Anemia of Chronic Disease: Pathophysiology and Laboratory Diagnosis

Abstract

Classic iron deficiency (ID) does not represent a challenge for the laboratory and physicians. The anemia that accompanies infection, inflammation, and cancer, commonly termed anemia of chronic disease (ACD), features apparently normal or increased iron stores. However, 20% of these patients have iron-restricted erythropoiesis (functional ID), an imbalance between the iron requirements of the erythroid marrow and the actual iron supply. Functional ID leads to a reduction in red cell hemoglobiniza-tion, causing hypochromic microcytic anemia. The diagnosis of functional ID in real time is based on measuring the hemoglobin content of reticulocytes. An examination of the biochemical markers of iron metabolism demonstrates weaknesses in the diagnosis of functional ID. We developed a diagnostic plot for the assessment of iron status in ACD and the detection of advancing ID in patients with ID, ACD, and the combined state of functional ID and ACD. The plot indicates the correlation between a marker of the iron supply for erythropoiesis (ie, the ratio of the soluble transferrin receptor value to the logarithm of the ferritin value) and the reticulocyte hemoglobin content and functions as a marker of iron demand. The diagnostic plot shows good selectivity for assessing the iron status of disease-specific anemias such as classic ID, end-stage renal failure, cancer-related anemia, and the anemia of infection and inflammation. The therapeutic implications of the diagnostic plot are to differentiate patients who should be administered oral iron supplements, recombinant human erythropoietin (r-HuEPO), or a combination of r-HuEPO and iron. The response of erythropoiesis to r-HuEPO depends on the iron supply and the proliferation of erythropoiesis. The lack of an increase or a decrease in reticulocyte hemoglobin levels indicates a nonresponder to r-HuEPO or functional ID.

Two Years Profile of Anemia in Systemic Lupus Erythematosus Patients at West Java’s Top Referral Hospital, Indonesia

“…Portillo et al 13 reported most patients with chronic disease in Spain have normocytic normochromic anemia, while Thomas et al 14 stated that iron deficiency causes microcytic hypochromic anemia to patients in Germany. 13,14 Nevertheless, it is not uncommon for anemia in SLE to manifest due to both chronic disease and IDA simultaneously. 5 This study also revealed that most subjects had either moderate anemia (50%) or mild anemia (42%).…”

Regulation of iron homeostasis in anemia of chronic disease and iron deficiency anemia: diagnostic and therapeutic implications

“…It is important to distinguish between ACD and ACD/IDA to appropriately guide therapeutic regimens, especially in respect to iron repletion strategies. 7,27 We used a rat model of inflammation-associated chronic anemia to investigate the regulation of body iron homeostasis in ACD. We observed increased expression of the iron storage protein ferritin in the spleen but not in the liver, a finding in accordance with previous data demonstrating divergent ferroportin regulation by hepcidin in duodenum and liver.…”

Mat á járnbúskap með mælingu á transferrínviðtökum

“…Tómasartaflan hefur þann kost að geta greint á milli starfraens járnskorts, það er ófullnaegjandi framboðs á járni til rauðkornskímfrumna þó að járnbirgðir séu naegar, og raunverulegs járnskorts og hún getur komið að gagni við val á meðferð við blóðleysi og við mat á árangri af þeirri meðferð. [6][7][8] CHr laekkar við járnskort eins og MCV en mun hraðar og eykst aftur í eðlilegt gildi á örfáum dögum þegar rauðkornskímfrumurnar fá aftur naegt járn. 9 sTfRferritín-vísir hefur verið talinn betri maelikvarði á járnhag en sTfR.…”

“…[6][7][8] Árangur af járngjöf getur komið fram í því að CHr eykst og/eða að sTfRferritín-vísir laekkar þannig að hnit sjúklingsins hliðrast upp á við og/eða til vinsri á mynd 1, jafnvel á milli flokka og flytjast þá í flokk með haerra CHr eða laegri sTfR-ferritín-vísi. Ef hnit sjúklings sem faer epóetín hliðrast í gagnstaeða átt getur það bent til þess að starfraenn járnskortur sé til staðar og þá gaeti betri árangur fengist með því að auka járngjöf eða baeta henni við meðferðina.…”

“…Sé niðurstaðan >28 pg virðist járnskortur ekki vera orsök blóð-leysis. [6][7][8] Ef CHr er 21-28 pg gaeti Tómasartafla komið að gagni við að greina á milli starfraens og raunverulegs járnskorts. Einnig maetti gefa járn og maela CHr aftur eftir til daemis 2-4 daga eftir járngjöf í aeð eða 1-2 vikur eftir járngjöf um munn.…”