Anemia of Chronic Diseases: Wider Diagnostics-Better Treatment?

Abstract

Anemia of chronic diseases is a condition that accompanies a specific underlying disease, in which there is a decrease in hemoglobin, hematocrit and erythrocyte counts due to a complex process, usually initiated by cellular immunity mechanisms and pro-inflammatory cytokines and hepcidin. This is the second most common type of anemia after iron deficiency anemia in the world. Its severity generally correlates with the severity of the underlying disease. This disease most often coexists with chronic inflammation, autoimmune diseases, cancer, and kidney failure. Before starting treatment, one should undertake in-depth diagnostics, which includes not only assessment of complete blood count and biochemical parameters, but also severity of the underlying disease. The differential diagnosis of anemia of chronic diseases is primarily based on the exclusion of other types of anemia, in particular iron deficiency. The main features of anemia of chronic diseases include mild to moderate lowering of hemoglobin level, decreased percentage of reticulocyte count, low iron and transferrin concentration, but increased ferritin. Due to the increasingly better knowledge of the pathomechanism of chronic diseases and cancer biology, the diagnosis of this anemia is constantly expanding with new biochemical indicators. These include: the concentration of other hematopoietic factors (folic acid, vitamin B₁₂), hepcidin, creatinine and erythropoietin. The basic form of treatment of anemia of chronic diseases remains supplementation with iron, folic acid and vitamin B₁₂ as well as a diet rich in the above-mentioned hematopoietic factors. The route of administration (oral, intramuscular or intravenous) requires careful consideration of the benefits and possible side effects, and assessment of the patient's clinical status. New methods of treating both the underlying disease and anemia are raising hopes. The novel methods are associated not only with supplementing deficiencies, but also with the administration of drugs molecularly targeted to specific proteins or receptors involved in the development of anemia of chronic diseases.

Keywords: anemia; biochemical parameters; erythropoiesis; hematological parameters; iron homeostasis; iron supplementation; nutrition; oxidative stress.

Figure 1

Fe³⁺ ions with food reach the stomach, where with the participation of hydrochloric acid and then (in duodenum) with ferric reductase enzyme (DCYTB) are transformed into Fe2+ ions. Bile secreted by the liver stabilizes iron by inhibiting its precipitation in the form of oxides. Thanks to DMT1 protein (divalent metal transporter 1), iron passes into the enterocyte and then it is released into the blood by ferroportin. Hepcidin produced by the liver limits the release of iron from enterocytes into the blood by binding to ferroportin. The divalent iron released into the blood is reoxidized with the contribution of hephaestin and ceruloplasmin to a trivalent ion, which, when combined with apotransferrin, forms transferrin and reaches the erythroblasts in the bone marrow.

Figure 2

Treatment of anemia of chronic diseases.