IRON SUCROSE
Clinical safety rating: caution
Comprehensive clinical and safety monograph for IRON SUCROSE (IRON SUCROSE).
Iron sucrose is a polynuclear iron(III)-hydroxide sucrose complex that, after intravenous administration, releases iron directly to transferrin, bypassing the gastrointestinal tract. The iron is then utilized in erythropoiesis to increase hemoglobin levels.
| Metabolism | Iron sucrose is dissociated into iron and sucrose by the reticuloendothelial system; iron is incorporated into hemoglobin or stored as ferritin, while sucrose is metabolized to carbon dioxide and water. |
| Excretion | Iron sucrose is primarily excreted via the reticuloendothelial system; negligible renal excretion of intact complex. Less than 1% of administered dose is excreted unchanged in urine. Iron is incorporated into hemoglobin and storage pools. |
| Half-life | Terminal elimination half-life is approximately 5–6 hours in patients with iron deficiency anemia. In healthy subjects, the half-life is about 6 hours. The clinical significance is that the drug is rapidly cleared from plasma, with iron being distributed to tissues. |
| Protein binding | Iron sucrose is rapidly dissociated in plasma; iron binds to transferrin (substantial binding) and ferritin in tissues. The complex itself does not have defined protein binding, but iron released binds to transferrin (about 30% saturation increases). |
| Volume of Distribution | Apparent volume of distribution is approximately 1.0–1.5 L/kg in patients with anemia, reflecting distribution into the reticuloendothelial system and erythroid precursor cells. Plasma volume is about 0.05 L/kg, so Vd indicates extensive tissue distribution. |
| Bioavailability | Bioavailability: Not applicable for intravenous iron sucrose, as it is administered IV. Oral absorption is negligible (iron sucrose is not absorbed orally due to its complex structure). |
| Onset of Action | Intravenous administration: onset of rise in hemoglobin is observed within 1–2 weeks, with improvement in symptoms (e.g., fatigue) occurring earlier. A single dose increases serum iron levels immediately. |
| Duration of Action | Duration of effect on hemoglobin depends on the total iron deficit; typically, treatment courses span several weeks. The drug itself is cleared from plasma within 24 hours, but iron is retained for erythropoiesis. |
100-200 mg elemental iron (as 5-10 mL) intravenously, up to 3 times per week, to a total cumulative dose based on iron deficit calculated by Ganzoni formula: Total iron deficit (mg) = body weight (kg) × (target Hb - actual Hb) (g/dL) × 2.4 + iron stores (500 mg if weight ≥35 kg, 15 mg/kg if <35 kg). Administer by slow IV injection (20 mg/min) or IV infusion over at least 30 minutes.
| Dosage form | INJECTABLE |
| Renal impairment | No dose adjustment required for GFR ≥15 mL/min. For GFR <15 mL/min (dialysis-dependent), use with caution due to oxidative stress risk; typical dosing unchanged but monitor iron parameters closely. No specific GFR-based dose reduction established. |
| Liver impairment | No dose adjustment recommended for Child-Pugh A or B. For Child-Pugh C, use with caution; consider reducing dose by 50% and monitor for iron overload due to reduced transferrin synthesis. |
| Pediatric use | Children ≥2 years: 0.15 mg/kg elemental iron (as 0.75 mL/kg) IV over 5 minutes, up to 3 times weekly, maximum single dose 100 mg; total dose per Ganzoni formula: iron deficit (mg) = weight (kg) × (target Hb - actual Hb) (g/dL) × 0.24 + 15 mg/kg (stores) for weight <35 kg. Infants <2 years: limited data; use with extreme caution. |
| Geriatric use |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for IRON SUCROSE (IRON SUCROSE).
| Breastfeeding | Excreted into human milk in negligible amounts. M/P ratio not established. Considered compatible with breastfeeding; minimal risk to infant due to poor oral bioavailability of iron from milk. No adverse effects reported. |
| Teratogenic Risk | FDA Pregnancy Category B. No evidence of teratogenicity in animal studies. Limited human data; however, iron sucrose does not cross the placenta in significant amounts (iron-carbohydrate complex is large). No increased risk of fetal malformations reported. Use only if clearly needed in pregnancy. |
■ FDA Black Box Warning
No FDA black box warning.
| Serious Effects |
["Hypersensitivity to iron sucrose or any of its components","Evidence of iron overload (e.g., serum ferritin > 1000 ng/mL or transferrin saturation > 50%)","Anemia not caused by iron deficiency"]
| Precautions | ["Risk of hypersensitivity reactions including anaphylaxis, which may be fatal; emergency equipment must be available.","Hypotension may occur; monitor blood pressure during infusion.","Iron overload can occur with excessive dosing; monitor iron indices.","Do not administer to patients with evidence of iron overload or anemia not caused by iron deficiency."] |
Loading safety data…
| No specific dose adjustment based on age alone; use lower end of dosing range (e.g., 100 mg IV) due to higher risk of adverse reactions (e.g., hypotension, anaphylaxis) and comorbidities. Administer at minimum recommended infusion rate (20 mg/min). |
| Fetal Monitoring |
| Monitor maternal hemoglobin, hematocrit, ferritin, and iron saturation levels periodically. Monitor for signs of hypersensitivity during infusion. In pregnancy, assess fetal growth and well-being if significant maternal anemia is present. |
| Fertility Effects | No direct adverse effects on fertility reported. Correction of iron deficiency may improve ovulatory function in women with iron-deficiency anemia. |