请输入您要查询的百科知识:

 

词条 Hemosiderin
释义

  1. Pathophysiology

  2. Diseases associated with hemosiderin deposition

  3. References

{{Multiple issues|{{expert-subject|date=September 2010}}{{refimprove|date=September 2010}}{{disputed|date=September 2010}}
}}

Hemosiderin or haemosiderin is an iron-storage complex. It is only found within cells (as opposed to circulating in blood) and appears to be a complex of ferritin, denatured ferritin and other material.[1][2] The iron within deposits of hemosiderin is very poorly available to supply iron when needed. Hemosiderin can be identified histologically with Perls' Prussian-blue stain; iron in hemosiderin turns blue to black when exposed to potassium ferrocyanide[3]. In normal animals, hemosiderin deposits are small and commonly inapparent without special stains. Excessive accumulation of hemosiderin is usually detected within cells of the mononuclear phagocyte system (MPS) or occasionally within epithelial cells of 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 to organ damage.

Hemosiderin is most commonly found in macrophages and is especially abundant in situations following hemorrhage, suggesting that its formation may be related to phagocytosis of red blood cells and hemoglobin. Hemosiderin can accumulate in different organs in various diseases.

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

Pathophysiology

Hemosiderin often forms after bleeding (haemorrhage).[4] When blood leaves a ruptured blood vessel, the red blood cell dies, and the hemoglobin of the cell is released into the extracellular space. Phagocytic cells (of the mononuclear phagocyte system) called macrophages engulf (phagocytose) the hemoglobin to degrade it, producing hemosiderin and biliverdin. 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).

Diseases associated with hemosiderin deposition

{{Main|Hemosiderosis}}

Hemosiderin may deposit in diseases associated with iron overload[5]. These diseases are typically diseases in which chronic blood loss requires frequent blood transfusions, such as sickle cell anemia and thalassemia.

References

1. ^{{cite journal|last1=Richter|first1=Goetz|title=A Study of Hemosiderosis with Aid of Electron Microscopy|journal=The Journal of Experimental Medicine|date=1 August 1957|volume=106|issue=2|pages=203–218|doi=10.1084/jem.106.2.203 |pmid=13449232|pmc=2136742}}
2. ^{{cite journal|last1=Fischbach|first1=FA|last2=Gregory|first2=DW|last3=Harrison|first3=PM|last4=Hoy|first4=TG|last5=Williams|first5=JM|title=On the structure of hemosiderin and its relationship to ferritin.|journal=Journal of Ultrastructure Research|date=December 1971|volume=37|issue=5|pages=495–503|doi=10.1016/S0022-5320(71)80020-5|pmid=5136270}}
3. ^{{Cite book|title=Robbins & Cotran Pathologic Basis of Disease, 9th Edition|last=Kumar, Abbas, Aster|first=Vinay, Abul K., Jon C.|publisher=Elsevier|year=2015|isbn=978-1-4557-2613-4|location=|pages=650}}
4. ^{{cite web |url=http://library.med.utah.edu/WebPath/FORHTML/FOR138.html |title=Forensic Pathology |website= |accessdate=}}
5. ^{{Cite news|url=https://tidsskriftet.no/en/2016/12/medical-history/hereditary-haemochromatosis-through-150-years#reference-19|title=Hereditary haemochromatosis through 150 years|last=|first=|date=|work=Tidsskrift for Den norske legeforening|access-date=2018-07-14|language=en}}
{{Pathology}}

3 : Iron metabolism|Hematology|Iron oxide pigments

随便看

 

开放百科全书收录14589846条英语、德语、日语等多语种百科知识,基本涵盖了大多数领域的百科知识,是一部内容自由、开放的电子版国际百科全书。

 

Copyright © 2023 OENC.NET All Rights Reserved
京ICP备2021023879号 更新时间:2024/9/20 16:28:50