Diagnose der Rheuma-Anämie

Anaemia of chronic disease is frequently accompanied by marked disturbances in iron metabolism driven, to a large part, by liver-derived hepcidin. Typically, there is reduced iron resorption from the intestine as well as increased uptake and retention of iron within cells of the reticuloendothelial system, resulting in a diversion of iron from the circulation to storage sites with a subsequent lack of iron for red progenitor cells and iron-deficient erythropoesis. In addition, gastrointestinal blood loss may aggravate the availability of iron. By using biochemical markers and special red blood cell indices, all three compartments of iron metabolism can be readily monitored. Serum ferritin represents storage iron, whereas the transferrin saturation (TSAT) is a measure for the amount of iron bound to transferrin. Determination of red cell indices such as% hypochromic erythrocytes or reticulocyte hemoglobin (CHr) or the soluble transferrin receptor (sTfR) provides direct information on iron availability for erythropoesis. An absolute iron deficiency is characterised by a serum ferritin<30 μg/L and reduced haemoglobin levels (iron deficiency anaemia). A latent iron deficiency is characterised by reduced iron stores with still normal haemoglobin values. Patients suffering from chronic inflammation might become anaemic (Hb reduced) in the presence of adequate iron stores (ferritin normal), due to hepcidin-mediated retention of iron in the reticuloendothelial system and subsequent iron-deficient erythropoesis. Iron-restricted blood formation may also occur during epoetin treatment, when the pharmacologically stimulated erythropoesis needs more iron than transferrin (low TSAT) is able to deliver to the bone marrow. Both scenarios would ultimately lead to iron-deficient erythropoesis, which is also called functional iron deficiency. Normally it is not necessary to determine all iron parameters in each and every case. The simultaneous evaluation of storage iron (ferritin) and iron availability to the bone marrow (% hypochromic red cells, CHr or sTfR) appears to be a rational first step to characterise complex disturbancies of iron homeostasis.