In a female patient admitted with enteric fever who has hemoglobin 8.2 g/dL, serum iron 30 µg/dL, total iron‑binding capacity 340 µg/dL, and ferritin 340 ng/mL without bleeding or jaundice, how should these findings be interpreted?

Interpretation of Iron Studies in Enteric Fever with Anemia

This patient has anemia of chronic disease (also called anemia of inflammation) caused by the acute infectious process of enteric fever, with possible coexisting functional iron deficiency. 1

Understanding the Laboratory Pattern

The key to interpretation is recognizing that ferritin is an acute-phase reactant that rises during inflammation, masking true iron status. 1

Calculating Transferrin Saturation

• Calculate transferrin saturation (TSAT) as (serum iron × 100) ÷ TIBC = (30 × 100) ÷ 340 = 8.8%, which is markedly reduced. 1, 2
• A TSAT < 20% in the presence of inflammation confirms functional iron deficiency even when ferritin appears elevated. 1

Interpreting the Ferritin Level

• Ferritin 340 ng/mL with elevated inflammatory markers indicates anemia of chronic disease, but the very low TSAT reveals that iron is sequestered and unavailable for erythropoiesis. 1, 2
• In the presence of inflammation (which enteric fever certainly causes), ferritin values up to 100 µg/L may still represent true iron deficiency; values between 30–100 µg/L suggest a mixed picture of iron deficiency plus anemia of chronic disease. 1
• When ferritin is > 100 µg/L AND TSAT < 20% in an inflammatory state, the diagnosis is anemia of chronic disease with functional iron deficiency. 1

The Pathophysiology

• Inflammatory cytokines, especially IL-6, induce hepatic production of hepcidin, which blocks iron release from macrophages, hepatocytes, and enterocytes, causing the characteristic hypoferremia and iron sequestration. 3
• This creates a state where total body iron stores may be adequate or even elevated (reflected by high ferritin), but iron is trapped and unavailable for red blood cell production (reflected by low serum iron and TSAT). 4, 3

Clinical Diagnosis

This patient has anemia of chronic disease secondary to enteric fever, characterized by:

• Hemoglobin 8.2 g/dL (moderate anemia in a female, below the WHO threshold of < 12 g/dL). 1
• Serum iron 30 µg/dL (low, indicating hypoferremia). 1
• TIBC 340 µg/dL (normal to low-normal, as transferrin is a negative acute-phase reactant). 1, 4
• TSAT 8.8% (markedly reduced, well below the 20% threshold). 1
• Ferritin 340 ng/mL (elevated due to acute-phase response). 1, 3

Management Approach

Primary Treatment

The cornerstone of management is aggressive treatment of the underlying enteric fever, as controlling inflammation will allow mobilization of sequestered iron stores. 1, 2

Iron Supplementation Decision

• Iron supplementation is NOT the primary intervention when ferritin > 100 µg/L with TSAT < 20% in the setting of acute inflammation. 1
• The sequestered iron will become available once the infection is controlled and hepcidin levels fall. 3
• If anemia persists after successful treatment of enteric fever and TSAT remains < 20%, reassess iron studies without inflammation present to determine if true iron deficiency exists. 1, 2

Monitoring Strategy

• Recheck complete blood count, iron studies, and inflammatory markers (CRP, ESR) after completing antibiotic therapy for enteric fever. 1
• If ferritin falls to 30–100 µg/L with persistent TSAT < 20% after inflammation resolves, this indicates true iron deficiency requiring supplementation. 1

Critical Pitfalls to Avoid

• Do not interpret the elevated ferritin as indicating adequate iron stores; ferritin > 100 µg/L in acute infection reflects inflammation, not iron repletion. 1, 5
• Do not start empiric iron supplementation based on low hemoglobin alone when ferritin is elevated and acute infection is present; iron will not be effectively utilized until inflammation resolves. 1, 3
• Do not rely on ferritin alone when inflammation is present; always calculate TSAT to assess functional iron availability. 1, 2
• Do not assume the anemia will self-correct; monitor hemoglobin response after treating the infection, as underlying iron deficiency may be unmasked once inflammation subsides. 1