Evaluation of Serum Markers of Iron Metabolism in Patients with chronic Liver Disease

Abstract

ron is essential for most living organisms. In an unbound state, however, it is highly reactive and leads to oxidative stress. Thus, iron is coupled to transferrin in serum, whereas it is stored in a ferritin-bound form in tissue. Small amounts of ferritin are load. Circulating iron constitutes a small, but highly dynamic iron transit compartment that becomes rapidly altered in disease states and increased serum iron load leads to emergence of the highly reactive non-transferrin bound iron (NTBI). The liver is a critical controller of iron metabolism as it represents a large iron storage compartment and a major producer of ferritin, transferrin and hepcidin. In chronic liver disease, low concentrations of hepcidin, which blocks the absorption of iron from the intestine and the release of iron from macrophages, contribute to parenchymal iron overload, whereas increased hepcidin concentrations, as observed during chronic inflammation, lead to the sequestration of iron within macrophages thereby promoting anaemia. As a negative acute phase protein, transferrin is downregulated during episodes of acute inflammation and in advanced liver disease, whereas the acute phase protein ferritin also serves as a surrogate of hepatocellular damage.