The pathogenesis of anemia of chronic disorders

Anemia of chronic diseases (ACD) has a complex etiopathogenesis that presents itself during the course of infective, immune and neoplastic pathologies. Rheumatoid arthritis (RA) is often considered to be a prototypic disease of ACD. This type of anemia is characterized by a slight or moderate normochromic-normocytic anemia with hemoglobin 9-11 g/dL, complete blood count 30-40% and by normal or slightly lower than normal reticulocyte count. Biochemical parameters show a reduction in serum iron (essential for a diagnosis of ACD), low transferrin saturation and a decrease in total iron binding capacity, in contrast to true iron deficiency in which there is an increase in total iron binding capacity. Furthermore, increased ferritin confirms that, in spite of the hyposideremia, the organic iron reserve is normal or higher than normal. Bone marrow cellularity is, on the whole, normal with scarse or a complete lack of erythroblastic hyperplasia. Non-hemoglobin iron staining (Perls reaction) shows a sharp reduction in normal values and an increase in macrophages containing hemosiderin. In patients with ACD, and in particular in female patients of child-bearing age or in cases with true iron deficiency (hemhorrage, reduced dietary intake or malabsorption of iron), a true hypochromic microcytic anemia is sometimes established. Anemia in rheumatoid arthritis (RA) correlates with the degree of disease activity but not disease duration. (1) The different mechanisms that determine ACD have still not been completely defined. However, these have been thought to be an alteration in iron metabolism, a slight reduction in the average erythrocyte age and in a modified proliferative response in the bone marrow erythroid compartment. (2)