Iron Deficiency Anaemia
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Direct answer
Roughly half of Indian women of reproductive age and two-thirds of under-five children are anaemic — NFHS-5 figures — and iron deficiency drives the largest share of that burden. Iron deficiency anaemia is a microcytic hypochromic anaemia in which stores fall to nothing: serum ferritin is the single best marker, transferrin and total iron-binding capacity rise, transferrin saturation drops below 16 per cent, and the marrow shows absent stainable iron. Causes divide into intake too low (dietary, pregnancy, adolescence) and loss too great (menstrual blood loss, hookworm in the tropics, gastrointestinal bleeding). The film shows microcytes, pencil cells, anisopoikilocytosis and a high RDW; koilonychia and pica are the bedside giveaways; Plummer-Vinson syndrome adds a post-cricoid web and raises squamous carcinoma risk.
What you must remember
- Iron kinetics: about 1-2 mg absorbed daily against 1-2 mg lost; absorption via DMT1 at duodenal enterocytes, regulated by hepcidin — inflammation raises hepcidin, blocking iron export through ferroportin, which is why anaemia of chronic disease coexists with high ferritin.
- Diagnostic ladder: low ferritin is specific for iron deficiency; low transferrin saturation with high TIBC and low serum iron completes the pattern; soluble transferrin receptor is raised (helps when ferritin is confounded by inflammation).
- Film and marrow: MCV under 80 fL, MCH low, RDW high (unlike thalassaemia trait, where RDW is often normal); microcytes, pencil cells, target cells; marrow iron stores absent on Perls stain with ring sideroblasts absent.
- Differential of microcytosis: iron deficiency, thalassaemia trait (MENTER index above 13 favours thalassaemia; HbA2 raised in beta trait), anaemia of chronic disease (ferritin normal or high), sideroblastic anaemia (ferritin high, ring sideroblasts).
- Causes in the Indian setting: hookworm (Necator, Ancylostoma) causing chronic gastrointestinal blood loss, heavy menstrual bleeding, repeated pregnancies, vegetarian diets low in haem iron, and co-existing folate or B12 deficiency producing dimorphic anaemia.
- Plummer-Vinson syndrome: iron deficiency plus dysphagia from a post-cricoid web, koilonychia and glossitis; lifelong squamous carcinoma surveillance is advised.
- Programme payload: Anaemia Mukt Bharat provides weekly iron-folic acid to adolescents (100 mg elemental iron) and daily IFA for 100 days in pregnancy, with deworming — asked in preventive-social medicine and pathology alike.
- Treatment arithmetic: oral iron yields reticulocytosis in 7-10 days and haemoglobin rise of about 2 g/dL in 3 weeks; therapy continues 3 months after haemoglobin normalises to refill stores.
Confirming iron deficiency in an Indian clinic
A 26-year-old vegetarian in her third pregnancy presents with fatigue, pallor and craving for ice. Send haemoglobin, indices, ferritin, TIBC and a peripheral film. If ferritin is low the diagnosis is made — below about 15 micrograms per litre in a non-pregnant adult it is essentially diagnostic. If ferritin is normal or high despite clinical deficiency — recent delivery, infection, tuberculosis — remember it is an acute-phase reactant: check transferrin saturation or soluble transferrin receptor, or go to a marrow Perls stain, the gold standard. Then find the cause: menstrual history, stool examination for hookworm ova, and if she is a man or a postmenopausal woman, endoscopy is mandatory because iron deficiency in those groups is gastrointestinal malignancy until excluded. Treat the cause alongside the iron — deworming without iron repletion, or iron without controlling menorrhagia, both fail. Children with pica (pagophagia, ice-craving) typically lose it within days of starting iron.
Where candidates slip
The ferritin trap heads the list: a normal or raised ferritin does not exclude iron deficiency in infection, inflammation or liver disease, and combining ferritin with transferrin saturation or CRP is the practical answer. Second slip — iron deficiency versus beta thalassaemia trait on indices alone: both are microcytic, but RDW is high in iron deficiency and usually normal in trait, the Mentzer index (MCV/red cell count above 13) favours trait, and confirmation is HbA2 electrophoresis. Third, dimorphic anaemia — microcytes mixed with macrocytes in a pregnant Indian woman — is missed when only one deficiency is treated; macrocytes emerging on iron therapy get mislabelled as a complication. Finally, parenteral iron (ferric carboxymaltose) is for intolerance, malabsorption, ongoing losses or late pregnancy with time constraints — not a routine shortcut.
Frequently asked questions
Why is ferritin the best single marker of iron deficiency?
Serum ferritin reflects storage iron and falls early; a value below about 15 micrograms per litre is essentially diagnostic, though it must be interpreted with CRP because it rises as an acute-phase reactant.
How do iron deficiency and beta thalassaemia trait differ on a blood film?
Iron deficiency shows high RDW with anisopoikilocytosis and pencil cells, while thalassaemia trait shows more uniform microcytosis with normal RDW and raised HbA2 on electrophoresis.
Which parasitic infection classically causes iron deficiency anaemia in India?
Hookworm infection with Ancylostoma duodenale or Necator americanus, causing chronic occult gastrointestinal blood loss of several millilitres daily, treatable alongside iron with albendazole.
What is Plummer-Vinson syndrome?
The triad of iron deficiency anaemia, dysphagia due to a post-cricoid oesophageal web, and koilonychia, carrying a long-term risk of post-cricoid squamous carcinoma.
How long should oral iron be continued after haemoglobin normalises?
For about three additional months, to replenish depot stores — stopping at correction of haemoglobin leaves ferritin low and guarantees relapse.