(s):

Randomized Controlled Trial ◽

Iron Deficiency ◽

Iron Deficiency Anemia ◽

Adverse Reactions ◽

Controlled Trial ◽

Oral Iron ◽

Deficiency Anemia ◽

Randomized Controlled ◽

Iv Iron ◽

Severe Adverse Reactions

Objective Iron-deficiency anemia (IDA) can have serious consequences for mothers and babies. Iron supplementation is recommended, but the administration route is controversial. We sought to conduct a randomized controlled trial (RCT) testing the effectiveness and safety of intravenous (IV) iron compared with oral iron on perinatal outcomes in pregnant women with IDA. Study Design This open-label RCT randomized patients with IDA (hemoglobin [hgb] <10 g/dL and ferritin <30 ng/mL) at 24 to 34 weeks' to oral iron or single 1,000-mg dose of IV low-molecular weight iron dextran over one hour. The primary outcome was maternal anemia at delivery (hgb < 11 g/dL). Secondary outcomes were mild/moderate or severe adverse reactions, maternal hgb and ferritin at delivery, blood transfusion, gestational age at delivery, birth weight, neonatal hgb and ferritin, and composite neonatal morbidity. Analysis was as per protocol. Results The trial was stopped early for logistical reasons, and the data analyzed as preliminary data to inform a larger, potentially externally funded, definitive trial. Of 55 patients approached, 38 consented. Of these, 15 were withdrawn: 5 received IV iron from their primary obstetrician after being randomized to oral iron and 10 declined to receive IV iron. Of the remaining 23 patients, who were included in the analytic population, 13 received oral iron and 10 received IV iron. The rate of maternal anemia at delivery (hgb < 11 g/dL) was high overall but significantly reduced with IV iron (40 vs. 85%, p = 0.039). Rates of maternal hgb < 10 g/dL were significantly lower in the IV iron group (10 vs. 54%, p = 0.029). There were no severe adverse reactions and similar rates of mild/moderate reactions between groups. Conclusion IV iron reduces rates of anemia at the time of admission for delivery, supporting a larger RCT comparing IV versus oral iron for the treatment of IDA of pregnancy powered for definitive clinical outcomes. However, issues uncovered in this RCT suggest that patient, clinician, and systems-level barriers associated with different IDA treatment modalities must be considered prior to conducting a larger RCT. This study is registered with clinicaltrials.gov with identifier no.: NCT03438227. Key Points

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