Iron Deficiency Anaemia — Symptoms, Causes & Treatment | MyMedicPlus

Iron deficiency anaemia (IDA) is the most common form of anaemia and the most prevalent nutritional deficiency worldwide, affecting approximately 30% of the global population. It occurs when iron stores are depleted, reducing haemoglobin synthesis and resulting in hypochromic (pale), microcytic (small) red blood cells with impaired oxygen-carrying capacity. IDA is characterized by serum ferritin below 30 µg/L (the most sensitive marker of iron depletion), low serum iron, elevated TIBC (total iron-binding capacity), and haemoglobin below 130 g/L in men and below 120 g/L in women. Iron deficiency anaemia (IDA) is the most prevalent nutritional deficiency and the most common cause of anaemia globally — affecting approximately 1.2 billion people, predominantly women of reproductive age, children under 5, and pregnant women in low-and-middle-income countries. The WHO defines anaemia as haemoglobin below 130 g/L in men (below 120 g/L in non-pregnant women; below 110 g/L in pregnant women), with IDA specifically characterised by microcytic hypochromic red blood cells and depleted iron stores (ferritin below 30 mcg/L). IDA develops through three progressive stages: iron depletion (reduced stores — low ferritin, normal haemoglobin), iron-deficient erythropoiesis (impaired red blood cell production — low serum iron, elevated TIBC, transferrin saturation below 16%), and frank IDA (low haemoglobin with microcytic, hypochromic red blood cells). All stages cause symptoms and impair function — treatment of iron depletion before anaemia develops improves outcomes.

Blood loss is the most common cause in adults: gastrointestinal blood loss (peptic ulcer, colorectal cancer, IBD, coeliac disease, hookworm — must be investigated in all adult males and post-menopausal women with IDA), heavy menstrual bleeding (most common cause in pre-menopausal women), urinary tract blood loss, and regular blood donation. Inadequate dietary intake: vegetarian and vegan diets (plant-based non-haem iron is poorly absorbed), infants fed cow's milk (low iron content), and malnourished elderly. Malabsorption: coeliac disease (most important), Crohn's disease affecting the duodenum, post-gastrectomy, and PPI use. Increased demand: pregnancy, infancy, and adolescence. The most common causes by mechanism: Blood loss is the leading cause in adults — menstrual blood loss (normal cycle: 30-40 mL/cycle; menorrhagia defined as above 80 mL/cycle causes negative iron balance, particularly in women with ferritin below 12 mcg/L), gastrointestinal blood loss from peptic ulcer disease (Helicobacter pylori infection causes up to 30% of iron deficiency — H. pylori eradication alone improves iron status), colorectal cancer (iron deficiency anaemia in a man or postmenopausal woman requires colonoscopy to exclude colorectal cancer until proven otherwise — colorectal cancer presents with IDA in 50% of cases), angiodysplasia (vascular malformations in elderly patients causing occult GI bleeding), and coeliac disease (25% of all IDA in adults — villous atrophy in the proximal small bowel impairs iron absorption from duodenum and jejunum). Malabsorption causes: gastric bypass surgery (reduces gastric acid and bypasses proximal small bowel — the primary site of iron absorption), atrophic gastritis (achlorhydria — gastric acid is required to reduce dietary ferric iron to ferrous form for absorption), and Crohn's disease (proximal small bowel involvement).

Anaemia symptoms reflect reduced oxygen delivery: fatigue, reduced exercise tolerance, breathlessness on exertion, palpitations, pallor (conjunctival, palmar), headache, and dizziness. Iron deficiency symptoms (can precede overt anaemia): hair loss, brittle nails, restless legs syndrome, impaired cognitive function, pica (craving for ice, clay, or non-food substances), and angular stomatitis (cracked corners of the mouth). Koilonychia (spoon-shaped nails) is a specific but late sign of IDA. Post-cricoid web formation (Plummer-Vinson syndrome) causes dysphagia in severe chronic IDA. In severe anaemia (haemoglobin below 70 g/L), high-output cardiac failure and angina may develop. The severity and spectrum of symptoms correlate with both the degree and rate of anaemia development — gradual anaemia allows compensatory mechanisms to develop (increased cardiac output, increased 2,3-DPG — right shift of oxyhaemoglobin dissociation curve) meaning significant anaemia may cause surprisingly few symptoms. Specific symptoms of iron deficiency (may precede anaemia): pica — the compulsive craving for non-food substances (most commonly pagophagia — ice craving, reported in up to 50% of women with IDA; also geophagi — dirt; amylophagia — starch); restless leg syndrome — unpleasant leg sensations at rest improving with movement, disrupting sleep (responds to IV iron even when haemoglobin is normal); koilonychia (spoon-shaped concave nail plates); angular cheilitis and glossitis. Symptoms of anaemia: pallor (scleral, palmar, and conjunctival pallor when haemoglobin below 90 g/L), progressive exertional dyspnoea, palpitations, headache, dizziness, tinnitus, and reduced exercise tolerance.

Full blood count: low haemoglobin, microcytic (MCV below 80 fL) hypochromic (MCH below 27 pg) red blood cells, elevated RDW (red cell distribution width). Serum ferritin below 30 µg/L confirms iron deficiency (note: ferritin is an acute phase reactant and may be falsely elevated in inflammation). Serum iron: low; TIBC: elevated; transferrin saturation: below 20%. Reticulocyte count rises early in response to treatment. Investigating the cause: colonoscopy and upper GI endoscopy in males and post-menopausal women; faecal occult blood testing; coeliac serology (anti-TTG antibodies); menstrual history. Interpreting ferritin in the context of inflammation: ferritin is an acute-phase reactant — elevated CRP (above 10 mg/L) raises ferritin independently of iron stores. In chronic inflammatory conditions (rheumatoid arthritis, IBD, CKD, cancer), ferritin may be within the normal reference range despite true iron deficiency — 'functional iron deficiency'. In this context, ferritin below 100 mcg/L combined with transferrin saturation below 20% and elevated CRP diagnoses functional iron deficiency requiring IV iron therapy. Reticulocyte haemoglobin content (CHr or RetHe) — the haemoglobin content of newly released reticulocytes — is a sensitive early marker of functional iron deficiency; below 29 pg indicates iron-limited erythropoiesis even before MCV falls. Obligatory investigation for cause: in all men and postmenopausal women with IDA, upper GI endoscopy (OGD — oesophagus, stomach, duodenum) and lower GI endoscopy (colonoscopy) are mandatory to exclude gastrointestinal malignancy, peptic ulcer, and coeliac disease (duodenal biopsy taken during OGD). Coeliac antibodies (IgA anti-tissue transglutaminase + total IgA for IgA deficiency control) should be checked in all cases.

Identify and treat the underlying cause — this is as important as replacing iron stores. Oral iron supplementation: ferrous sulfate 200 mg (65 mg elemental iron) once or twice daily — the most cost-effective first-line treatment. Take on an empty stomach or with vitamin C to maximize absorption. Common side effects include GI upset, nausea, constipation, and dark stools; alternate-day dosing may improve tolerance with similar efficacy. Continue oral iron for 3 months after haemoglobin normalization to replenish stores. IV iron (ferric carboxymaltose, iron sucrose, iron isomaltoside) is preferred when oral iron is not tolerated, absorbed, or fast enough (active bleeding, pre-surgery, pregnancy, IBD, or chronic kidney disease). Optimising oral iron absorption: ferrous (Fe2+) preparations are better absorbed than ferric (Fe3+) preparations — ferrous sulfate, ferrous fumarate, and ferrous gluconate are equivalent in efficacy when corrected for elemental iron content. Enteric-coated preparations reduce GI side effects but also reduce absorption by 40-70% — not recommended unless standard preparations are truly intolerable. Ascorbic acid (vitamin C 250 mg taken simultaneously) reduces ferric iron to ferrous form, increasing absorption by 30-50%. Avoid concurrent tea, coffee, milk, antacids, calcium supplements, and proton pump inhibitors — all significantly reduce iron absorption. Alternate-day dosing (every other day) — supported by emerging evidence including RCTs — may achieve equivalent iron repletion to daily dosing by avoiding hepcidin upregulation; hepcidin (hepatic iron regulatory hormone) is induced by iron absorption and inhibits further absorption for approximately 24 hours, meaning twice-daily dosing and daily dosing may be less efficient than alternate-day dosing. IV iron is preferred over oral in: inflammatory bowel disease (oral iron worsens gut inflammation and is poorly absorbed), post-bariatric surgery, CKD on erythropoietin stimulating agents (IV iron dramatically improves response — reduces ESA dose requirement by 30-50%), and perioperative setting when oral iron cannot be given.

Untreated severe anaemia causes high-output cardiac failure from compensatory increases in heart rate and cardiac output. In pregnancy, IDA increases risk of preterm birth, low birth weight, postpartum hemorrhage, and impaired neonatal neurodevelopment. In children, IDA causes impaired cognitive development, reduced school performance, and behavioral problems that may be irreversible if prolonged. The underlying cause of IDA may itself carry serious consequences: undiagnosed colorectal cancer (the most dangerous missed diagnosis), untreated coeliac disease causing long-term complications, or severe menorrhagia impairing quality of life.

Dietary optimization: consume haem iron (meat, poultry, fish) which is absorbed 2–3 times more efficiently than non-haem iron (legumes, tofu, fortified cereals, dark leafy greens). Consume non-haem iron alongside vitamin C (citrus, peppers, tomatoes) to enhance absorption. Avoid consuming iron with calcium-rich foods, tea, coffee, or high-phytate foods (bran) — these inhibit absorption. Universal iron fortification of staple foods (flour, salt) is an effective public health strategy in high-prevalence regions. Supplementation in pregnancy (400 mcg folic acid plus 30–60 mg elemental iron daily) prevents IDA and neural tube defects. Women with heavy periods should discuss investigation and treatment options.

Seek emergency care immediately for: severe shortness of breath at rest, chest pain, or palpitations with haemoglobin below 70 g/L (severe anaemia causing high-output cardiac failure) — may require emergency blood transfusion. See your GP within 1–2 weeks if: you are a man of any age with iron deficiency anaemia (cause must be investigated — exclude GI malignancy urgently); you are a post-menopausal woman with IDA (same rule — colonoscopy and upper GI endoscopy required); you have dark or tarry stools, blood in stools, or unexplained weight loss alongside IDA (urgent 2-week-wait cancer pathway referral). See your GP within 4 weeks for: fatigue and breathlessness on exertion with pallor; hair loss, brittle nails, or restless legs that may reflect iron deficiency without overt anaemia (check serum ferritin — treat if below 30 µg/L). If haemoglobin fails to rise after 4 weeks of oral iron, see your GP — the cause may be malabsorption (check coeliac serology), ongoing blood loss, or the need for IV iron infusion. In pregnancy, all women should have haemoglobin checked at booking and 28 weeks — IDA in pregnancy requires prompt treatment to protect fetal neurodevelopment and reduce delivery complications.