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Hemosiderin

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Iron-storage complex
This articleneeds morereliable medical references forverification or relies too heavily onprimary sources. Please review the contents of the article andadd the appropriate references if you can. Unsourced or poorly sourced material may be challenged andremoved.Find sources: "Hemosiderin" – news ·newspapers ·books ·scholar ·JSTOR(November 2021)
Histopathology of a case of chronic pulmonary congestion, showing interstitium with hemosiderin deposition (black arrow), edema and collagenous thickening. The alveolus contains asiderophage (white arrow, characterized by coarse brown pigment, which is slightly refractile).
Hemosiderin image of a kidney viewed under a microscope. The brown areas represent hemosiderin

Hemosiderin orhaemosiderin is aniron-storage complex that is composed of partially digested ferritin andlysosomes. The breakdown ofheme gives rise tobiliverdin and iron.[1][2] The body then traps the released iron and stores it as hemosiderin in tissues.[3] Hemosiderin is also generated from the abnormal metabolic pathway offerritin.[3]

It is only found within cells (as opposed to circulating in blood) and appears to be a complex offerritin, denatured ferritin and other material.[4][5] The iron within deposits of hemosiderin is very poorly available to supply iron when needed. Hemosiderin can be identified histologically withPerls' Prussian blue stain; iron in hemosiderin turns blue to black when exposed to potassium ferrocyanide.[6] In normal animals, hemosiderin deposits are small and commonly inapparent without special stains. Excessive accumulation of hemosiderin is usually detected within cells of themononuclear phagocyte system (MPS) or occasionally withinepithelial cells of the liver and kidney.

Several disease processes result in deposition of larger amounts of hemosiderin in tissues; although these deposits often cause no symptoms, they can lead toorgan damage.

Hemosiderin is most commonly found inmacrophages and is especially abundant in situations followinghemorrhage, suggesting that its formation may be related tophagocytosis ofred blood cells andhemoglobin. Hemosiderin can accumulate in differentorgans in variousdiseases.

Iron is required by many of thechemical reactions (i.e., oxidation-reduction reactions) in the body but istoxic when not properly contained. Thus, many methods of iron storage have developed.

Pathophysiology

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Hemosiderin often forms after bleeding (haemorrhage).[7] When blood leaves a ruptured blood vessel, thered blood cell dies, and the hemoglobin of the cell is released into the extracellular space. Phagocytic cells (of themononuclear phagocyte system) called macrophages engulf (phagocytose) the hemoglobin to degrade it, producing hemosiderin andbiliverdin. Excessive systemic accumulations of hemosiderin may occur in macrophages in the liver, lungs, spleen, kidneys, lymph nodes, and bone marrow. These accumulations may be caused by excessive red blood cell destruction (haemolysis), excessive iron uptake/hyperferraemia, or decreased iron utilization (e.g., anaemia of copper toxicity) uptake hypoferraemia (which often leads to iron deficiency anemia).

Cellular iron is found as either ferritin or hemosiderin. It is identified in cells by the Perls or Prussian blue reaction, in which ionic iron reacts with acid ferrocyanide to impart a blue color.<Wintrobe's Clinical Hematology>

Diseases associated with hemosiderin deposition

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Main article:Hemosiderosis

Hemosiderin may deposit in diseases associated with iron overload.[8] These diseases are typically diseases in which chronic blood loss requires frequentblood transfusions, such assickle cell anemia andthalassemia.

References

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  1. ^"Hemosiderin".Definition, Staining, Function and Treatment. 2019-05-04. Retrieved2019-05-04.
  2. ^Kalakonda, Aditya; John, Savio (2018-10-27)."Physiology, Bilirubin".NCBI Bookshelf.PMID 29261920. Retrieved2019-05-04.
  3. ^abLitwack, Gerald (2018). "Micronutrients (Metals and Iodine)".Human Biochemistry. Elsevier. pp. 591–643.doi:10.1016/b978-0-12-383864-3.00019-3.ISBN 978-0-12-383864-3.S2CID 90250940.
  4. ^Richter, Goetz (1 August 1957)."A Study of Hemosiderosis with Aid of Electron Microscopy".The Journal of Experimental Medicine.106 (2):203–218.doi:10.1084/jem.106.2.203.PMC 2136742.PMID 13449232.
  5. ^Fischbach, FA; Gregory, DW; Harrison, PM; Hoy, TG; Williams, JM (December 1971). "On the structure of hemosiderin and its relationship to ferritin".Journal of Ultrastructure Research.37 (5):495–503.doi:10.1016/S0022-5320(71)80020-5.PMID 5136270.
  6. ^Kumar, Abbas, Aster, Vinay, Abul K., Jon C. (2015).Robbins & Cotran Pathologic Basis of Disease, 9th Edition. Elsevier. p. 650.ISBN 978-1-4557-2613-4.{{cite book}}: CS1 maint: multiple names: authors list (link)
  7. ^"Forensic Pathology".
  8. ^"Hereditary haemochromatosis through 150 years".Tidsskrift for den Norske Legeforening. Retrieved2018-07-14.
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