1. Differentiate between absolute and functional iron deficiency in the context of ACD and IDA.
Absolute iron deficiency is when the stores of iron are depleted and bone marrow iron is absent, resulting in low serum ferritin and low transferrin saturation. Simple absolute iron deficiency usually results in iron deficiency anemia and can be resolved with iron supplementation. Functional iron deficiency results in anemia of chronic disease/inflammation, where infections, connective tissue disorders, or other diseases can cause inflammatory cytokines to be released. These inflammatory cytokines inhibit survival of erythroid progenitor cells, reduce EPO production, and cause excess hepcidin production, which decreases the amount of iron absorbed by enterocytes and blocks the release of iron stored in macrophages. In this case, the iron stores in the body are adequate, but are not being released for use, resulting in hypoferremia and creating a pathological basis for ACD.
2. Explain why transferrin levels in the blood are not increased in ACD patients, unlike in IDA patients.
Transferrin is a transport protein that is responsible for mediating the exchange of iron between tissues. Most of the iron transferred is derived from the iron stored in the macrophages and not from iron absorbed via the digestive tract. This affects transferrin levels in the blood in ACD because transferrin is a negative acute phase reactant. This means that during an infection or inflammation, the levels of transferrin in the blood decrease as the body tries to minimize the amount of iron accessible to pathogens and sequesters iron within macrophages. Also, most iron-bound transferrin is delivered to the bone marrow for erythropoiesis or tissues for storage, leaving the bloodstream. On the contrary in IDA, transferrin levels in the blood increase because the body is trying to accumulate iron by increasing the level of transferrin.