| Condition (examples) | Pattern | Management implications |
Iron overload - Hereditary hemochromatosis
- Transfusional iron overload
- Ineffective erythropoiesis (eg, thalassemia)
| Progressive/cumulative increase in ferritin over time, eventually causing organ damage if not treated. TSAT will be high (typical value >45%). | Close monitoring with iron removal once there is evidence of excess tissue deposition (from MRI or tissue biopsy) or the ferritin level exceeds a certain threshold (eg, >1000 ng/mL). Phlebotomy is often used in individuals without anemia; iron chelation is generally used for individuals with anemia. |
| Massive cell/tissue death | Rapid rise in ferritin to very high levels (eg, >3000 ng/mL), usually in the setting of acute illness with immune dysregulation. TSAT will not be increased (typical value <45%). | Aggressive therapy for the underlying condition is usually indicated. Ferritin level may be a useful marker of disease activity. |
Inflammatory block - Anemia of chronic disease/anemia of inflammation (ACD/AI, as in diabetes, cancer, chronic infection, or autoimmune disorders)
- Anemia of chronic kidney disease
- Chronic liver disease
| Chronic, modest increase in ferritin (approximately two to three times normal). Ferritin is an acute phase reactant. TSAT will not be increased (typical value <45%). | May be helpful in distinguishing ACD/AI from iron deficiency, but ferritin by itself is a poor indicator of iron stores in the setting of chronic inflammation. A search for the cause may be indicated if not immediately apparent. Therapy is directed to the underlying condition. |
