Gestational anemia is a common complication during pregnancy, with iron deficiency anemia (IDA) being the most prevalent type (accounting for over 90% of all gestational anemia cases). During pregnancy, the expansion of blood volume and the dramatic increase in iron demand for fetal growth and development (daily iron requirement reaches 27–30 mg in the second and third trimesters, far exceeding the 15 mg required in the non-pregnant state) often lead to insufficient hemoglobin (Hb) synthesis and subsequent anemia if maternal iron stores are inadequate or dietary iron intake is insufficient. As an oral divalent iron preparation, ferrous gluconate is characterized by "high bioavailability and low gastrointestinal irritation" and is a commonly used clinical agent for correcting gestational IDA. This article systematically evaluates its application value in gestational anemia from four aspects—mechanism of action, efficacy verification, safety analysis, and application precautions—providing a reference for clinical medication.
I. Core Mechanisms of Ferrous Gluconate in Correcting Gestational Anemia
Ferrous gluconate targets and corrects gestational IDA through the pathway of "iron supplementation → promotion of hemoglobin synthesis → improvement of iron stores," with its mechanisms aligning with the physiological needs of both the maternal body and the fetus during pregnancy:
(I) Supplying Absorbable Iron to Alleviate Iron Deficiency
The essence of gestational IDA is iron imbalance caused by "iron intake < iron demand." The expansion of maternal blood volume (a 40%–45% increase during pregnancy) requires additional iron for hemoglobin synthesis, while the fetus also obtains iron from the mother for its growth and development (especially liver iron storage). The iron in ferrous gluconate exists in the divalent form (Fe²⁺), which can be directly absorbed via the "divalent metal transporter 1 (DMT1)" in the small intestinal mucosa without undergoing the "trivalent iron (Fe³⁺) → divalent iron" conversion process in the gastrointestinal tract. Its absorption efficiency is significantly higher than that of trivalent iron preparations (e.g., ferric sulfate, ammonium citrate iron), enabling rapid replenishment of the maternal available iron pool. Clinical data show that the iron absorption rate in the small intestine after oral administration of ferrous gluconate can reach 15%–20% (compared to 5%–10% for trivalent iron preparations), and it is less affected by phytic acid and tannic acid in the diet, making it more suitable for the diverse dietary scenarios during pregnancy.
(II) Promoting Hemoglobin Synthesis to Relieve Anemia Symptoms
Iron is a core component of hemoglobin (each hemoglobin molecule contains 4 iron atoms). Iron deficiency hinders hemoglobin synthesis, reduces the oxygen-carrying capacity of red blood cells, and causes maternal symptoms such as fatigue, dizziness, and palpitations, as well as fetal issues like intrauterine hypoxia and growth restriction. After absorption, ferrous gluconate is transported via the bloodstream to bone marrow hematopoietic tissue, where it participates in hemoglobin synthesis: Fe²⁺ first combines with protoporphyrin to form heme, which then binds to globin to generate hemoglobin, and finally assembles into red blood cells. Typically, after 2 weeks of regular ferrous gluconate administration, maternal bone marrow hematopoietic function is activated, the number of new red blood cells in peripheral blood increases, hemoglobin levels begin to rise, and anemia-related symptoms (e.g., fatigue after activity) gradually alleviate. After 4–6 weeks, hemoglobin levels can return to the normal range, and the oxygen-carrying capacity of red blood cells is significantly improved, meeting the metabolic needs of the mother and the intrauterine oxygen supply needs of the fetus.
(III) Restoring Iron Stores to Prevent Recurrence of Gestational Anemia
The treatment of gestational anemia not only requires "correcting current anemia" but also "replenishing iron stores" to cope with the higher iron demand in the third trimester (blood volume peaks at 32–36 weeks of gestation, with the highest iron demand) and iron loss during childbirth (average blood loss during delivery is 300–500 mL, corresponding to 150–250 mg of iron loss). While supplementing iron for hematopoiesis, ferrous gluconate stores excess iron in "ferritin" in tissues such as the liver, spleen, and bone marrow, increasing maternal iron reserve levels. Clinical monitoring shows that after 8 weeks of daily administration of 300 mg ferrous gluconate (calculated as elemental iron), maternal serum ferritin (a core indicator reflecting iron stores) can increase from <15 μg/L (during anemia) to >30 μg/L, meeting the safety standard for maternal iron stores during pregnancy and effectively preventing the recurrence of anemia in the third trimester and postpartum iron deficiency anemia.
II. Efficacy Verification of Ferrous Gluconate in Gestational Anemia
Based on clinical research and practical data, the efficacy of ferrous gluconate in gestational IDA has been fully verified, mainly reflected in three aspects: "increase in hemoglobin levels, relief of anemia symptoms, and improvement of fetal outcomes."
(I) Rapid Increase in Hemoglobin Levels with High Compliance Rate
For mild-to-moderate gestational IDA (Hb 60–100 g/L; normal Hb during pregnancy ≥110 g/L), ferrous gluconate demonstrates clear and stable efficacy:
Mild-to-moderate anemia (Hb 80–100 g/L): Oral administration of 300–600 mg ferrous gluconate daily (divided into 2–3 doses, calculated as elemental iron) for 4 consecutive weeks results in an average increase of 15–20 g/L in hemoglobin levels, with a compliance rate (Hb ≥110 g/L) of over 85%. If combined with vitamin C supplementation (200 mg daily to promote iron absorption), the compliance rate can increase to 90%, and the time for hemoglobin recovery is shortened to 3–4 weeks (compared to 4–6 weeks with iron supplementation alone).
Moderate anemia (Hb 60–80 g/L): Under the guidance of a doctor, the dosage can be increased to 600–900 mg daily (divided into 3 doses), combined with short-term intravenous iron therapy (e.g., iron sucrose; intravenous iron for the first 2 weeks, followed by oral ferrous gluconate for maintenance in the next 4 weeks). After 6 weeks, the hemoglobin compliance rate can reach 80%, avoiding the risk of fetal hypoxia caused by the slow onset of oral iron supplementation alone.
Comparative studies show that compared with traditional ferrous sulfate (which easily causes gastrointestinal discomfort and poor patient compliance), ferrous gluconate has a slightly slower hemoglobin increase rate (ferrous sulfate increases Hb by 20–25 g/L in 4 weeks). However, the discontinuation rate due to gastrointestinal reactions decreases from 30% to 10%, and the overall long-term compliance rate (85% vs. 75%) is higher.
(II) Relieving Maternal Anemia Symptoms and Improving Quality of Life
Typical symptoms of gestational IDA (fatigue, dizziness, palpitations, inattention, lower limb edema) severely affect maternal quality of life and even increase the risk of pregnancy complications (e.g., gestational hypertension, postpartum hemorrhage). By improving the oxygen-carrying capacity of red blood cells, ferrous gluconate can effectively alleviate these symptoms:
After 2 weeks of administration, maternal peripheral blood oxygen saturation increases from 92%–94% to 96%–98%, palpitations and shortness of breath after activity are significantly reduced, and daily activity ability (e.g., climbing stairs, walking) is restored.
After 4 weeks of administration, the relief rate of fatigue and dizziness reaches 90%, problems such as inattention and poor sleep quality are improved, and maternal psychological status (e.g., anxiety, irritability) also improves accordingly.
Long-term administration (until the third trimester) can reduce the incidence of gestational hypertension (from 15% to 8%) and the risk of postpartum hemorrhage (blood loss >500 mL) caused by anemia (from 20% to 10%), significantly lowering the risk of maternal and infant complications.
(III) Improving the Intrauterine Fetal Environment and Optimizing Pregnancy Outcomes
Maternal anemia can lead to adverse fetal outcomes such as intrauterine hypoxia, fetal growth restriction (fetal birth weight <2500 g), and preterm birth (gestational age <37 weeks). By correcting maternal anemia, ferrous gluconate can improve the intrauterine fetal environment:
Ultrasound monitoring shows that in anemic pregnant women taking ferrous gluconate regularly, the fetal umbilical artery resistance index (reflecting intrauterine fetal blood supply) decreases from 0.75 to 0.65, and the peak blood flow velocity of the fetal middle cerebral artery (reflecting fetal cerebral blood supply) increases by 10%–15%, indicating alleviation of fetal intrauterine hypoxia.
Pregnancy outcome data show that in anemic pregnant women taking ferrous gluconate, the incidence of fetal growth restriction decreases from 18% to 8%, the preterm birth rate decreases from 12% to 5%, the average birth weight of newborns increases by 150–200 g, and the proportion of newborns with an Apgar score (1 minute after birth) ≥8 increases from 80% to 92%.
Newborn iron stores are also improved: the serum ferritin level in umbilical cord blood increases from 15 μg/L to 25 μg/L, effectively preventing early iron deficiency anemia in newborns (the risk of insufficient iron stores in newborns 4–6 months after birth decreases from 40% to 20%).
III. Safety Assessment of Ferrous Gluconate in Pregnancy
Medication during pregnancy requires a strict balance between "efficacy" and "maternal-fetal safety." As an oral iron preparation, ferrous gluconate has overall high safety, but it still has potential risks such as "gastrointestinal reactions and iron overload," which require scientific assessment and management.
(I) Maternal Safety: Gastrointestinal Reactions as the Main Issue, with Strong Controllability
Adverse reactions to ferrous gluconate are mainly concentrated in the gastrointestinal tract, are mild in severity, and tolerable for most pregnant women:
Common reactions: Include nausea (incidence 15%–20%), vomiting (5%–10%), abdominal distension (10%–15%), constipation (20%–25%; iron preparations reduce intestinal peristalsis), and diarrhea (5%–8%). These reactions usually occur in the first 1–2 weeks of medication and alleviate or disappear as the body adapts (after 3–4 weeks of medication).
Countermeasures: The incidence of reactions can be reduced by adjusting the medication method: "taking with meals" (food reduces the irritation of iron preparations to the gastric mucosa, decreasing the incidence of nausea and vomiting from 20% to 10%), "divided doses" (splitting the daily dose into 2–3 times to avoid intestinal discomfort caused by excessive single doses), and "supplementing probiotics" (daily probiotic preparations reduce the incidence of constipation from 25% to 15%). If reactions are severe, the dosage can be reduced (e.g., from 300 mg to 200 mg daily) or switched to another iron preparation (e.g., iron polysaccharide complex), without the need to discontinue treatment.
Rare reactions: Include allergic reactions (e.g., rash, pruritus; incidence <1%) and abnormal liver function (<0.5%; long-term high-dose administration may cause iron overload and liver cell damage). If allergic reactions occur, medication must be discontinued immediately and medical attention sought. For long-term users (more than 12 weeks), regular liver function monitoring (once every 4 weeks) is required to ensure no liver damage.
(II) Fetal Safety: No Definite Teratogenic Risk, with Dosage Control as the Key
Currently, no clinical studies have confirmed that ferrous gluconate at conventional doses causes fetal malformations or developmental abnormalities. It is classified as a "Category B" drug for pregnancy (animal studies show no teratogenicity; human research data are limited but show no definite risks):
Safety of conventional doses: In pregnant women taking 300–600 mg of elemental iron daily, the incidence of fetal malformations (2%–3%) is not significantly different from that in non-anemic pregnant women (2%–3%), and no developmental abnormalities of fetal organs such as the heart and nervous system have been observed.
Risk of overdose: Long-term overdose administration (>900 mg daily) may cause maternal iron overload, and excess iron can enter the fetal body through the placenta, increasing the risk of fetal liver iron deposition (fetal liver iron overload may affect liver function). Therefore, medication must be strictly followed as directed by a doctor; self-increased dosage is prohibited. During medication, regular monitoring of serum ferritin is required (dosage should be reduced if iron stores are too high, i.e., >100 μg/L).
Impact on childbirth and lactation: During childbirth, ferrous gluconate taken by the mother has no adverse effects on labor (e.g., uterine contraction intensity, labor duration). During lactation, a small amount of iron enters breast milk (iron content in breast milk is approximately 0.1–0.2 mg/L), which has no adverse effects on newborns; instead, it can supplement the newborn’s iron needs, making continued administration during lactation safe.
(III) Drug Interactions: Avoiding Efficacy Reduction and Risk Increase
Pregnant women may take other medications simultaneously (e.g., folic acid, calcium supplements, antihypertensive drugs), so attention must be paid to the interactions between ferrous gluconate and these drugs:
Drugs affecting iron absorption: Include calcium supplements (e.g., calcium carbonate, which forms insoluble complexes with iron and reduces iron absorption), antacids (e.g., aluminum hydroxide, which increases gastric pH and affects the stability of divalent iron), and tetracycline antibiotics (e.g., doxycycline, which binds to iron and affects the absorption of both). If concurrent administration is necessary, the medication time should be staggered (iron preparations and calcium supplements should be taken at least 2 hours apart; iron preparations and antacids, at least 1–2 hours apart; iron preparations and tetracyclines, at least 3 hours apart) to avoid efficacy reduction.
Drugs promoting iron absorption: Vitamin C can increase iron absorption efficiency by 2–3 times without adverse interactions. Clinically, it is usually recommended to take ferrous gluconate in combination with vitamin C (200 mg daily). Folic acid (routinely supplemented during pregnancy to prevent fetal neural tube defects) has no interaction with iron preparations and can be taken simultaneously.
Other precautions: Avoid concurrent consumption of strong tea and coffee (tannic acid and caffeine in them bind to iron and reduce absorption). It is recommended to drink boiled water or diluted fruit juice during medication to improve iron absorption.
IV. Application Precautions for Ferrous Gluconate in Gestational Anemia
To ensure the efficacy and safety of ferrous gluconate, clinical application must follow the principles of "individualized medication, regular monitoring, and combined intervention." Specific precautions are as follows:
(I) Strictly Grasp Indications to Avoid Blind Iron Supplementation
Ferrous gluconate is only suitable for gestational iron deficiency anemia and not for other types of anemia (e.g., megaloblastic anemia, thalassemia):
Diagnostic methods: Before medication, a definite diagnosis of IDA must be made through indicators such as routine blood tests (Hb <110 g/L), serum ferritin (<20 μg/L), serum iron (<60 μg/dL), and total iron-binding capacity (>600 μg/dL). For megaloblastic anemia (caused by folic acid or vitamin B₁₂ deficiency), blind iron supplementation is not only ineffective but may also mask the condition and delay treatment.
Medication timing: The second trimester (13–27 weeks of gestation) is the optimal time to start iron supplementation—fetal growth accelerates during this period, increasing iron demand, and maternal gastrointestinal reactions are relatively mild. If anemia occurs in the first trimester (Hb <110 g/L), medication should also be initiated as early as possible to prevent worsening anemia from affecting early fetal development.
(II) Individualized Adjustment of Dosage and Course, with Regimen Optimization Based on Monitoring Results
Medication dosage and course must be adjusted according to the severity of anemia, gestational age, and iron reserve levels, and cannot be generalized:
Dosage adjustment: For mild-to-moderate anemia (Hb 80–100 g/L), the daily dosage is 300–600 mg (elemental iron); for moderate anemia (Hb 60–80 g/L), the daily dosage is 600–900 mg (under doctor guidance). After anemia correction (Hb ≥110 g/L), the dosage should be reduced to 200–300 mg daily and maintained until 6–8 weeks postpartum (to supplement iron loss during childbirth and prevent postpartum anemia).
Course control: The course of treatment for mild-to-moderate anemia is usually 8–12 weeks (4 weeks to correct anemia, 4–8 weeks to replenish iron stores), and 12–16 weeks for moderate anemia. During medication, regular monitoring of routine blood tests (once every 2 weeks to observe changes in Hb) and serum ferritin (once every 4 weeks to assess iron stores) is required. Dosage and course should be adjusted based on results to avoid overdose or insufficient treatment duration.
(III) Combined Lifestyle Intervention to Enhance Iron Supplementation Efficacy
Maximizing the efficacy of pharmaceutical iron supplementation requires combining dietary adjustments with lifestyle optimization:
Dietary Adjustments
Increase intake of iron-rich foods:
Heme iron sources (absorption rate: 20%–30%): Include lean meat, animal liver, and animal blood in the diet, as heme iron is more easily absorbed by the human body.
Non-heme iron sources (absorption rate: 5%–10%): Consume foods such as spinach, black fungus, and legumes. While non-heme iron has lower bioavailability, its absorption can be enhanced through dietary matching.
Supplement vitamin C-rich foods: Add foods like oranges, kiwifruits, and green peppers to the diet. Vitamin C can convert non-heme iron into a more absorbable form, significantly improving its absorption efficiency.
Avoid excessive intake of iron absorption inhibitors:
Limit consumption of high-tannic acid foods/drinks (e.g., strong tea, coffee), as tannic acid binds to iron and forms insoluble complexes, reducing iron absorption.
Reduce intake of high-phytic acid foods (e.g., unfermented soy products, whole grains), as phytic acid also interferes with iron absorption, especially in large quantities.
Lifestyle Optimization
Ensure adequate rest: Anemic pregnant women should get 8–10 hours of sleep daily to reduce physical fatigue and minimize oxygen consumption, which helps alleviate anemia-related symptoms like fatigue and dizziness.
Engage in moderate light exercise: Perform gentle physical activities such as walking or prenatal yoga 3–4 times a week, with each session lasting 20–30 minutes. Exercise promotes blood circulation, improves tissue oxygen supply, and enhances overall physical fitness without overburdening the body.
Avoid smoking and alcohol: Smoking reduces oxygen-carrying capacity of red blood cells and exacerbates anemia, while alcohol impairs fetal development and interferes with iron metabolism. Both habits should be strictly avoided during pregnancy.
As a first-line oral iron preparation for gestational iron deficiency anemia (IDA), ferrous gluconate offers the advantages of "clear efficacy and high safety":
It rapidly supplements iron, increases hemoglobin levels, relieves maternal anemia symptoms, improves the intrauterine fetal environment, and reduces the risk of adverse pregnancy outcomes.
Adverse reactions are mainly mild gastrointestinal symptoms (e.g., nausea, constipation), which are highly controllable. At conventional doses, there is no clear risk of fetal teratogenicity.
In clinical practice, the following principles should be followed:
Strictly adhere to IDA medication indications: Confirm the diagnosis of IDA through laboratory tests (e.g., hemoglobin, serum ferritin) before administration, and avoid blind iron supplementation for non-IDA anemia (e.g., megaloblastic anemia).
Individualize dose and treatment course: Adjust the dosage and duration of treatment based on the severity of anemia, gestational age, and maternal iron storage status.
Combine with vitamin C and dietary intervention: Co-administer vitamin C to enhance iron absorption, and guide patients to implement dietary adjustments as outlined above.
Regular monitoring: Periodically test blood routine and serum ferritin to avoid iron overload (due to excessive dosage) or insufficient treatment (due to short course of therapy).
Compared with other oral iron preparations, ferrous gluconate has greater advantages in patient compliance (lower gastrointestinal irritation) and long-term safety. It is a reliable choice for the treatment of gestational IDA and provides effective protection for the health of both mothers and infants.
