Anaemia of Chronic Disorders (ACD) Lecture Notes PDF

Anaemia of chronic disorders (ACD) by Dr. Teeb M. Jaafar MBCh.B / F.I.C.M.S. (Path)  Topics Definition of anemia of chronic disorders. Causes Pathogenesis Laboratory investigation Differential diagnosis Peripheral blood sme...

Anaemia of chronic disorders (ACD) by Dr. Teeb M. Jaafar MBCh.B / F.I.C.M.S. (Path)  Topics Definition of anemia of chronic disorders. Causes Pathogenesis Laboratory investigation Differential diagnosis Peripheral blood smear and bone marrow study ESR and CRP comparison Treatment  Objectives At the end of the lecture you will be able to : Define anemia of chronic disorders and enumerate its causes. Explain its pathogenesis. Mention its important lab. Investigation. Differentiate between it and similar conditions. Enumerate the peripheral blood and bone marrow finding in each causative underlying disease. Compare between ESR and CRP. Summarize its treatment.  Anaemia of chronic disorders (ACD) Many of the anemias seen in clinical practice occur in patients with systemic disorders and are the result of a number of contributing factors. The anaemia of chronic disorders (ACD) is of central importance and occurs in patients with a variety of chronic inflammatory and malignant diseases. Usually, both the erythrocyte sedimentation rate (ESR) and C‐reactive protein (CRP) are raised. It may be complicated by additional hematological changes due to the disease such as anemias from other causes (e.g. iron or folate deficiency, bone marrow infiltration, hypersplenism or endocrine abnormality).  Causes Chronic inflammatory diseases  Infectious (e.g. pulmonary abscess, tuberculosis, osteomyelitis, pneumonia, bacterial endocarditis and some viral and parasitic infection)  Non‐infectious (e.g. rheumatoid arthritis, systemic lupus erythematosus and other connective tissue diseases, sarcoid, Crohn’s disease and liver cirrhosis) Malignant disease (e.g. carcinoma, lymphoma, sarcoma, myeloma). Chronic Renal failure. Chronic Liver diseases  Pathogenesis 1. Decreased release of iron from macrophages to plasma because of raised serum hepcidin levels: Hepcidin is a polypeptide produced by liver cells. It is the major hormonal regulator of iron homeostasis. It inhibits iron release from macrophages and from intestinal epithelial cells by its interaction with the transmembrane iron exporter, ferroportin. It accelerates degradation of ferroportin mRNA. Raised hepcidin levels therefore profoundly affect iron metabolism by reducing its absorption and release from macrophages. When iron stores are adequate or high, increased hepcidin expression inhibits: 1. intestinal iron absorption. 2. release of recycled iron from macrophages. 3. its transport across the placenta. Hepcidin synthesis is increased by: a. transferrin saturation. b. Inflammation. while hepcidin synthesis is reduced by: a. Increased erythropoiesis. b. Erythropoietin. c. Hypoxia. d. Matriptase. 2. Reduced red cell lifespan. 3. An inadequate erythropoietin response to anaemia caused by the effects of cytokines and tumor necrosis factor (TNF) on erythropoiesis : The plasma levels of various cytokines, especially interleukin (IL – 1& IL – 6) and tumor necrosis factor (TNF) are raised and reduce erythropoietin secretion.  Clinical features These patients usually presented with signs and symptoms of anemia (pallor, dizziness, tiredness, palpitation, etc.) in addition to signs and symptoms of the underlying disease.  Lab. Findings 1. Mild to moderate anaemia (hemoglobin rarely