Iron Deficiency Anaemia — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Iron deficiency anaemia (IDA) occurs when inadequate body iron stores fail to support normal haemoglobin synthesis, leading to hypochromic microcytic anaemia. It is the most common nutritional deficiency and the most prevalent cause of anaemia worldwide, affecting approximately 1.2 billion people. Iron is essential for haemoglobin production, oxygen transport, mitochondrial function, and DNA synthesis. The body contains approximately 3-4 g of total iron: 60-70% incorporated in haemoglobin, 25% stored as ferritin or haemosiderin, and the remainder in myoglobin and enzymes. IDA can arise from inadequate intake, poor absorption, increased requirements (pregnancy, growth), or chronic blood loss — the most important cause in adult males and postmenopausal women being gastrointestinal bleeding, which requires investigation to exclude colorectal cancer. The global prevalence of IDA disproportionately affects women of reproductive age, pregnant women, infants, and young children, particularly in low- and middle-income countries where dietary iron intake is insufficient and infectious diseases causing occult blood loss remain endemic and undertreated.

Chronic blood loss is the most common cause in adults: gastrointestinal bleeding (peptic ulcers, colorectal cancer, angiodysplasia, coeliac disease, inflammatory bowel disease, chronic NSAID use), menorrhagia (heavy menstrual bleeding — most common cause in premenopausal women), haematuria (bladder cancer, kidney cancer), and frequent blood donation. Inadequate dietary intake: vegetarian and vegan diets (plant-based non-haem iron is less bioavailable than haem iron from meat), poverty, malnutrition. Malabsorption: coeliac disease (damages duodenal mucosa where iron absorption occurs), Helicobacter pylori gastritis, post-gastrectomy, and inflammatory bowel disease affecting the duodenum. Increased requirements: pregnancy (iron demand increases by 1,000 mg over the third trimester), infancy and adolescence (rapid growth). Risk factors include frequent pregnancy, heavy periods, vegetarianism, and chronic NSAID use.

Symptoms result from reduced oxygen delivery and impaired cellular iron-dependent enzyme function. Classic symptoms: fatigue, reduced exercise tolerance, pallor (conjunctival, palmar, and nail bed pallor), breathlessness on exertion, palpitations, dizziness, and headache. Iron deficiency-specific symptoms (even before frank anaemia): pica (unusual cravings for non-food substances such as ice, clay, or chalk — particularly pagophagia/ice eating), restless legs syndrome, hair loss, brittle nails, smooth tongue (atrophic glossitis), and mouth ulcers. Koilonychia (spoon-shaped nails) is a classical but rare finding in severe chronic IDA. Plummer-Vinson syndrome (iron deficiency, dysphagia from oesophageal web, and atrophic glossitis) is a rare but important complication associated with increased hypopharyngeal cancer risk. In children: developmental delay, poor school performance, and behavioural difficulties.

Full blood count (FBC): microcytic (MCV below 80 fL) hypochromic (MCHC below 315 g/L) anaemia with low haemoglobin (below 130 g/L in men, below 120 g/L in non-pregnant women, below 110 g/L in pregnancy). Serum ferritin below 30 mcg/L is diagnostic of IDA (ferritin is an acute phase reactant — in inflammation, ferritin may be falsely elevated even with iron deficiency; a level below 100 mcg/L with elevated CRP still indicates relative iron deficiency). Additional iron studies: low serum iron, low transferrin saturation (below 20%), elevated total iron binding capacity (TIBC). Blood film: microcytes, hypochromia, anisocytosis, pencil cells, target cells. Identify and investigate the underlying cause: coeliac disease antibodies (anti-TTG IgA), faecal immunochemical test (FIT) for GI bleeding, urine dipstick, endoscopy in adults over 50 with new-onset IDA.

Oral iron is first-line: ferrous sulphate 200 mg (65 mg elemental iron) twice or three times daily on an empty stomach for optimal absorption — take with vitamin C to enhance non-haem iron absorption; separate from tea, coffee, calcium, and antacids by 2 hours. Side effects (constipation, nausea, black stools) reduce adherence — alternative preparations include ferrous gluconate and ferrous fumarate. Alternate-day dosing (rather than daily) has been shown to achieve equivalent or better absorption by minimising hepcidin upregulation. Expect haemoglobin to rise by approximately 20 g/L per week with treatment; continue for 3 months after haemoglobin normalises to replenish stores. Intravenous iron (ferric carboxymaltose, iron sucrose) is indicated when oral iron is not tolerated, malabsorption is present, severe anaemia requires rapid correction, or in pregnancy. Treat the underlying cause — simply replacing iron without addressing the source is inadequate.

Untreated iron deficiency anaemia causes progressive deterioration across multiple body systems. Severe IDA (Hb below 70 g/L) leads to high-output cardiac failure — the heart increases cardiac output to compensate for impaired oxygen delivery, resulting in left ventricular dilatation, cardiomegaly, and decompensated heart failure. In children, iron deficiency — even at subclinical levels before frank anaemia — causes irreversible neurodevelopmental damage: impaired cognitive development, reduced IQ, poor school performance, behavioural difficulties, and motor delay. In pregnancy, severe IDA significantly increases risk of preterm birth, low birth weight, perinatal and maternal mortality, and impaired foetal brain development. Plummer-Vinson syndrome — occurring in a minority of severe chronic IDA cases — causes oesophageal web formation and dysphagia, with significantly increased risk of hypopharyngeal squamous cell carcinoma requiring endoscopic dilatation. Chronic IDA impairs immune function, increases susceptibility to infections, and reduces physical work capacity. Missing the underlying cause of IDA (particularly colorectal cancer in adults over 50) results in delayed cancer diagnosis and worse oncological outcomes.

Dietary iron optimisation: include haem iron sources (red meat, poultry, fish) and non-haem sources (legumes, dark leafy vegetables, fortified cereals, nuts, seeds). Pair non-haem iron foods with vitamin C (citrus, tomatoes, peppers) to triple absorption. Avoid simultaneous tea, coffee, dairy, or antacid consumption — they inhibit iron absorption. Routine iron supplementation is recommended in pregnancy (from 12 weeks in the UK), infancy, and menstruating adolescents in high-prevalence regions. Iron fortification of wheat flour, salt, and rice is a public health strategy reducing IDA in developing countries. Treat heavy menstrual bleeding with hormonal contraception or tranexamic acid. Early endoscopic investigation of iron deficiency in adults over 50 enables early detection of gastrointestinal malignancy — do not dismiss IDA as diet-related without appropriate investigation.

See a doctor promptly if you notice pallor, extreme fatigue, shortness of breath, or palpitations — these require a blood test to check for anaemia. Urgently seek care for chest pain, severe breathlessness, or haemodynamic instability caused by acute blood loss. Investigate new-onset iron deficiency anaemia in any adult over 50 for gastrointestinal malignancy with faecal immunochemical testing and colonoscopy — this is a red flag requiring same-week investigation. In men and postmenopausal women, iron deficiency anaemia has no benign dietary explanation — a structural gastrointestinal source must be excluded. Refer children with iron deficiency for developmental assessment. Women with heavy menstrual bleeding causing anaemia should be referred to gynaecology for management.