Situation: A 34-year-old woman is brought to the emergency room (ER) because she nearly fainted at work. She reports fatigue, shortness of breath on climbing stairs, and heavy menstrual periods for the past year. Her heart rate is 118/min and blood pressure 104/66 mmHg. She has no chronic illness and no known drug allergies. Her results are: Hemoglobin: 62 g/L (6.2 g/dL) Mean corpuscular volume: 70 fL (normal 80–100) Serum iron: low Total iron-binding capacity: high Serum ferritin: 5 ng/mL (5 µg/L) Reticulocyte count: low The provider diagnoses iron deficiency anemia. A student nurse notes that anemia of inflammation can also cause a low serum iron and small red cells. In which pair do BOTH results differ from what is expected in anemia of inflammation?

In anemia of inflammation, hepcidin traps iron in storage, so serum iron is low but ferritin is normal or high and total iron-binding capacity (TIBC) is low or normal; red cells can be small and reticulocytes are low. In iron deficiency the stores are empty, so ferritin is low and TIBC rises. Only low ferritin and high TIBC both depart from the pattern of inflammation.

Core mechanism
Iron deficiency anemia and anemia of inflammation share a superficial laboratory overlap: both can show low serum iron and microcytosis. The difference lies in how the body handles stored iron and transport capacity. In iron deficiency, total body iron stores are depleted, so serum ferritin falls and the liver increases total iron-binding capacity (TIBC) to capture whatever iron is available. In anemia of inflammation, the hepatic peptide hepcidin rises, blocking ferroportin-mediated iron release from macrophages and enterocytes. Iron remains trapped in storage, so ferritin is normal or elevated and TIBC is low or normal, even though serum iron is low.

The only pair in which both values move away from the inflammation pattern is low ferritin plus high TIBC. That combination signals empty iron stores, not sequestered iron.

Marker	Iron deficiency anemia	Anemia of inflammation
Serum iron	Low	Low
Serum ferritin	Low	Normal or high
Total iron-binding capacity	High	Low or normal
Mean corpuscular volume	Low	Low or normal
Reticulocyte count	Low	Low

Watch out! Do not use serum iron alone to separate these two anemias. Both conditions depress serum iron, so it is a shared finding, not a discriminating one.

Key point! Ferritin is an acute-phase reactant. In inflammation it rises even when bioavailable iron is low. Therefore, a ferritin below the lower limit of normal in a patient with chronic disease strongly suggests coexisting iron deficiency.

Applying the evidence to this patient
The woman’s hemoglobin of 62 g/L (6.2 g/dL) and MCV of 70 fL confirm a hypochromic microcytic anemia. Her ferritin of 5 ng/mL (5 µg/L) is markedly low, and her TIBC is high. The low reticulocyte count reflects an inadequate marrow response because iron substrate is missing for hemoglobin synthesis. In the study by Nigotia et al., patients with anemia of chronic disease typically demonstrated low serum iron and low transferrin saturation, but their ferritin was not low and their TIBC was not high; bone marrow iron stores were preserved or increased ^[1]. That pattern is the opposite of what is seen here.

A low ferritin in the setting of chronic heavy menstrual bleeding indicates depleted iron stores, and a high TIBC reflects the liver’s compensatory upregulation of transferrin. These two findings together exclude isolated anemia of inflammation as the primary process.

Why the other options are not correct
Option 1 pairs low serum iron with low MCV. Both can occur in anemia of inflammation, so this pair does not depart from the inflammation pattern. Option 3 pairs low serum iron with high TIBC. The low serum iron is expected in inflammation, so only one of the two values differs. Option 4 pairs low ferritin with low reticulocyte count. The low reticulocyte count is expected in anemia of inflammation, so again only one value differs. Only option 2 contains two findings—low ferritin and high TIBC—that are both inconsistent with anemia of inflammation.

Clinical reasoning for nursing care
The priority is to recognize that this patient’s iron deficiency is severe enough to cause near-syncope and tachycardia of 118/min. Nursing assessment should include orthostatic vital signs, oxygen saturation, activity tolerance, and a thorough menstrual and dietary history. Because she has no known drug allergies and no chronic illness, oral iron replacement is typically first-line, but a hemoglobin this low may warrant intravenous iron or transfusion depending on hemodynamic stability and institutional protocol. Monitoring reticulocyte response after iron therapy helps confirm the diagnosis: reticulocytes should rise within 5–10 days if iron deficiency is the cause.