Diagnosis of iron-deficient states

Abstract

The diagnosis of iron deficiency anemia is typically straightforward, especially when classic biochemical and hematological changes are present in a subject at risk. It can be challenging in the presence of diseases or when it is due to inherited defects of iron metabolism. The identification of iron deficiency prior to anemia development is also difficult. New hematological parameters such as reticulocyte Hb content have expanded the classic ones such as MCV, MCH and MCHC. A variety of hematology analyzers now provide novel parameters to assess cellular hypochromia and microcytosis in both reticulocytes and mature red blood cells. The repertoire of biochemical markers has also been expanded, with iron, transferrin and ferritin being supplemented by circulating transferrin receptor and hepcidin. Molecular identification of functional variants of key iron metabolism determinants has provided explanations for the heritability of some iron metabolism biomarkers. Genetic defects in some of these molecules are responsible for hereditary microcytic anemias, also called atypical microcytic anemias. In this review, we examine the most significant hematological and biochemical markers for iron metabolism, as well as relevant genetic polymorphisms and defects affecting iron handling.

Lower mean corpuscular hemoglobin concentration is associated with poorer outcomes in intensive care unit admitted patients with acute myocardial infarction

“…Increased inflammatory markers, such as CRP, predict poor prognosis of AMI (29,30), and anti-inflammatory agents such as corticosteroid can decrease mortality in AMI patients (31). Inflammatory response may lead to iron deficiency (32,33), which decrease MCHC (34). Therefore, similar to RDW (35), MCHC can be regarded as an inflammatory marker and thus can affect the prognosis after AMI.…”

Positive Iron Balance in Chronic Kidney Disease: How Much is Too Much and How to Tell?

“…As an acute phase reactant, serum ferritin levels are increased in the setting of inflammation (as is often observed in CKD). Serum ferritin levels can also be impacted by sex, age, race/ethnicity, infection, malignancy, hyperthyroidism, liver disease, ascorbic acid status, and heavy alcohol intake [30, 31]. Thus, serum ferritin concentrations should not be used as the sole factor guiding iron therapy [32, 54].…”

“…As a negative acute phase reactant, transferrin levels are reduced by inflammation [70]. Transferrin levels, and by extension TSAT, can therefore also be impacted by infection, malignancy, progesterone, and recent iron intake [30]. TSAT should be measured in the morning after ≥8 h of fasting to reduce the impact of diurnal variation, and at least 1 week after high-dose IV iron to avoid spurious elevations [30, 71].…”

“…In the setting of normal total body iron stores, increased iron demands can still result in a supply-demand mismatch. The result is functional iron deficiency, a state of inadequate delivery of iron to the bone marrow in the setting of adequate iron stores caused by impaired iron mobilization (from the reticuloendothelial system [RES]) and/or increased bone marrow iron demand (as might be secondary to reduced red cell life span and/or erythropoiesis-stimulating agents [ESA] use) [4, 7, 30]. Even among patients with increased total body iron, reduced iron availability can result in functional iron deficiency.…”

“…Transferrin levels, and by extension TSAT, can therefore also be impacted by infection, malignancy, progesterone, and recent iron intake [30]. TSAT should be measured in the morning after ≥8 h of fasting to reduce the impact of diurnal variation, and at least 1 week after high-dose IV iron to avoid spurious elevations [30, 71]. Although current guidelines do not recommend initiating IV iron when TSAT >30%, there is some evidence that targeting TSAT >30% (and <50%) can reduce ESA usage by increasing “responsiveness” to erythropoiesis [72].…”