Ferritin
Your iron storage protein — and an inflammation alarm in disguise
A low ferritin is diagnostic of iron deficiency — the only reason it falls. But a high ferritin tells a different story: it's an acute-phase reactant that rises sharply with inflammation, liver disease, and several serious systemic conditions entirely unrelated to iron.
Ferritin is the body's primary iron storage protein — a hollow spherical cage that stores up to 4,500 iron atoms. Serum ferritin correlates closely with iron stores under normal conditions. However, ferritin is also an acute-phase reactant: inflammation, liver disease, and malignancy dramatically elevate it independent of iron status. A low ferritin always means iron deficiency; an elevated ferritin requires clinical context to interpret.
Reference Ranges
How clinicians interpret Ferritin (Serum) results — from optimal to concerning.
⚠ Reference ranges vary by laboratory and assay. Always interpret your result in context of your laboratory's own reference intervals and your clinical presentation.
What raises Ferritin (Serum)
IL-1, IL-6, TNF all increase ferritin synthesis — normal ferritin can hide iron deficiency in inflamed patients.
Hepatocytes are the primary source — alcoholic hepatitis, NAFLD, hepatitis B/C cause ferritin up to 10,000 µg/L.
Progressive iron loading — ferritin > 1,000 with transferrin saturation > 45% is the hallmark.
Lymphoma, leukaemia, MDS — ferritin > 5,000 via macrophage activation and cellular necrosis.
Ferritin > 10,000 µg/L (often > 50,000) is a diagnostic criterion for this macrophage activation emergency.
What lowers Ferritin (Serum)
A low ferritin always means iron deficiency — it cannot be masked by inflammation.
Rises 10–15 µg/L per month of adequate oral iron. Continue until ferritin > 50 µg/L, not just until Hgb normalises.
In haemochromatosis, weekly venesection reduces ferritin by 30–50 µg/L per session. Target 50–100 µg/L.
Conditions this biomarker signals
When Ferritin (Serum) is outside normal range, these are the most clinically significant possibilities.
Ferritin < 30 is diagnostic — even with normal Hgb. Sensitivity falls in concurrent inflammation; add transferrin saturation.
Ferritin > 300 men / > 200 women with transferrin saturation > 45% triggers HFE C282Y genetic testing.
Ferritin > 10,000 in a febrile patient with cytopenias and hepatosplenomegaly = HLH until proved otherwise. ICU emergency.
Normal or elevated ferritin with low iron saturation — iron trapped in macrophages by hepcidin. Treat underlying disease.
Which tests measure this biomarker
Ferritin (Serum) may be included in or ordered alongside these panels.
Always interpret ferritin alongside transferrin saturation for complete iron status.
The dual identity of ferritin: iron store and acute-phase reactant
Hepcidin, the master iron regulator, creates ferritin's diagnostic trap. Inflammation raises hepcidin via IL-6, locking iron inside macrophage ferritin — simultaneously causing anaemia of chronic disease and inflating the serum ferritin reading. A patient with both iron deficiency and active inflammation can have ferritin in the "normal" range while genuinely iron-depleted. Each ferritin molecule stores up to 4,500 iron atoms — oxidising ferrous iron (Fe²⁺, toxic) to ferric iron (Fe³⁺, safe) via intrinsic ferroxidase activity.
Each ferritin cage stores up to 4,500 iron atoms
Ferritin is a 24-subunit hollow protein shell (apoferritin). Iron enters through specific channels and is oxidised from Fe²⁺ to Fe³⁺ before storage. Free Fe²⁺ generates hydroxyl radicals via the Fenton reaction — causing oxidative cell damage. Ferritin's storage function is, at its core, a toxicity-prevention mechanism.
Hepcidin controls the ferritin-iron relationship
Hepcidin from the liver binds ferroportin (the cellular iron exporter) causing its degradation — trapping iron inside macrophages. In inflammation, IL-6 drives hepcidin surge, locking iron in cells and elevating serum ferritin while reducing availability for erythropoiesis. This is why treating the underlying condition matters more than giving iron in anaemia of chronic disease.
L-ferritin stores; H-ferritin protects
L-chains (liver/spleen) are primarily storage ferritin. H-chains (heart/brain) have ferroxidase activity protecting against iron toxicity. Serum ferritin is predominantly L-chain and reflects hepatic iron stores. Measuring the H-chain:L-chain ratio can help distinguish iron-loading from inflammatory ferritin elevation.
Clinical use — when and why this is ordered
How clinicians use Ferritin (Serum) in practice — the real-world scenarios where it changes decisions.
Iron deficiency screening
Ferritin < 30 µg/L diagnoses iron deficiency. In symptomatic patients (fatigue, pica, restless legs), treat at ferritin < 50 regardless of Hgb.
Haemochromatosis monitoring
Monthly phlebotomy until ferritin < 50 µg/L, then maintenance every 3–4 months. Ferritin guides frequency, not just diagnosis.
Hyperferritinaemia workup
Ferritin > 1,000 without clear infection or haematological cause triggers workup for adult-onset Still's disease, HLH, and lymphoma.
CKD anaemia (pre-EPO treatment)
KDIGO guidelines target ferritin > 200 µg/L in dialysis patients before EPO — iron must be replete for EPO to work.