Guidelines for Complications of Cancer Treatment Vol VIII Part B

system. There is an upregulation of specific inflammatorycytokines such as interleukin-1 (IL-1), gamma interferon (IFN-) and tumor necrosis factor alpha (TNF- ) which causedecreased differentiation of erythroid precursors, interferencewith normal iron utilization and inhibition of normal hypoxiadrivenEPO production [4,5] . Renal impairment, caused bynephrotoxic agents and a blunted response EPO response toanemia in cancer patients further compound the problem. [6-8]Chronic anemia in some cancer patients may be exacerbatedby an anemia-inducing factor, generated by tumor cells, whichcauses a diminished erythrocyte life span. [9,10] .Absolute or functional iron deficiency is another factor in theaetio-pathogenesis of anemia in cancer patients. (11) Absoluteiron deficiency (ID), defined by the exhaustion of iron storesin macrophages and hepatocytes, is reflected in the serumferritin values (40 to 100 ng /ml). However, despite this irondeficient erythropoiesis may still occur or paradoxically mayeven be elevated. This is called functional ID, defined as animbalance between iron needs in the bone marrow and ironsupply by macrophages. Common causes for absolute irondeficiency in cancer patients include poor dietary iron,compromised oral intake and blood loss. Altered ironhomeostasis by the over expressed cytokines interfere withthe iron homeostasis by trapping iron within macrophagesmaking it unavailable for utilization. Blunted response of theerythroid progenitors to the erythropoietin also adds to thefunctional iron deficiency in cancer patients. (12)Diagnosis of CIASerum ferritin, although useful for diagnosing absolute irondeficiency, may not be a reliable indicator of iron stores incancer patients on recombinant human erythropoietin(rHuEPO). Serum ferritin increases with inflammation, andhigh levels may be seen in patients with ACD and cancer. The479