Transcription
Hey, welcome back. Now let's talk about iron studies. In the previous video, we have talked about iron absorption. You cannot understand it without the previous video, so please go ahead and watch our previous video about iron absorption. Okay.
Of course, we're talking about anemia: tired and pale, pale and tired. Sometimes I have a murmur; sometimes I can get angina. Okay, let's go. First, ferritin. We've said before that ferritin is this storage protein that binds iron; iron protein ferritin; storage protein that binds iron. Okay. Ferritin is in the macrophages of the bone marrow, also in the liver. Remember, ferritin is synthesized in greater quantities in case of inflammation, why? Due to interleukin 6. What's the function of ferritin? It keeps iron in a bound form, in a non-toxic form, because iron, if left free, will lead to the Fenton reaction, as we've said in the previous video. It's stored in the macrophages of the bone marrow, again, degraded by lysosomes to give us hemosiderin. And hemosiderin is stained blue by the Prussian blue; stained blue with blue. Okay. For ferritin, there is a correlation between ferritin here in the serum and ferritin stored in the macrophages. So, one microgram of ferritin correlates with eight milligrams of stored iron. Remember that. Ferritin is decreased in iron deficiency, of course. If I, I cannot store iron, because where does the storage come from? From the iron itself. And increased in iron overload diseases, such as sideroblastic anemia, such as hemochromatosis, and also in any chronic disease, because we'll discuss later that in any chronic disease, I have iron that I cannot use. Why? It's bound to the ferritin, and it's kept in store.
Next, we have the serum iron; we're in the plasma. Okay. So, the iron in the plasma will be carried on transferrin. I cannot leave iron free due to the Fenton reaction. Perfect. So, RBCs, senescent RBCs, get destructed; macrophage; iron; iron bound to transferrin. Okay. Transferrin carries the iron to the storage ferritin, the storage protein. So that's the story of iron. We have senescent RBCs give us hemoglobin; heme and globin; and the heme has iron and protoporphyrin; iron; macrophage; iron in the plasma bound to transferrin; stored as ferritin. Serum iron, of course, is decreasing in deficiency anemia. There is, I'm not getting iron, so there is no iron in the plasma. Also, in anemia of chronic disease, that serum iron is low, as we said. I mean, if chronic disease, I have iron that is stored as ferritin but not available in the plasma, in the blood. So, the serum iron will be low in anemia of chronic disease, and we will discuss anemia of chronic disease later. Also, serum iron is increasing in iron overload diseases, such as hemochromatosis, sideroblastic anemia. That's fine.
Or else, serum total iron-binding capacity, or TIBC. TIBC is basically the transferrin, the protein that carries iron: ferrous or ferric. Okay. Transferrin carries the ferric; transferrin carries the ferric. Okay. Where does TIBC, or transferrin, come from? It's synthesized in the liver, of course. Okay. The iron on the transferrin, where does it come from? From macrophages in the bone marrow or from the duodenum absorption. Transferrin carries that iron, and this iron will be carried to erythroid precursors to form what? RBCs. Perfect. Remember, there is an inverse relation between ferritin and transferrin. Whenever ferritin increases, transferrin decreases; whenever ferritin decreases, transferrin increases. Please remember that.
Next, we have the iron saturation percentage, aka transferrin saturation. Percent saturation is, okay, how many receptors, or how many positions on the transferrin, are occupied by iron? In other words, iron over the transferrin. And we have said that transferrin is the same as the TIBC. So let's say that this transferrin, okay, has one-third of it occupied by iron; there will be 33% saturated. Okay. If the transferrin has everything, like this, iron in all locations, will be 100% saturation. This is not normal; this is not natural. Normally, we have 33%; only one-third of the transferrin is occupied by iron. The percent saturation is decreasing in iron deficiencies, in anemia, why? Because iron is low; low in iron deficiency anemia. Okay. That percent saturation is increased in case of iron overload, why? Because the iron will be high. Okay, pretty simple. Okay, that's it. But there is one more thing; it's called the soluble transferrin receptor concentration, or sTfR. So, its main purpose is to differentiate between iron deficiency anemia and anemia of chronic disease. The sTfR is increased in iron deficiency anemia and normal in anemia of chronic disease. Think, think about that. As transferrin, or TIBC, it's increased in iron deficiency anemia, but TIBC is low in anemia of chronic disease. However, that receptor concentration is normal. So just remember, sTfR is increased in iron deficiency anemia, and you will be fine. And I'll see you next video.