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Hematology›Condition·Updated Jul 11, 2026·v1

Iron Deficiency Anemia

Iron deficiency anemia (IDA) is a microcytic hypochromic anemia caused by insufficient iron stores for erythropoiesis. It is the most prevalent anemia globally, affecting ~1/3 of the population, with highest burden in women and children. The hepcidin-ferroportin axis is central to pathophysiology: low iron stores suppress hepcidin to enhance absorption. IDA progresses through three stages (iron depletion, iron-deficient erythropoiesis, frank anemia). Diagnosis relies on low ferritin (≤30 ng/mL) and low TSAT (<16%). Management begins with oral ferrous sulfate (65 mg elemental iron daily). For intolerance, severe cases, or ongoing losses, IV iron - preferably ferric derisomaltose 1000 mg - is indicated. Transfusion is reserved for hemodynamic instability or Hb <7 g/dL. The key to long-term cure is identifying and treating the underlying cause: GI bleeding (requires bidirectional endoscopy for patients ≥45 years), heavy menstrual bleeding, malabsorption (celiac, autoimmune gastritis, bariatric surgery), or H. pylori infection. Genetic causes like IRIDA (TMPRSS6 mutation) should be considered in refractory pediatric cases. Prognosis is excellent when the driver is addressed.

High Evidence141 references·2,839 words·12 min read·v1
iron deficiency anemiamicrocytic anemiahepcidinhematologyiron therapyferritin

Quick Reference

RxDrug of choiceOral ferrous sulfate 325 mg (65 mg elemental iron) once daily; IV ferric derisomaltose 1000 mg single dose for intolerance/severity.
AltAlternatives[[Ferric carboxymaltose]] IV (monitor for hypophosphatemia), [[iron sucrose]] IV (multiple doses), [[liposomal iron]] for pediatric GI intolerance.
⊘AvoidIV iron in first trimester of pregnancy (relative); avoid [[rivaroxaban]] in women with heavy menstrual bleeding; do not transfuse asymptomatic stable children.
DxTest of choiceSerum ferritin; if ≤30 ng/mL, confirms IDA (97-99% specific). For equivocal cases, bone marrow Perls stain is gold standard.
ScKey scoreWHO grading of anemia severity by hemoglobin: mild 10-12 g/dL (F)/11-13 g/dL (M), moderate 7-10 g/dL, severe <7 g/dL.
→When to referRefractory to oral iron beyond 6 weeks; suspected IRIDA; unexplained IDA requiring bidirectional endoscopy; severe anemia with hemodynamic instability; need for bone marrow biopsy.
IDA is the most common anemia worldwide; treat with oral iron first, correct underlying cause (especially GI bleeding, H. pylori, celiac), and escalate to IV iron (preferably ferric derisomaltose) for intolerance, ongoing losses, or severe disease. Transfusion reserved for unstable or Hb <7 g/dL.
Iron deficiency anemia (IDA) is a microcytic hypochromic anemia resulting from insufficient iron stores for erythropoiesis. It is the most prevalent anemia worldwide, often signaling an underlying condition such as gastrointestinal blood loss, malabsorption, or increased demand. Prompt diagnosis and treatment of both the anemia and its cause are essential to prevent complications like heart failure and developmental impairment. This concise guide covers classification, pathophysiology, clinical presentation, diagnosis, management, and prevention.

Overview and Recommendations

Background

  • •Iron deficiency anemia (IDA) affects roughly 1 in 3 persons globally, with South Asia and sub-Saharan Africa bearing the highest burden; among women of reproductive age, prevalence reaches nearly 30%, and in children under 5 it remains the leading cause of anemia worldwide.
  • •The hepcidin-ferroportin axis governs iron homeostasis: the liver-derived hormone binds to on enterocytes and macrophages, internalizing it and blocking both dietary iron absorption and iron release from stores. In IDA, low iron stores suppress hepcidin, permitting maximal absorption - but when demands exceed supply (e.g., chronic blood loss, pregnancy, malabsorption), this homeostatic response fails, depleting stores and impairing erythropoiesis.
  • •IDA progresses through three sequential stages: (1) prelatent iron depletion - serum ferritin <30 ng/mL with normal hemoglobin; (2) latent iron-deficient erythropoiesis - transferrin saturation (TSAT) <16%, rising TIBC, still normal Hb; (3) frank IDA - microcytic hypochromic anemia with reduced Hb, MCV, and MCH. Ferritin is the earliest and most specific marker in the absence of inflammation.
  • •Underlying causes fall into three categories: chronic blood loss (GI bleeding from , , or heavy menstrual bleeding), malabsorption ( , , ), and increased demand (pregnancy, growth). In up to 71% of patients with IDA, pan-endoscopy reveals a potential bleeding lesion, most commonly in the small bowel.
  • •A genetic form, (IRIDA), results from biallelic mutations causing elevated hepcidin and poor response to oral iron; affected children present with severe microcytic anemia and require IV iron. Heterozygous variants also modify
    penetrance.

Evaluation

  • •Suspect IDA in any patient with unexplained fatigue, weakness, exercise intolerance, pallor, or less specific complaints like restless legs syndrome (RLS) or pica - craving for ice, clay, or bricks. Ask specifically about these symptoms, as they often go unreported.
  • •Explore the history for potential causes: heavy menstrual bleeding (ask about pad/tampon count, flooding), GI blood loss (melena, hematochezia, occult blood), dietary inadequacy (vegetarian/vegan, restrictive diets), prior , family history of anemia or thalassemia, and chronic medications (NSAIDs, anticoagulants, particularly which has a 2.7-fold increased risk of abnormal uterine bleeding).
  • •Examine for signs of anemia: conjunctival and palmar pallor, glossitis (smooth red tongue), angular cheilitis, koilonychias (spoon nails), and signs of underlying disease (abdominal masses, telangiectasias in , neurologic signs of B12 deficiency if autoimmune gastritis suspected).
  • •Order a with indices (looking for low MCV <80 fL, low MCH <27 pg), reticulocyte count, serum ferritin, transferrin saturation (TSAT), total iron-binding capacity (TIBC), and a (showing microcytic hypochromic red cells, pencil cells, and often reactive thrombocytosis).
  • •Diagnostic thresholds: a serum ferritin ≤30 ng/mL in the absence of inflammation is 97-99% specific for absent iron stores and confirms IDA. TSAT <16% indicates insufficient iron for erythropoiesis. In equivocal cases (ferritin 30-100 ng/mL, especially with inflammation), consider with Perls stain as the gold standard for iron stores, or measure hepcidin (low in simple IDA, high in IRIDA and ).
  • •Interpret the blood film: microcytes, hypochromia, pencil cells, and target cells. Reactive thrombocytosis (platelet count >450,000) is seen in up to one-third of cases and resolves with iron repletion - if thrombocytosis is extreme or persists, consider alternative diagnoses (myeloproliferative neoplasm). Basophilic stippling suggests thalassemia or lead poisoning.
  • •In children with unexplained microcytic anemia refractory to oral iron, suspect IRIDA: age <2 years, severe microcytosis, inappropriately normal/high hepcidin, and only partial response to IV iron. Order gene sequencing to confirm.
  • •Once IDA is confirmed, the evaluation must identify the underlying cause. For adults ≥45 years with new IDA (or younger with alarm symptoms), perform bidirectional endoscopy ( and ) to exclude GI malignancy - IDA carries an odds ratio of 3.56 for early-onset . If endoscopy is negative, test for (tTG IgA), (stool antigen or biopsy), and autoimmune gastritis (parietal cell antibodies, gastrin).
  • •Additional testing: if iron studies suggest (low TSAT but ferritin >100 ng/mL), measure or consider bone marrow. In young women with heavy menstrual bleeding and recurrent IDA, consider screening (VWF level, especially VWF p.Tyr1584Cys variant).

Management

  • •Initiate oral iron therapy for all patients with confirmed IDA without contraindications. First-line is providing 60-200 mg of elemental iron daily. Standard dose: 325 mg ferrous sulfate (65 mg elemental iron) once daily, preferably on an empty stomach or with vitamin C (orange juice) to enhance absorption. Daily dosing delivers the best total iron load, though alternate-day dosing (e.g., 65 mg every other day) may be used for patients with intolerance.
  • •Counsel patients to separate iron from calcium-rich foods, antacids, and calcium supplements by at least 2 hours. Common side effects include dark stools, constipation, and epigastric discomfort; these can be mitigated by starting at a low dose and gradually escalating, taking with food (though this reduces absorption by ~40%), or switching to a slower-release formulation.
  • •If oral iron is not tolerated or ineffective after 4-6 weeks (Hb rise <1 g/dL, persistent low ferritin), switch to intravenous iron. Preferred agent: (FDI) at a total dose of 1000 mg as a single 15-20 minute infusion, which repletes stores in one visit. (FCM) is an alternative (single dose up to 1000 mg over 15 minutes), but use with caution due to risk of hypophosphatemia and associated fracture risk; choose FDI when available.
  • •IV iron is also first-line for patients with severe ongoing blood loss (e.g., , dialysis-dependent CKD), malabsorption (celiac disease, post-bariatric surgery), moderate-to-severe IDA in late pregnancy (after first trimester), or when rapid correction is needed preoperatively.
  • •Dosing for IV iron: ferric derisomaltose 1000 mg as a single dose; ferric carboxymaltose 750-1000 mg single dose (depending on weight); iron sucrose 200 mg per dose, typically 3-5 doses administered on separate days. Always reconstitute and infuse according to manufacturer guidelines. Have resuscitation equipment available for rare hypersensitivity reactions.
  • •Reserve packed red blood cell transfusion for patients with: hemodynamic instability, active bleeding, symptomatic severe anemia (Hb <7 g/dL with cardiac ischemia, heart failure, or altered mental status), or inability to receive/completion of IV iron. Transfusion threshold: target Hb 7-8 g/dL in most patients; individualize for acute coronary syndrome (symptom-guided). Avoid transfusing asymptomatic children with IDA (ASH-ASPHO Choosing Wisely).
  • •Address the underlying cause aggressively: if infection is identified (prevalence >50% in refractory IDA), eradicate with standard triple therapy (PPI + amoxicillin + clarithromycin or metronidazole for 14 days); this permanently resolves IDA in 64-75% of infected patients. If is found, initiate strict gluten-free diet and monitor iron status. For (20-27% of unexplained IDA), monitor for B12 deficiency (serum B12, methylmalonic acid) and consider periodic gastroscopy for dysplasia surveillance.
  • •For heavy menstrual bleeding (HMB) as the cause, manage gynecologically: consider hormonal therapy (combined oral contraceptive, levonorgestrel IUD), tranexamic acid, or endometrial ablation. In women on who develop IDA from HMB, switch to , , or a vitamin K antagonist to reduce bleeding risk.
  • •In patients with (HHT) and recurrent IDA from epistaxis/GI bleeding, consider systemic therapy: 4 mg daily (reduces Epistaxis Severity Score by 0.94 points vs placebo) or antifibrinolytics. Percutaneous left atrial appendage closure (LAAC) should be considered over anticoagulation if HHT patients need stroke prevention.
  • •Monitor response: recheck hemoglobin and reticulocyte count at 2-4 weeks after starting oral iron; a rise in Hb ≥1 g/dL by 4 weeks indicates adequate response. Ferritin is not reliable during the first 4 weeks as it may transiently increase; recheck 8-12 weeks after therapy initiation. Continue oral iron for at least 3 months after Hb normalizes to replenish stores (target ferritin >50 μg/L).
  • •For patients on IV iron, a single dose typically raises Hb by 1-2 g/dL within 2-4 weeks. Recheck Hb and ferritin at 4-8 weeks post-infusion. If inadequate response, consider: ongoing blood loss, an incorrect diagnosis (e.g., thalassemia trait, anemia of chronic disease), IRIDA, or need for additional IV doses.
  • •What NOT to do: do not prescribe platelet transfusion for reactive thrombocytosis in IDA - it resolves with iron repletion. Do not use cytoreductive agents (hydroxyurea, anagrelide) for reactive thrombocytosis. Do not transfuse packed RBCs for asymptomatic IDA in children. Do not administer IV iron in early pregnancy (first trimester). Do not combine oral and IV iron concurrently.
  • •When to refer: to for bidirectional endoscopy if IDA is unexplained and patient ≥45 years or younger with alarm symptoms. To if: refractory to oral iron or IV iron not tolerated, suspected IRIDA or inherited anemia, need for bone marrow biopsy, or unexplained persistent thrombocytosis. To if heavy menstrual bleeding is the cause and hormonal/device management is needed. To follow-up clinic for post-surgical patients.
  • •Discharge criteria for hospitalized patients: hemoglobin stable or rising >7 g/dL, no active bleeding, hemodynamic stability, plan for iron repletion (oral or IV continuation) and follow-up arranged for underlying cause evaluation. Ensure patient understands need for medication adherence and return if symptoms recur.

Board Review — High Yield

  • •Ferritin, earliest and most specific marker of iron stores; value ≤30 ng/mL confirms IDA in absence of inflammation.
  • •TSAT <16%, hallmark of iron-deficient erythropoiesis; combined with low ferritin establishes the diagnosis.
  • •TMPRSS6 mutation, causes iron-refractory IDA (IRIDA) with inappropriately high hepcidin; unresponsive to oral iron, partial response to IV.
  • •Pica, craving for non-nutritive substances (ice, clay, bricks); classic symptom of IDA.
  • •Restless legs syndrome (RLS), common association with IDA; resolves with iron repletion.
  • •Hepcidin, central regulator; low in simple IDA, elevated in IRIDA and anemia of chronic disease (ACD).
  • •71% of IDA patients have a potential bleeding lesion on pan-endoscopy; IDA is a red flag for GI malignancy.
  • •Reactive thrombocytosis, occurs in ~30% of IDA due to altered MEP lineage commitment; resolves with iron therapy.
  • •H. pylori eradication, cures IDA in 64-75% of infected patients even without additional iron; test in refractory cases.
  • •Ferric derisomaltose preferred over ferric carboxymaltose, FCM causes hypophosphatemia and increased fracture risk (validated in large database).

Deep Dive — Evidence Details

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