A 72-year-old man with chronic heart failure (ejection fraction 30%) attends a heart failure clinic that uses the European Society of Cardiology (ESC) definition of iron deficiency: ferritin below 100 µg/L, or ferritin 100-299 µg/L with transferrin saturation below 20%. Results: hemoglobin 124 g/L (12.4 g/dL) (reference 130-170), MCV 84 fL, RDW 15.8% (reference 11.5-14.5%), serum iron 8 µmol/L (45 µg/dL) (reference 10-30 µmol/L), TIBC 62 µmol/L (346 µg/dL) (reference 45-70 µmol/L), ferritin 182 µg/L (reference 30-400), CRP 9 mg/L (reference below 5) and eGFR 58 mL/min/1.73 m². Using the clinic's definition, how should his iron status be reported?

Iron deficiency, by a transferrin saturation of 13%

Not assessable until the CRP returns to normal

Anemia of inflammation alone, with adequate stores

Iron replete, because ferritin is above 100 µg/L

A 69-year-old woman with polymyalgia rheumatica has an anemia that has not responded to 3 months of oral iron. Results: hemoglobin 96 g/L (9.6 g/dL), MCV 82 fL, CRP 38 mg/L (reference below 5), ferritin 140 µg/L (reference 15-150) and transferrin saturation 9% (reference 20-50%). To separate iron deficiency from anemia of inflammation, a marrow aspirate and trephine biopsy are taken. The Perls-stained aspirate smears contain only cell trails with no marrow particles, and no stainable iron is seen; sideroblasts are 3% of erythroblasts. The trephine was decalcified overnight in a rapid hydrochloric acid decalcifier, and its Perls stain also shows no iron. How should the marrow iron stores be reported?

Not assessable on this material

Absent, confirming iron deficiency

Absent, excluding anemia of inflammation

Normal, because sideroblasts are present

A woman with iron deficiency anemia starts oral iron and takes it correctly. Which finding is the earliest sign that she is responding?

Reticulocyte rise peaking at about 7 to 10 days

Normal hemoglobin within the first week

Normal ferritin within the first week

Normal MCV within the first 3 days

Iron deficiency and anemia of inflammation

19 DOH Abu Dhabi (HAAD) lab licensing practice questions on Iron deficiency and anemia of inflammation, part of Hematology. The first 19 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

Question 1 · Hard
A 72-year-old man with chronic heart failure (ejection fraction 30%) attends a heart failure clinic that uses the European Society of Cardiology (ESC) definition of iron deficiency: ferritin below 100 µg/L, or ferritin 100-299 µg/L with transferrin saturation below 20%. Results: hemoglobin 124 g/L (12.4 g/dL) (reference 130-170), MCV 84 fL, RDW 15.8% (reference 11.5-14.5%), serum iron 8 µmol/L (45 µg/dL) (reference 10-30 µmol/L), TIBC 62 µmol/L (346 µg/dL) (reference 45-70 µmol/L), ferritin 182 µg/L (reference 30-400), CRP 9 mg/L (reference below 5) and eGFR 58 mL/min/1.73 m². Using the clinic's definition, how should his iron status be reported?
1. ANot assessable until the CRP returns to normal
2. BAnemia of inflammation alone, with adequate stores
3. CIron deficiency, by a transferrin saturation of 13%
4. DIron replete, because ferritin is above 100 µg/L
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Answer: C · Iron deficiency, by a transferrin saturation of 13%
Transferrin saturation = serum iron ÷ TIBC × 100 = 8 ÷ 62 × 100 = 13%. His ferritin of 182 µg/L lies in the 100-299 µg/L band, so with a saturation below 20% he meets the ESC definition of iron deficiency, even though the ferritin is inside the laboratory reference range. Heart failure is a low-grade inflammatory state in which ferritin rises as an acute-phase protein and no longer reflects stores, which is why the definition pairs a higher ferritin cut-off with the saturation. The high-normal TIBC and the raised RDW also point to iron-deficient red cell production rather than inflammation alone, in which TIBC is usually low. In heart failure, iron deficiency is treated even without anemia, because intravenous iron improves symptoms and exercise capacity.
- A: The definition is designed for this inflammatory state, so testing need not wait for a normal CRP.
- B: The definition is met, and the high-normal TIBC points to a lack of iron, not inflammation alone.
- D: Under the ESC definition, ferritin of 100-299 µg/L with saturation below 20% counts as iron deficiency.
Question 2 · Hard
A 69-year-old woman with polymyalgia rheumatica has an anemia that has not responded to 3 months of oral iron. Results: hemoglobin 96 g/L (9.6 g/dL), MCV 82 fL, CRP 38 mg/L (reference below 5), ferritin 140 µg/L (reference 15-150) and transferrin saturation 9% (reference 20-50%). To separate iron deficiency from anemia of inflammation, a marrow aspirate and trephine biopsy are taken. The Perls-stained aspirate smears contain only cell trails with no marrow particles, and no stainable iron is seen; sideroblasts are 3% of erythroblasts. The trephine was decalcified overnight in a rapid hydrochloric acid decalcifier, and its Perls stain also shows no iron. How should the marrow iron stores be reported?
1. AAbsent, confirming iron deficiency
2. BAbsent, excluding anemia of inflammation
3. CNot assessable on this material
4. DNormal, because sideroblasts are present
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Answer: C · Not assessable on this material
Storage iron lies in macrophages within marrow particles, so an aspirate with only cell trails cannot show whether stores are present, and an apparent absence of iron is unreliable; several particles are needed for a valid grade. Strong acid decalcification leaches iron from a trephine, so a negative Perls stain on this core is also unreliable, whereas EDTA decalcification preserves it. The report should say that iron stores cannot be assessed and why, rather than suggest a diagnosis. Her raised CRP, ferritin near the top of the range and low saturation fit anemia of inflammation with possible co-existing iron deficiency, which a soluble transferrin receptor or a repeat aspirate with particles could help settle. Sideroblasts are reduced in both conditions, so they say nothing about the stores.
- A: With no particles and an acid-decalcified core, an absence of iron cannot be trusted.
- B: Absent iron is not proven on this material, and inflammation can co-exist with iron deficiency.
- D: Sideroblasts are reduced in both iron deficiency and inflammation and do not show the stores.
Question 3 · Easy
Where is most of the body's iron found in a healthy adult?
1. AFerritin in the liver
2. BHemoglobin in red cells
3. CTransferrin in plasma
4. DMyoglobin in muscle
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Answer: B · Hemoglobin in red cells
About two-thirds of body iron, roughly 2 to 2.5 g in an adult man, is in the hemoglobin of red cells and their precursors. Storage iron in ferritin and hemosiderin, mainly in the liver, spleen and marrow macrophages, makes up most of the rest. Myoglobin and enzymes hold a smaller amount, and transferrin carries only about 3 to 4 mg at any time. This is why chronic blood loss is the most common cause of iron deficiency in adults.
- A: Storage iron is the second largest pool, smaller than the iron in hemoglobin.
- C: Transferrin carries only a few milligrams of iron at any time.
- D: Myoglobin holds only a small share of body iron.
Question 4 · Medium
A woman with iron deficiency anemia starts oral iron and takes it correctly. Which finding is the earliest sign that she is responding?
1. AReticulocyte rise peaking at about 7 to 10 days
2. BNormal hemoglobin within the first week
3. CNormal ferritin within the first week
4. DNormal MCV within the first 3 days
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Answer: A · Reticulocyte rise peaking at about 7 to 10 days
Once iron is available, the marrow releases more reticulocytes within days, and the count peaks at about 7 to 10 days. Hemoglobin then rises, and an increase of about 20 g/L (2 g/dL) within 3 to 4 weeks is usually taken as an adequate response. The MCV corrects slowly as new normocytic cells replace old microcytic ones, giving a dimorphic picture for a while. Iron is usually continued for about 3 months after hemoglobin normalizes to refill stores, which is when ferritin rises.
- B: Hemoglobin takes weeks, not days, to return to normal.
- C: Ferritin rises late, once stores refill after hemoglobin recovers.
- D: The MCV corrects slowly as new cells replace old microcytic cells.
Question 5 · Medium
In anemia of inflammation, which cytokine is the main driver of increased hepcidin production?
1. AInterleukin-2
2. BInterleukin-6
3. CInterleukin-4
4. DInterleukin-5
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Answer: B · Interleukin-6
Interleukin-6, released in infection, autoimmune disease and cancer, activates the JAK-STAT3 pathway in hepatocytes and switches on the hepcidin gene. Hepcidin then traps iron in macrophages and reduces absorption, so serum iron falls within hours to days. This limits the iron available to microbes but also to the marrow, causing anemia of inflammation. Drugs that block IL-6 can raise hemoglobin in conditions such as rheumatoid arthritis.
- A: IL-2 drives T cell growth and is not the main inducer of hepcidin.
- C: IL-4 drives Th2 and IgE responses, not hepcidin.
- D: IL-5 drives eosinophil production.
Question 6 · Hard
A patient on hemodialysis receiving an erythropoiesis-stimulating agent (ESA) has a falling hemoglobin. Results: ferritin 380 µg/L (reference 30-400), transferrin saturation 14% (reference 20-50%), reticulocyte hemoglobin 24 pg (reference 28-35), normal CRP, and normal B12 and folate. The most likely explanation is:
1. AFunctional iron deficiency during ESA therapy
2. BIron overload from intravenous iron
3. CAnemia of inflammation from infection
4. DAbsolute iron deficiency with empty stores
Answer and explanation in LearnFree account
Question 7 · Medium
Which factor increases the absorption of non-heme iron from a meal?
1. ALong-term proton pump inhibitor use
2. BAscorbic acid taken with the meal
3. CTea or coffee taken with the meal
4. DCalcium supplements taken with it
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Question 8 · Hard
A 58-year-old man has had chronic osteomyelitis for 4 months. Results: Hb 98 g/L (9.8 g/dL), MCV 82 fL, serum iron 6 µmol/L (34 µg/dL) (reference 10-30 µmol/L), TIBC 38 µmol/L (212 µg/dL) (reference 45-70 µmol/L), ferritin 480 µg/L (reference 30-400), CRP 65 mg/L and a soluble transferrin receptor within its reference range. The most likely diagnosis is:
1. AIron deficiency anemia
2. BIron deficiency with anemia of inflammation
3. CAnemia of inflammation
4. DSideroblastic anemia
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Question 9 · Hard
A 24-year-old woman with light periods has iron deficiency anemia (Hb 92 g/L [9.2 g/dL], ferritin 5 µg/L, reference 15-150). After 3 months of oral iron taken correctly, Hb is 94 g/L (9.4 g/dL) and ferritin 6 µg/L. Fecal occult blood tests are negative. Which test is the most appropriate next step?
1. ABone marrow aspirate with iron stain
2. BHemoglobin A2 and Hb F quantitation
3. CSerum vitamin B12 and folate
4. DTissue transglutaminase IgA with total IgA
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Question 10 · Medium
A low reticulocyte hemoglobin content (CHr or Ret-He) shows that:
1. ARed cells are being destroyed faster than normal
2. BIron supply to the marrow has been short in recent days
3. CFolate supply to the marrow is inadequate
4. DErythropoietin output from the kidney is low
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Question 11 · Hard
A woman with active Crohn's disease has Hb 101 g/L (10.1 g/dL), CRP 40 mg/L, ferritin 100 µg/L and soluble transferrin receptor (sTfR) 4.4 mg/L. The laboratory reports the sTfR-ferritin index (sTfR ÷ log10 ferritin): below 1 suggests anemia of inflammation alone, above 2 suggests coexisting iron deficiency. What is the index, and what does it suggest?
1. A0.96: anemia of inflammation alone
2. B0.044: anemia of inflammation alone
3. C0.45: anemia of inflammation alone
4. D2.2: coexisting iron deficiency
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Question 12 · Hard
A 15-month-old drinks about 1.2 L of cow's milk a day and eats little solid food. Results: Hb 79 g/L (7.9 g/dL), MCV 57 fL, RDW 21% (reference 11.5-14.5%), platelets 560 × 10^9/L (reference 150-450) and ferritin 3 µg/L (reference 12-150). What is the most likely cause of the anemia?
1. ALead poisoning
2. BIron deficiency from excess cow's milk
3. CBeta-thalassemia major
4. DAnemia of chronic inflammation
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Question 13 · Hard
A 30-year-old woman on oral iron has blood drawn 2 hours after her morning tablet. Results: Hb 108 g/L (10.8 g/dL), MCV 74 fL, serum iron 38 µmol/L (212 µg/dL) (reference 10-30 µmol/L), transferrin saturation 62% (reference 20-50%) and ferritin 7 µg/L (reference 15-150). The best interpretation is:
1. ARecent iron intake, with stores still depleted
2. BIron overload from too much oral iron
3. CAnemia of inflammation with iron trapping
4. DHereditary hemochromatosis with iron overload
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Question 14 · Easy
Dietary iron is absorbed mainly in the:
1. AStomach
2. BTerminal ileum
3. CColon
4. DDuodenum
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Question 15 · Medium
Why can serum ferritin fall within the reference range in a patient who has both iron deficiency and active inflammation?
1. ATransferrin carries extra ferritin in inflammation
2. BInflammation blocks the ferritin immunoassay
3. CFerritin rises as an acute-phase protein
4. DInflammation releases iron from hemoglobin
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Question 16 · Easy
Hepcidin, the main hormone controlling iron balance, is made mainly by the:
1. ALiver
2. BBone marrow
3. CKidneys
4. DDuodenum
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Question 17 · Medium
In uncomplicated iron deficiency, serum hepcidin is expected to be:
1. AHigh, blocking iron absorption
2. BNormal, as it tracks only inflammation
3. CHigh, increasing iron absorption
4. DLow, allowing more iron absorption
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Question 18 · Hard
A 6-year-old has had microcytic anemia since infancy that does not respond to oral iron and improves only partly with intravenous iron. Results: Hb 85 g/L (8.5 g/dL), MCV 58 fL, transferrin saturation 4% (reference 20-50%), ferritin 25 µg/L (reference 15-150), normal Hb A2 and Hb F, negative celiac serology, and a serum hepcidin that is not low. Which gene defect best explains these findings?
1. AALAS2 mutation
2. BBeta-globin gene mutation
3. CHFE C282Y homozygosity
4. DTMPRSS6 (matriptase-2) deficiency
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Question 19 · Medium
Microcytic, hypochromic red cells with pencil cells and a high red cell distribution width (RDW) most suggest which condition?
1. AVitamin B12 deficiency
2. BIron deficiency anemia
3. CAplastic anemia
4. DBeta-thalassemia trait
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Iron deficiency and anemia of inflammation

Where is most of the body's iron found in a healthy adult?

A woman with iron deficiency anemia starts oral iron and takes it correctly. Which finding is the earliest sign that she is responding?

In anemia of inflammation, which cytokine is the main driver of increased hepcidin production?

Which factor increases the absorption of non-heme iron from a meal?

A low reticulocyte hemoglobin content (CHr or Ret-He) shows that:

A 15-month-old drinks about 1.2 L of cow's milk a day and eats little solid food. Results: Hb 79 g/L (7.9 g/dL), MCV 57 fL, RDW 21% (reference 11.5-14.5%), platelets 560 × 10^9/L (reference 150-450) and ferritin 3 µg/L (reference 12-150). What is the most likely cause of the anemia?

Dietary iron is absorbed mainly in the:

Why can serum ferritin fall within the reference range in a patient who has both iron deficiency and active inflammation?

Hepcidin, the main hormone controlling iron balance, is made mainly by the:

In uncomplicated iron deficiency, serum hepcidin is expected to be:

Microcytic, hypochromic red cells with pencil cells and a high red cell distribution width (RDW) most suggest which condition?