Anaemia of Chronic Disease (ACD) ; A Guide for Primary Care Clinicians

Anaemia of Chronic Disease (ACD) — also known as anaemia of inflammation — is the second most common type of anaemia after iron deficiency anaemia. It typically occurs in the context of:

Chronic infections (e.g. TB, HIV)
Inflammatory or autoimmune conditions (e.g. RA, SLE)
Malignancy
Chronic kidney disease (CKD)

Pathophysiology of Anaemia of Chronic Disease

Mechanism	Key Pathway	Clinical Impact
Iron dysregulation	↑IL-6 → ↑Hepcidin → ↓iron absorption (gut) + ↑iron sequestration (macrophages)	↓Serum iron, but normal or ↑ferritin
Suppressed erythropoiesis	↑TNF-α, ↑IL-1 → ↓EPO production + ↓bone marrow responsiveness	↓RBC production → normocytic or mild anaemia
Shortened RBC lifespan	Chronic inflammation → ↑RBC phagocytosis by macrophages	Contributes to anaemia
Impaired iron utilisation	Iron stores present but unavailable for erythropoiesis (functional deficiency)	↓Transferrin saturation (TSAT)

In ACD, chronic inflammation — through cytokines like interleukin-6 (IL-6) — stimulates the liver to produce hepcidin, a key regulator of iron homeostasis.

Hepcidin acts by:

Inhibiting ferroportin, the only known cellular iron exporter, found on enterocytes (gut), hepatocytes (liver), and macrophages.
This blocks iron absorption from the gut and prevents iron release from macrophages and liver stores.

As a result, iron becomes sequestered in storage sites, leading to low serum...

Try our Free Plan to get the full article.