Have you heard of hemosiderin? What is hemosiderin? It is a yellow-gold or brown pigment with a granular or crystalline appearance derived from hemoglobin when there is more iron than necessary in the body. It consists of micellar aggregates of ferritin, whose function is to serve as an iron reservoir.
Hemosiderin is formed by the decomposition of hemoglobin into globin and the heme group. later into hemosiderin and biliverdin. It is detected by fresh staining with Prussian Blue.
Pathophysiology:
Hemosiderin deposits are present in the phagocytic cells of the spleen, liver, bone marrow, and lymph nodes. When blood levels are very high, it is an indicator of pathology. Its pathological deposit is hemosiderosis, either in organs or the lungs. It can be, in turn, localized or generalized.
When there is a local or general excess of iron, ferritin forms hemosiderin granules. Thus, hemosiderin corresponds to conglomerates of micelles with an amorphous constitution of ferritin. In many disease states, excess iron causes hemosiderin to accumulate in cells.
What causes hemosiderin?
A decrease in red blood cells or a greater rapidity due to blood loss, bleeding, or nutritional deficiency can cause iron deficiency anemia. The author addresses the iron cycle, its metabolism in humans, and the causes, symptoms, diagnosis, prevention, and treatment of iron deficiency anemia.
In general, the prevalence of iron deficiency anemia in women of childbearing age is 2%, in children from 2.5 to 5.7%, and in adult men and non-menstruating women, it is less than 0.4%.
Other groups susceptible to other types of anemia are strict vegetarians, mainly due to vitamin B12 deficiency, although they also have a certain risk due to iron deficiency. Although less frequently than iron (Fe), Folic acid deficiency can also cause anemia, especially during pregnancy and in premature infants. Due to its higher prevalence, we will focus on iron-deficiency anemia that causes hemosiderin.
How is hemosiderin formed?
Iron metabolism includes several important processes, such as regulation of intestinal iron absorption, transport of iron to cells, storage of iron, incorporation of iron into proteins, and recycling of iron after iron degradation.
The erythrocytes
Under normal conditions, as there is no active iron excretion mechanism, iron homeostasis is strictly controlled at the level of intestinal absorption. The average iron content in the body is 3-4 g, distributed in erythrocytes, macrophages of the reticuloendothelial system (RES), liver, bone marrow, muscles, and other tissues.
A dynamic balance is maintained by iron in the circulation between the various compartments: almost all of the iron released by the breakdown of hemoglobin (Hb) from senescent erythrocytes, about 20-25 mg/day, is reused, and only they lose 1-2 mg of iron per day, which must be replenished in the diet. That is when hemosiderin follows.
How to stop hemosiderin from taking place?
A normal balanced diet contains 5-6 mg of iron for every 1,000 Kcal, corresponding to a daily intake of 12-18 mg of total iron/day, of which 1-2 mg are absorbed. Although only a small proportion of dietary iron is absorbed, with considerable inter- and intra-individual differences observed, a balanced diet will provide the body with sufficient iron under normal circumstances. The increased demands for iron lead to increased absorption, but it hardly exceeds 3-5 mg of iron per day.
Iron can be classified as heme and non-heme iron. Heme iron in meat, fish, and poultry exhibits high bioavailability. Although it normally represents only a small fraction of the total iron content of foods, it contributes a considerable amount of absorbed iron. Up to 20-30% of dietary heme iron is absorbed, and its uptake is not affected by other dietary components. Non-heme iron is available in variable amounts in all plant-based foods and makes up the majority of dietary iron (often more than 90%). Its bioavailability is strongly affected by the presence of inhibiting or enhancing factors. Phytates (e.g., bran and seeds), oxalates (e.g., fruit and vegetables), polyphenols (e.g., tea), calcium, various dairy proteins, eggs, soy, and certain pharmaceuticals inhibit non-heme iron absorption. At the same time, muscle tissue (e.g., meat, fish, poultry) and vitamin C have a potentiating effect.
Therefore, the bioavailability of iron is estimated to be 15% in diets rich in vitamin C and animal protein, 10% in diets rich in cereals and vitamin C but low in animal protein, and 5% in diets rich in cereals and vitamin C but low in animal protein diets low in vitamin C and animal protein. If you take care of your diet and follow the above quotient, it is easy to keep hemosiderin at bay.
How iron storage and its use triggers hemosiderin
In healthy people, about 25% of total body iron (800-1,000 mg) represents iron from stores, main ferritin in the liver, spleen, and skeletal muscle. Ferritin is present in almost all cell types, and the small amounts of ferritin in serum are related to the amount of hepatic ferritin. As such, serum ferritin is an indicator of iron stores.
Ferritin is a cytosolic protein composed of 24 polypeptide chains arranged circularly around a polynuclear iron (III)-oxyhydroxide phosphate core. The core comprises a maximum of eight sub-units with a large surface area that allows rapid iron turnover. Sequestered iron is a non-toxic, redox-inactive form and is immediately available to meet the needs of cells.
Another storage protein, hemosiderin, appears to be derived from ferritin. Its structure has not yet been well defined, and iron availability is less than ferritin. Under physiological conditions, ferritin is the main iron storage protein, whereas hemosiderin accumulates only in small amounts in the spleen and RES cells. Under iron overload, especially in hereditary hemochromatosis and thalassemia, the proportion of iron stored increases.
Conclusion:
Hemosiderin is achieved after a hematological examination. For the diagnosis of iron deficiency anemia to be correct, it must be shown that there is a depletion of body iron stores.
In most cases, there is microcytosis. For the differential diagnosis of iron deficiency anemia and those secondary to a chronic inflammatory process, it is necessary to look at the ferritin values. In iron-deficiency anemias, it remains elevated until the reserves have been restored.
The transferrin saturation coefficient is decreased below 16%, indicating an insufficient iron supply to the erythroblasts. Once the iron deficiency is known, hemosiderin must be sought.
To treat hemosiderin, get in touch with USA Vein Clinics.
