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Immune activation and the anaemia associated with chronic inflammatory disorders
Author(s) -
Fuchs Dietmar,
Hausen Arno,
Reibnegger Gilbert,
Werner Ernst R.,
WernerFelmayer Gabriele,
Dierich Manfred P.,
Wachter Helmut
Publication year - 1991
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1991.tb00524.x
Subject(s) - erythropoietin , immune system , haematopoiesis , iron deficiency , bone marrow , immunology , erythropoiesis , inflammation , medicine , tumor necrosis factor alpha , anemia , hypoxia (environmental) , endocrinology , biology , stem cell , chemistry , genetics , organic chemistry , oxygen
Chronic inflammatory disorders are associated with an increased risk of patients developing anaemia. There is some evidence that cytokines released during cell‐mediated immune responses are capable of inhibiting bone marrow haematopoiesis. In vitro , interferon gamma and tumournecrosis factor alpha inhibit growth of erythroid precursor cells. The mode of action of these cytokines is probably associated with their antiproliferative capacity. Decrease of serum iron and increase of storage iron in patients appears to be a consequence of the defense strategy of macrophages during long‐lasting inflammatory disorders. Decreased serum iron correlates to decreased haemoglobin concentrations. In view of this, the development of anaemia seems likely to result from the altered iron metabolism induced by stimulated macrophages. Low haemoglobin levels and associated hypoxia up‐regulate the release of erythropoietin, which can explain why increased circulating erythropoietin is usually found in patients with anaemia.