๐Ÿฉธ
Microcytosis — Assessment & ManagementIron deficiency 2WW GI investigation · Mentzer index thalassaemia · Hb electrophoresis · IV iron Ferinject · ACD iron studies · coeliac anti-tTG · bidirectional endoscopy BSG
Progress0 / 9
The full reasoning pathway โ€” ferritin is the pivot: low = iron deficiency (find the source); normal/high with low MCV = think thalassaemia trait or chronic disease. Classify, refer (NG12), counsel, and safety-net.StartDecisionInvestigateActionReferStop / Admit
PresentationLow MCV (<80 fL)
Check ferritin and review the full blood count, indices and any family/ethnic origin.
Step 3 ยท Decision ยท FerritinIs ferritin low?
Low ferritin confirms iron deficiency. Normal/high ferritin with a disproportionately low MCV points elsewhere.
Low ferritin
Iron deficiency
Find the source โ€” see the iron-deficiency pathway. Coeliac serology; GI work-up.
Normal ferritin + low MCV
Thalassaemia trait
Disproportionately low MCV, normal/raised RBC count (low Mentzer index) โ†’ Hb electrophoresis / HbA2.
High ferritin + inflammation
Anaemia of chronic disease
Inflammation raises ferritin; transferrin saturation helps separate from iron deficiency.
ReferEscalation
2WW NICE NG12 iron-deficiency anaemia in men / post-menopausal women, or age 60+ โ†’ GI cancer pathway (FIT, endoscopy). Antenatal / haematology thalassaemia trait โ€” partner testing & pre-conception counselling.
Step 8 ยท modifiable factors
Step 8 ยท Lifestyle & modifiable factorsIron repletion vs avoiding pointless iron
For iron deficiency: iron-rich diet + vitamin C, treat heavy menstrual bleeding, gluten-free diet if coeliac (and complete the GI work-up). For thalassaemia trait, do not give long-term iron โ€” it doesn't help and risks overload; provide genetic/partner counselling. In anaemia of chronic disease, treat the underlying inflammatory condition.
Step 9 ยท monitoring & safety-net
Step 9 ยท Monitoring & safety-netRecheck & close the loop
Recheck Hb/MCV/ferritin after iron replacement; if no response, reconsider thalassaemia trait or ongoing loss (electrophoresis, GI work-up). Action FIT/endoscopy results. Same-day for symptomatic severe anaemia (chest pain, breathlessness at rest), or black/bloody stools.
โš ๏ธ Low MCV with a normal ferritin is not iron deficiency. Suspect thalassaemia trait โ€” confirm with electrophoresis and avoid pointless long-term iron.
1
Safety

Red Flags โ€” Severe Anaemia, Thalassaemia Major & Malignancy

Microcytosis + Hb <70 g/L + tachycardia + dyspnoea at rest + chest pain Severe iron deficiency anaemia with haemodynamic compromise. โ†’ Hospital same-day. Consider transfusion (2 units pRBC if cardiac compromise). Identify and control bleeding source. IV iron (Ferinject) after resuscitation.
Microcytosis + post-menopausal woman or man of any age with no obvious blood loss GI malignancy causing occult blood loss. โ†’ 2WW colorectal + quantitative FIT. OGD + colonoscopy required (bidirectional). Anti-tTG IgA. Do not assume dietary cause.
MCV <70 fl + Hb very low + splenomegaly + ethnic background (Mediterranean, South/Southeast Asian, Middle Eastern, African) Consider thalassaemia major/intermedia. โ†’ Urgent haematology. Haemoglobin electrophoresis + HPLC. Transfusion-dependent thalassaemia = iron chelation therapy mandatory (defer osamine/desferrioxamine). Genetic counselling.
Microcytosis + normal or high ferritin + high CRP in patient with chronic inflammatory disease Anaemia of chronic disease with co-existing iron deficiency (functional iron deficiency). โ†’ Check transferrin saturation <20% + serum iron (confirms iron deficiency despite elevated ferritin). IV iron preferred (oral iron absorbed poorly in inflammation).
Microcytic anaemia + blood transfusion history + iron overload symptoms (bronze skin + hepatomegaly + diabetes + heart failure) Transfusional haemosiderosis. Serum ferritin >2,500 mcg/L + liver MRI (iron quantification). Iron chelation urgently.
Microcytosis + sideroblastic anaemia features + history of lead exposure, alcohol, or isoniazid use Sideroblastic anaemia โ€” ringed sideroblasts in bone marrow. โ†’ Haematology. Lead level if exposure suspected. Pyridoxine (B6) trial (hereditary sideroblastic anaemia).
Microcytosis (MCV below 80 fl) combined with an iron deficiency pattern in a man or post-menopausal woman is a red flag for gastrointestinal malignancy that must not be attributed to dietary causes without investigation โ€” the BSG guidelines are explicit: iron deficiency anaemia in a post-menopausal woman or a man of any age mandates bidirectional GI investigation (OGD + colonoscopy) regardless of whether there are GI symptoms. Approximately 10-15% of IDA in these groups has an underlying GI malignancy (colorectal, gastric, or oesophageal cancer). The investigation must be bidirectional because approximately 10% of patients have lesions in both the upper and lower GI tract. Coeliac disease should also be excluded in every patient with IDA (anti-tTG IgA + total IgA) โ€” it is present in approximately 5-7% of IDA patients. The GP who prescribes iron without investigating the cause in a post-menopausal woman or man has made a clinical error, regardless of whether there are GI symptoms.
2
Diagnose

Causes of Microcytosis โ€” Classification

Iron deficiency (most common)
Causes: blood loss (GI most important in men + post-menopausal women; menstruation most common in pre-menopausal women), reduced absorption (coeliac disease, achlorhydria, post-gastrectomy, H. pylori, IBD), increased demand (pregnancy, growth, EPO therapy), inadequate intake (vegan/vegetarian diet, poverty). Serum ferritin <15 mcg/L = definite deficiency. MCV typically <80 fl. Hypochromic microcytic red cells on film. Pencil cells characteristic.
Thalassaemia (alpha and beta)
Alpha-thalassaemia: 1 or 2 gene deletions = thalassaemia trait (asymptomatic, MCV low, Hb normal). 3 deletions = HbH disease (haemolytic anaemia, splenomegaly). 4 deletions = hydrops fetalis (stillbirth). Normal Hb electrophoresis in alpha-thal trait โ€” DNA testing required. Beta-thalassaemia trait: HbA2 elevated >3.5% on Hb electrophoresis. Beta-thal major: Hb F predominant, severe anaemia from infancy, transfusion-dependent.
Anaemia of chronic disease (ACD)
Microcytosis less common than in IDA โ€” ACD usually normocytic or borderline microcytic. Mechanism: hepcidin rise (from IL-6 in inflammation) blocks intestinal iron absorption + releases iron from macrophages into plasma. Ferritin: normal or elevated (acute phase reactant). Serum iron: low. TIBC: low or normal (unlike IDA where TIBC is elevated). Transferrin saturation <20% in both IDA and ACD. MCV usually 75-85 fl in ACD.
Sideroblastic anaemia
Hereditary (ALAS2 X-linked โ€” pyridoxine-responsive) or acquired (MDS, alcohol, lead toxicity, isoniazid, chloramphenicol). Microcytic hypochromic cells + elevated serum iron + elevated ferritin + elevated transferrin saturation (iron-loaded but cannot be incorporated into haem). Ring sideroblasts in bone marrow (mitochondrial iron loading). Haematology-led diagnosis.
The Mentzer index is a quick discriminating tool between IDA and thalassaemia trait โ€” calculated as MCV (fl) divided by the RBC count (ร—10ยนยฒ/L): a result below 13 suggests thalassaemia trait (RBC count is elevated or maintained despite small cell size, because the bone marrow produces more small cells to maintain oxygen delivery); a result above 13 suggests IDA (RBC count is reduced along with MCV reduction). This calculation is immediately available from any FBC report and takes 10 seconds. Its sensitivity is approximately 75-85% โ€” not definitive, but highly useful for triaging which patients need haemoglobin electrophoresis for thalassaemia confirmation. The clinical importance: giving iron supplementation to a patient with thalassaemia trait (who has normal iron stores) is not harmful, but it is ineffective and may cause unnecessary investigation anxiety. Conversely, missing IDA in a patient thought to have thalassaemia trait can cause ongoing investigation for a 'genetic condition' while GI blood loss goes untreated.
3
Diagnose

Investigation Strategy โ€” Iron Studies Interpretation

Iron deficiency โ€” confirming the pattern
Definitive deficiency (ferritin <15 mcg/L): treat + investigate cause. Borderline ferritin (15-30 mcg/L): check serum iron + TIBC + transferrin saturation. Transferrin saturation <20% = iron deficient. Serum ferritin + serum iron + TIBC + transferrin saturation together give the most reliable picture. CRP: if >5, ferritin is unreliable (acute phase reactant) โ€” use transferrin saturation as the primary marker in inflammation. Soluble transferrin receptor (sTfR): elevated in IDA, not in ACD โ€” available in specialist labs, useful for distinguishing the two when ferritin is misleading.
IDA vs ACD vs mixed: iron study pattern
IDA: Ferritin LOW | Serum iron LOW | TIBC HIGH | TS <20%
ACD: Ferritin NORMAL/HIGH | Serum iron LOW | TIBC LOW/NORMAL | TS <20%
Mixed IDA+ACD: Ferritin VARIABLE | Serum iron LOW | TIBC LOW | TS <20%
Thalassaemia workup
Hb electrophoresis + HPLC (beta-thal trait: HbA2 >3.5%; alpha-thal trait: normal electrophoresis) · DNA analysis (alpha-thalassaemia confirmation if electrophoresis normal + Mentzer <13) · Ferritin (thalassaemia trait: normal ferritin โ€” confirms not IDA) · Partner testing (if confirmed thalassaemia carrier โ€” pregnancy implications, both partners must be screened)
The iron studies pattern is one of the most useful and underutilised diagnostic discriminators in haematology โ€” the combination of serum ferritin, serum iron, TIBC, and transferrin saturation reliably distinguishes iron deficiency anaemia from anaemia of chronic disease in the majority of cases. The key distinguishing feature: in IDA, the body depletes iron stores (low ferritin) and upregulates iron absorption by producing more transferrin (high TIBC). In ACD, inflammation-driven hepcidin blocks iron release from macrophage stores โ€” iron is actually trapped in the reticuloendothelial system (ferritin is elevated as an acute phase protein; TIBC is low or normal because the liver reduces transferrin synthesis in response to IL-6). The transferrin saturation (serum iron รท TIBC ร— 100%) is below 20% in both conditions โ€” it does not discriminate. The clinical trap: in a patient with both IDA and ACD (common in IBD, RA with GI blood loss from NSAID use, or malignancy with nutritional iron deficiency), the ferritin may appear normal because the ACD component elevates it while the IDA component depletes it โ€” the sTfR (elevated only in IDA, not ACD) is the most reliable test in this scenario.
4
Diagnose

Thalassaemia โ€” Carrier Identification & Pregnancy Planning

UK antenatal thalassaemia screening
All pregnant women in the UK are offered haemoglobinopathy screening (ideally before 10 weeks). High-prevalence areas (South and East London, Midlands, parts of Yorkshire): all women screened. Low-prevalence areas: family origin questionnaire first. If mother is a carrier: partner testing offered. If both parents are carriers: prenatal diagnosis (chorionic villus sampling at 11-14 weeks or amniocentesis at 15 weeks) offered for each pregnancy. Affected fetus (beta-thal major or HbSS): counselling about termination or prenatal treatment options.
GP-identified thalassaemia trait
Incidental finding of persistent microcytosis with normal ferritin and normal Hb: order Hb electrophoresis + HPLC. Beta-thalassaemia trait (HbA2 >3.5%): explain it is a carrier state, not a disease, with no symptoms. Document in clinical record. Advise: inform partner, who should also be tested if pregnancy planned. Genetic counselling referral if partner also a carrier (25% risk of affected child per pregnancy).
Haemoglobin variants
HbS (sickle cell trait + sickle cell disease โ€” SS, SC, S-beta). HbC, HbE, HbD-Punjab: variable severity when combined with HbS or each other. HbH disease (alpha-thal 3 deletions): mild-moderate haemolytic anaemia, splenomegaly, no transfusion needed in most cases. Haemoglobin electrophoresis or HPLC (high performance liquid chromatography) identifies and quantifies all haemoglobin variants.
Partner thalassaemia testing after a carrier is identified in primary care is a critical step that is frequently not completed โ€” the clinical consequence of missed partner testing is a couple where both partners are thalassaemia trait carriers who conceive without knowing their risk, and present in pregnancy at 20+ weeks with a thalassaemia major fetus on anomaly scan. This is avoidable: if thalassaemia trait is identified in a patient of reproductive age, their partner must be tested before the next pregnancy, and ideally before conception. The GP's responsibility: document thalassaemia trait clearly in the clinical record, provide patient education, and advise partner testing. If the patient is pregnant at the time of diagnosis, the antenatal team will coordinate partner testing โ€” but if identified outside pregnancy, the GP must take proactive action. The Sickle Cell and Thalassaemia Society (sicklecellsociety.org) provides excellent patient information resources.
5
Refer

Referral Pathways

Same-day hospital
Hb <70 g/L + haemodynamic compromise ยท Acute significant GI bleeding causing IDA
2WW colorectal
IDA in post-menopausal woman or man of any age โ†’ OGD + colonoscopy ยท FIT >10 mcg Hb/g + microcytosis ยท Macroscopic rectal bleeding + IDA
Haematology
Thalassaemia major/intermedia requiring transfusion management ยท Sideroblastic anaemia ยท Suspected MDS with microcytic pattern ยท IDA not responding to oral iron after 4 months (malabsorption) ยท Combined haemoglobinopathy in pregnancy
Gastroenterology / gastroenterology referral
Confirmed coeliac disease causing IDA ยท Persistent IDA after normal bidirectional endoscopy โ†’ capsule endoscopy (small bowel angiodysplasia) ยท H. pylori eradication for IDA
Genetic counselling
Both partners carrying thalassaemia trait or haemoglobinopathy ยท Single gene disorders with reproductive implications ยท Antenatal: CVS or amniocentesis counselling
GP management
IDA with identified source: oral iron + treat cause. Thalassaemia trait: reassurance + partner testing advice + pregnancy counselling. Coeliac + IDA: GFD + iron + annual monitoring. Metformin IDA: B12 check + oral iron.
The bidirectional GI investigation requirement for IDA โ€” OGD plus colonoscopy โ€” must both be performed, not performed sequentially only if the first is normal. The BSG IDA guideline states clearly that both investigations should be arranged simultaneously in men and post-menopausal women with IDA, because approximately 10% of patients have relevant pathology in both the upper and lower GI tract. Common clinical errors: (1) arranging OGD only (finding oesophagitis and attributing IDA to it, missing a concurrent right-sided colorectal cancer); (2) arranging colonoscopy only (finding left-sided polyps but missing gastric cancer); (3) arranging FIT alone without endoscopy โ€” FIT is a screening tool, not a diagnostic tool; a negative FIT does not exclude upper GI pathology and does not eliminate the need for OGD in a man with IDA. The GP referral should request both OGD and colonoscopy simultaneously, with a cover letter explaining: IDA confirmed (ferritin level + Hb), sex and menopausal status, GI symptoms if any, family history of CRC or gastric cancer.
6
Treat

Iron Replacement โ€” Oral and IV (See Low Ferritin Algorithm)

Oral iron โ€” dosing and administration
Ferrous sulphate 200 mg BD (65 mg elemental iron per tablet): take on empty stomach + vitamin C (orange juice) to maximise absorption. Separate from antacids, calcium, PPIs, tea/coffee by 2 hours. Expected response: Hb rises 10-20 g/L per month. Reticulocyte peak at day 7-10 (confirms diagnosis). Continue for 3 months after Hb normalises (replete stores; target ferritin >30 mcg/L). Tolerability issues (constipation, nausea): switch to ferrous gluconate 300 mg BD (lower elemental iron, better tolerated) or alternate-day dosing (BALTAR trial: equivalent efficacy to daily with fewer side effects from reduced hepcidin rise).
IV iron โ€” indications
Oral iron intolerance (confirmed โ€” not poor compliance). Confirmed malabsorption (coeliac, IBD, post-bariatric). Severe IDA in pregnancy (Hb <85 g/L or oral iron inadequate). Pre-operative optimisation (cardiac/orthopaedic surgery). CKD on EPO (functional iron deficiency). Active IBD (inflammation prevents oral absorption). Preferred: ferric carboxymaltose (Ferinject) 1,000 mg IV over 15 minutes (single dose repletes stores in most patients). Monitor phosphate at 2 weeks (hypophosphataemia risk from FGF23 stimulation).
Treating the cause alongside iron
Menorrhagia: LNG-IUS (Mirena) โ€” reduces blood loss 90%. Tranexamic acid 1g QDS during period. H. pylori eradication (IDA + H. pylori โ€” eradication restores acid + absorption). Coeliac disease: strict GFD restores iron absorption within 3-6 months. NSAID-related GI blood loss: stop NSAID if possible; PPI gastroprotection if essential. Reduce dietary inhibitors: stop tea/coffee with meals.
IV ferric carboxymaltose (Ferinject) management in primary care is an area where UK pathways are actively expanding โ€” many ICBs now have pathways for GP-initiated IV iron infusion in day units without specialist referral for specific indications (confirmed IDA with failed/intolerable oral iron, IBD, pre-operative anaemia, obstetric anaemia). GPs who identify patients meeting these criteria should: (1) check local ICB formulary for the IV iron pathway; (2) arrange pre-infusion blood tests (FBC, ferritin, CRP, renal function); (3) refer to the appropriate day unit with a completed referral form; (4) arrange post-infusion monitoring (FBC + ferritin at 4-6 weeks, serum phosphate at 2 weeks). The GIRFT (Getting It Right First Time) programme has highlighted that IV iron is significantly underutilised in UK primary care, resulting in avoidable hospital admissions for severe IDA and unnecessary delays in surgical procedures.
7
Treat

Thalassaemia Management โ€” GP Role

Thalassaemia trait (carrier state)
No treatment required. Normal life expectancy. No anaemia or only very mild anaemia. Do NOT prescribe iron (iron stores are normal โ€” unnecessary + potentially harmful long-term). Ensure ferritin is normal (exclude concurrent IDA). Document clearly in clinical record: "Thalassaemia trait โ€” iron treatment not required; refer to genetics if pregnancy planned." Avoid misdiagnosis as IDA and repeated unnecessary iron treatment.
HbH disease (alpha-thalassaemia, 3 deletions)
Chronic mild-moderate haemolytic anaemia (Hb typically 7-10 g/dL). Splenomegaly. Jaundice. Haemolysis exacerbated by: infections, oxidant drugs (dapsone, primaquine, sulfonamides โ€” check before prescribing). Haematology follow-up. Folic acid 5 mg OD (increased erythropoiesis demand). Transfusion only if Hb drops acutely (haemolytic crisis). Avoid iron supplementation unless concurrent iron deficiency confirmed.
Beta-thalassaemia major (transfusion-dependent)
GP awareness: patients on monthly transfusion + iron chelation (deferasirox, deferoxamine). GP role: manage intercurrent infections promptly (infection precipitates haemolytic crisis), monitor chelation side effects (deferasirox: renal function + LFTs annually; audiology and ophthalmology for deferoxamine). Annual cardiac MRI (iron overload monitoring). Hydroxyurea in some patients (increases HbF โ€” reduces transfusion requirement). HSCT: only curative option. Haematology-led.
Pregnancy with thalassaemia trait
Refer early to obstetrician/haematologist with haemoglobinopathy experience. Ensure partner tested. Folic acid 5 mg OD from pre-conception. If beta-thal trait + partner beta-thal trait: 25% risk of beta-thal major per pregnancy โ€” prenatal diagnosis (CVS or amniocentesis) offered. Register with haemoglobinopathy specialist centre.
Iron supplementation must not be given to patients with thalassaemia trait without confirming concurrent iron deficiency โ€” this is a common and important prescribing error in primary care. Thalassaemia trait causes microcytosis and a mildly low MCV that looks superficially identical to early IDA. However, in thalassaemia trait, the iron stores are normal (ferritin is normal or elevated), and the microcytosis is caused by reduced haemoglobin chain synthesis rather than iron deficiency. Prescribing iron to a thalassaemia trait patient who does not also have IDA: (1) is ineffective (MCV and Hb will not improve); (2) exposes the patient to unnecessary GI side effects; and (3) if continued long-term, may cause iron overload (particularly in alpha-thalassaemia carriers who may have slightly elevated ferritin even at baseline). The safe practice: always check ferritin before prescribing iron for microcytosis. If ferritin is normal and Mentzer index is below 13: arrange haemoglobin electrophoresis before starting iron.
8
Lifestyle

Iron Absorption Optimisation & Thalassaemia Carrier Awareness

Maximising dietary iron absorption Haem iron (meat/fish/poultry): 15-35% absorption โ€” not significantly affected by dietary factors. Non-haem iron (plants/fortified foods): 2-8% absorption โ€” highly variable. Enhancers: vitamin C (orange juice, peppers, kiwi, broccoli โ€” increases Fe3+ to Fe2+ reduction). Meat factor (MFP factor โ€” eating meat alongside plant iron increases non-haem iron absorption). Inhibitors: tea and coffee (polyphenols โ€” separate by 1 hour from iron-rich meals), calcium/dairy (separate by 2 hours from iron tablets), phytates in wholegrains (soaking/sprouting reduces), zinc supplements (compete with iron).
Iron tablet tips for tolerability Take with orange juice (not water alone). If nausea/constipation on BD dose: switch to OD dose with food (reduces absorption approximately 25% but dramatically improves compliance โ€” net effect is better). Alternate-day dosing (BALTAR trial): equivalent efficacy to daily with significantly fewer GI side effects. Ferrous gluconate 300mg BD: better tolerated than ferrous sulphate at similar elemental iron doses. Ferric maltol (Feraccru): licensed for IDA in IBD โ€” good tolerance, superior absorption profile.
Vegetarian and vegan iron strategies Iron requirement on plant-based diet approximately 1.8x higher than omnivore diet. Key plant iron sources: fortified breakfast cereals (up to 8mg/serving), lentils (3.3mg/100g cooked), tofu (3.5mg/100g), pumpkin seeds (9mg/100g), spinach (2.7mg/100g cooked). Always combine with vitamin C. Annual ferritin check for vegans with any symptoms or risk factors. Cooking in cast-iron cookware contributes small amounts of iron.
Thalassaemia carrier awareness and pregnancy Every patient with known thalassaemia trait should understand: it is a carrier state, not a disease. It affects your children only if your partner is also a carrier. Before pregnancy: tell your partner, encourage them to get tested. If both carriers: 25% chance of an affected child per pregnancy โ€” prenatal diagnosis is available. Sickle Cell and Thalassaemia Society (sicklecellsociety.org) โ€” patient information and support. UK Thalassaemia Society (ukts.org).
Antenatal iron monitoring Hb <110 g/L in first trimester or <105 g/L in second/third trimester: treat with iron. Ferritin <30 mcg/L in pregnancy: treat even if Hb normal (depleted stores indicate risk of developing IDA). IV iron (Ferinject) in pregnancy: safe after first trimester; rapid response. Neonatal iron stores depend on maternal iron status โ€” severe maternal IDA risks neonatal iron deficiency.
Monitoring after GI investigation for IDA If OGD + colonoscopy normal: capsule endoscopy consideration (small bowel angiodysplasia or Crohn). Annual ferritin monitoring for unexplained recurrent IDA. Document: investigations performed, results, action taken, safety-netting. Recurrence of IDA without new GI pathology identified โ†’ gastroenterology for capsule endoscopy.
Exercise in iron deficiency anaemia Endurance athletes (runners, cyclists): IDA causes significantly reduced VO2max and performance. Annual ferritin check for symptomatic athletes. Exercise-related IDA: foot-strike haemolysis (microtrauma to RBCs during running), GI blood loss (exercise-induced ischaemic colitis), sweat iron losses, increased erythropoiesis demand. Running shoe cushioning improvements reduce foot-strike haemolysis. IV iron increasingly used in elite athletic preparation.
Adherence support for iron treatment Iron treatment requires 3-4+ months for full store repletion โ€” poor adherence is extremely common because patients feel better once Hb is normalised (typically 4-8 weeks) and stop taking tablets. Explain: stopping iron when you feel better leaves your stores depleted, which will cause IDA to return within months. Set a clear end-date: "take iron tablets every day until [date โ€” 3 months after Hb normalised]." Pill organiser or phone alarm.
The duration of iron supplementation after Hb normalisation is one of the most important patient education points that prevents IDA relapse โ€” most patients stop taking iron when their symptoms resolve (usually 4-8 weeks into treatment). However, at the point when the Hb normalises, the iron stores (ferritin) are still depleted. The bone marrow's priority is to restore the Hb to normal first, using all available iron for haemoglobin synthesis โ€” only after this is the remaining iron stored. Stopping iron when Hb normalises leaves a patient with replete Hb but near-empty stores (ferritin often still below 10-15 mcg/L), meaning the next episode of increased demand (heavy period, minor illness, dietary restriction) will cause IDA to return rapidly. The message to patients: 'We will check your blood test in 3 months โ€” you need to keep taking the iron tablets until then, even when you feel completely better. This is because it takes your body longer to refill its iron stores than it takes to fix the anaemia.'
9
Safety

Follow-Up & Safety-Netting

IDA treatment monitoring
FBC at 4-6 weeks (confirm Hb response: 10-20 g/L per month). Ferritin at 3-4 months (target >30 mcg/L = stores repleted). Continue iron 3 months after Hb normalises. If no Hb response at 4 weeks: check compliance, absorption, ongoing loss.
After GI investigation
OGD + colonoscopy results reviewed and documented. If both normal: capsule endoscopy via gastroenterology (small bowel pathology). Annual ferritin check for unexplained IDA with normal investigation. Close the loop: confirm referral outcome received.
Thalassaemia trait management
Document in clinical record + summary. Advise partner testing if reproductive age. Genetic counselling referral if both partners carriers. Avoid prescribing iron without confirming concurrent IDA (ferritin).
Coeliac-related IDA
Annual: anti-tTG IgA (dietary compliance monitoring), FBC + ferritin, B12, folate, calcium, vitamin D. DEXA at diagnosis. Dietitian review annually. Iron normalises within 3-6 months of strict GFD.
Urgent referral
IDA in post-menopausal woman or man without GI investigation โ†’ 2WW now ยท No Hb response at 6 weeks on oral iron โ†’ IV iron consideration + malabsorption screen ยท Thalassaemia both partners carriers + pregnancy โ†’ urgent genetics + obstetrics
Within 2 weeks
New GI symptoms during iron treatment โ†’ OGD or colonoscopy urgently ยท Ferritin not normalising after 3 months iron โ†’ malabsorption screen (coeliac, H. pylori) ยท Microcytosis with normal ferritin in high-risk ethnic group โ†’ Hb electrophoresis
The clinical governance requirement for closed-loop referral management applies critically in the IDA context โ€” IDA is one of the most common diagnoses associated with missed cancer diagnoses in UK medicolegal claims. The typical claim pattern: GP identifies IDA in a 62-year-old man โ†’ prescribes iron without arranging GI investigation โ†’ patient's Hb improves on iron โ†’ GP assumes problem resolved โ†’ patient returns 8 months later with symptomatic stage IV colorectal cancer. Prevention: every diagnosis of IDA in a man or post-menopausal woman must be followed by: (1) arrangement of bidirectional GI investigation (OGD + colonoscopy); (2) documentation that the referral was sent; (3) a system to confirm the referral was received and acted upon; and (4) review of the results when available. If a patient declines investigation, this must be documented: 'Patient fully informed of investigation requirement and cancer risk. Patient declines investigation โ€” reasons documented. Patient safety-netted to attend urgently if symptoms develop.'
Educational use only. Based on BSG Iron Deficiency Anaemia Guidelines (Goddard 2011), NICE NG20 Coeliac Disease, NHS Antenatal Haemoglobinopathy Screening Programme, NICE NG88 Heavy Menstrual Bleeding, BNF iron replacement prescribing.