Related Subjects:
| Alpha Thalassaemia
| Anaemia of Chronic Disease
| Acute Myeloblastic Leukaemia (AML)
π Anaemia of Chronic Disease (ACD), also called anaemia of inflammation, is one of the most common anaemias in hospitalised patients.
It is characterised by reduced haemoglobin levels despite normal or increased iron stores, due to impaired iron utilisation and blunted erythropoiesis.
π ACD typically accompanies chronic infections, autoimmune conditions, malignancy, or renal failure.
π§Ύ Aetiology
- Chronic inflammation diverts iron into storage sites, limiting its availability for red cell production.
- Inflammatory cytokines (especially IL-6) β hepcidin β blocks ferroportin β β intestinal iron absorption & β iron release from macrophages β "functional iron deficiency".
- Reduced responsiveness to erythropoietin β impaired erythropoiesis.
- Additional factors: erythrophagocytosis, bone marrow infiltration by tumour or infection.
π Causes
- Rheumatological: Rheumatoid arthritis, SLE, PMR, vasculitis, sarcoidosis.
- Infective: TB, osteomyelitis, HIV/AIDS, chronic viral, bacterial, fungal, protozoal infections.
- Gastrointestinal: Crohnβs disease, ulcerative colitis.
- Renal: Chronic kidney disease (reduced erythropoietin production).
- Oncological: Solid tumours, haematological malignancies.
- Cardiac: Chronic heart failure, endocarditis.
π§ͺ Investigations
- FBC: Hb β (usually normocytic/normochromic; can be microcytic), low reticulocyte count.
- Iron studies:
- Serum iron: β or normal
- TIBC: β (key discriminator from iron deficiency)
- Ferritin: normal or β (acute phase reactant)
- Bone marrow iron: β (stores present but not mobilised)
- Inflammatory markers: ESR and CRP β.
- Serum transferrin receptor: Normal (vs β in iron deficiency anaemia).
- Zinc protoporphyrin: β due to impaired haem synthesis.
βοΈ Management
- 1οΈβ£ Treat underlying cause: Control of infection, autoimmune disease, or malignancy often improves anaemia.
- 2οΈβ£ Exclude other causes: Always rule out coexistent iron deficiency anaemia.
- 3οΈβ£ ESAs: Erythropoiesis-stimulating agents (e.g. Epoetin alfa) in CKD or severe cases; usually combined with iron therapy.
- 4οΈβ£ Parenteral iron: Oral iron often ineffective (blocked absorption); IV iron can help in selected patients despite high ferritin.
- 5οΈβ£ Blood transfusion: Reserved for severe/symptomatic anaemia (Hb <8β9 g/dL).
π References
π§ββοΈ Case Examples β Anaemia of Chronic Disease (ACD)
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Case 1 (Rheumatoid Arthritis): π¦΄
A 62-year-old woman with long-standing rheumatoid arthritis presents with fatigue and pallor. Bloods show Hb 9.8 g/dL, MCV 86 fL, ferritin raised, serum iron low, and TIBC low.
Diagnosis: Anaemia of chronic disease secondary to chronic inflammation.
Management: Optimise RA control with DMARDs/biologics; no role for iron unless deficiency coexists. Monitor symptoms and haemoglobin.
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Case 2 (Chronic Kidney Disease): π
A 70-year-old man with CKD stage 4 reports increasing tiredness. FBC shows normocytic anaemia (Hb 9.5 g/dL). Ferritin is normal, transferrin saturation low, and reticulocyte count reduced.
Diagnosis: Anaemia of chronic disease due to reduced erythropoietin production in CKD.
Management: Exclude concurrent iron deficiency, then initiate erythropoiesis-stimulating agent (ESA) with iron supplementation if required.
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Case 3 (Malignancy β Lung Cancer): ποΈ
A 68-year-old man with non-small cell lung cancer undergoing chemotherapy presents with fatigue and pallor. Hb 8.9 g/dL, MCV 88 fL, ferritin raised, serum iron low, CRP elevated.
Diagnosis: Anaemia of chronic disease associated with malignancy and systemic inflammation.
Management: Treat underlying malignancy, consider blood transfusion for symptomatic relief, and avoid unnecessary iron therapy unless true deficiency is proven.