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Anemia in women

Anaemia ferripriva

Iron-deficiency anemia (IDA) is a pathological condition in which hemoglobin levels drop due to an absolute iron deficiency in the body. Women of reproductive age constitute one of the primary risk groups for this pathology due to a constant imbalance between the demand for this micronutrient and its actual availability.

HemoglobinThe normal range for women is 120–140 g/L.
FerritinThe target level to confirm a cure is strictly >40–60 ng/mL.
Latent deficiencyIron deficiency manifests as overt anemia in only 30% of cases.
WHO dosage120 mg/day of elemental iron for treatment, 60 mg/day for prophylaxis.
4 min readFor medical studentsUpdated 10.10.2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesPending instructor review

Pathogenesis and the hidden threat of iron deficiency

The development of iron-deficiency anemia is based on a simple yet dangerous imbalance: the body spends or loses more of the micronutrient than it receives and absorbs. In women of reproductive age, this is frequently associated with menstrual blood loss or pathological bleeding (e.g., uterine fibroids).

A crucial epidemiological detail: in the overwhelming majority of cases (about 70%), the deficiency is occult. This condition is termed latent iron deficiency. Blood hemoglobin levels remain within the normal range (120–140 g/L), but tissue stores (depots) are already critically depleted. Such a deficiency can be diagnosed only by a decrease in serum ferritin levels. The goal of treatment at the latent deficiency stage is to raise ferritin to over 40–60 ng/mL and achieve complete regression of sideropenic syndrome symptoms.

Fundamental treatment principles

IDA is a condition that is 100% curable if therapy is selected correctly. The primary rule is the elimination of the source of blood loss or the cause of the deficiency. Without eliminating the root cause (surgical treatment of fibroids with menorrhagia, treatment of peptic ulcer disease), any iron supplementation will yield only a short-term effect.

The mainstay of medical treatment is oral iron therapy:

  • Drug selection: Preference is given to ferric (Fe3+) iron preparations because they are tolerated much better than ferrous (Fe2+) ones. Ascorbic, citric, or succinic acid is often added to improve absorption.
  • Administration regimen: The modern approach allows for low doses in short courses (two weeks per month) or an alternate-day regimen. This provides excellent clinical efficacy with minimal side effects compared to the classic administration of high doses several times a day.
  • Combination therapy: Since anemias are frequently of a mixed nature, folic acid preparations are often included in the regimen to compensate for concomitant folate deficiency.

It is important to remember that the normalization of hemoglobin is not yet a cure. True recovery occurs only when tissue iron stores are replenished, which is confirmed by the normalization of ferritin.

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Pregnancy and the postpartum period

The management of pregnant women requires special caution. Routine prescription of iron supplements "just in case" when hemoglobin is normal is not recommended, as there is no proven benefit for the mother or fetus. However, prophylaxis (60 mg/day) is indicated for risk groups (e.g., vegans). According to WHO guidelines, it is advisable to prescribe iron prophylactically in the 2nd and 3rd trimesters and the first six months of lactation.

If moderate or severe anemia is detected in a pregnant woman during the 2nd or 3rd trimester and oral forms are ineffective or not tolerated, parenteral (intravenous) ferric iron preparations are prescribed. The dose is calculated strictly on an individual basis depending on body weight and total deficit.

For postpartum anemia (mild to moderate with stable hemodynamics), oral preparations of Fe2+ or Fe3+ are prescribed at a dose of 40–100 mg/day. The course of treatment should be at least three months.

Treatment efficacy assessment and refractoriness

The body's response to correctly selected oral therapy unfolds according to a clear schedule:

  1. Day 2–3: Ret-He levels rise (activation of erythropoiesis).
  2. Day 7–10: Reticulocyte crisis — the reticulocyte count increases by 2–3% from baseline.
  3. By the end of week 4: Hemoglobin increases by at least 10 g/L, and hematocrit by 3%.
  4. In 1–1.5 months: Clinical manifestations disappear.
  5. In 3–6 months: Serum ferritin normalizes (>30 ng/mL), and stores are fully replenished.

If there is no response to treatment, it most often indicates an inadequate regimen or an erroneous diagnosis. In rare cases, the physician must rule out IRIDA (iron-refractory iron deficiency anemia), a hereditary autosomal recessive anemia unresponsive to standard iron therapy.

Class and exam questions

Can iron-deficiency anemia be cured through diet alone?

No, dietary therapy is purely supportive. Although meat is the best source of heme iron with maximum bioavailability, eliminating an already developed deficiency requires pharmacological doses (about 120 mg/day) that cannot be obtained from food alone.

Why continue taking pills if hemoglobin has already reached 130 g/L?

The normalization of hemoglobin does not mean a complete cure. It is necessary to continue taking medications (usually up to 3–6 months) to replenish tissue iron stores (depots), targeting the achievement of the target ferritin level.

In which cases is iron administered intravenously?

Parenteral therapy is indicated for malabsorption syndrome, severe and moderate anemia (including in the 2nd and 3rd trimesters of pregnancy), as well as in cases of tablet intolerance or ineffectiveness. Only modern ferric iron preparations are used.

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What else to study on this topic

  • Specifics of intravenous iron administration and prevention of anaphylactoid reactions
  • Prevention and treatment of IDA in patients after bariatric surgery
  • Management tactics for anemia in malignancies
  • The role of folic acid in the treatment of mixed anemias
  • Late anemia of prematurity (constitutional) as a specific variant of IDA

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