Ferritin is important in iron homeostasis. It is the main iron-storage protein, composed of two partially homologous subunits, heavy and light chains. Ferritin molecules in cells containing high levels of iron tend to be rich in light chains, and may have a long-term storage function, whereas heavy-rich ferritins are more active in iron metabolism (1-2). Mutations in the ferritin gene cause the hereditary hyperferritinemia-cataract syndrome and neuroferritinopathy, associated with inflammation. Elevated levels of ferritin are reported as characteristic of adult-onset Still's disease and hemophagocytic syndrome, also associated with inflammation (3). Microfilaments and increased levels of exogenous ferritin are excreted directly into the bile by way of a second microfilament-independent, chloroquine-insensitive pathway, supporting a possible physiological mechanism for the release of ferritin from the liver (4).

WB, IHC