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Hemosiderin
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Hemosiderin image of a kidney viewed under a microscope. The brown areas represent hemosiderin
Heme. Iron is at center.Hemosiderin or haemosiderin is an iron-storage complex. It is always found within cells (as opposed to circulating in blood) and appears to be a complex of ferritin, denatured ferritin and other material. The iron within deposits of hemosiderin is very poorly available to supply iron when needed.

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.

[edit] Pathophysiology
Hemosiderin often forms after bleeding (hemorrhage).[1] When blood leaves a ruptured blood vessel, the cell dies and the hemoglobin of the red blood cells is released into the extracellular space. White blood cells called macrophages engulf (phagocytose) the hemoglobin to degrade it, producing hemosiderin and porphyrin.

[edit] Diseases associated with hemosiderin deposition
Main article: Hemosiderosis
Hemosiderin may deposit in diseases associated with iron overload. These diseases are typically diseases in which chronic blood loss requires frequent blood transfusions, such as sickle cell anemia and thalassemia.

Experimental hemosiderosis: relationship between skin pigmentation and hemosiderin.


Tsuji T

Acta Derm Venereol 1980; 60:109-14.

Abstract
Iron (totalling 7.5 mg per mouse in three doses) was injected into hairless mice to determine the relationship between skin pigmentation and hemosiderin deposition. The skin color reached its maximum 24 to 48 hours after the last injection and then gradually faded over the subsequent 8 months. In the skin, hemosiderin granules were present extracellularly between collagen bundles as well as within dermal macrophages, Langerhans cells and indeterminate dendritic cells of the epidermis. A larger amount of iron was deposited in the facial than in the dorsal skin, resulting in darker pigmentation of the former. This study suggests that brownish discoloration of skin in hemochromatosis might be attributable in some degree to accumulation of hemosiderin and that pronounced hyperpigmentation of the face in hemochromatosis might be due to increased activation of melanocytes by a high content of hemosiderin.

MeSH
Animals; Hemochromatosis; Hemosiderin; Hemosiderosis; Iron; Melanins; Mice; Mice, Nude; Skin; Skin Pigmentation

CAS Registry Number (Substance Name)
0 (Melanins), 7439-89-6 (Iron), 9011-92-1 (Hemosiderin)

MEDLINE record details


Publication Type:
Journal Article


ISSN:
0001-5555


Country:
SWEDEN


Language:
eng


Date of Entry:
19800728


Unique Identifier:
6155014


Journal Subset:
IM

In 2002, Dr. Zamboni noted that positive urine hemosiderin- a disease marker used to assess the severity of chronic venous disease- was administered to MS patients while they were in the midst of relapse. All of the MS patients tested positive. After he published a paper on this, he received an e-mail from Dr. FA Schelling- which referred him to Dr. Torben Fog’s paper- “Topography of Plaques in MS” The note from Dr. Schelling stated that perhaps Dr. Zamboni would now find what he was looking for...that the lesions of MS spread counter current from normal venous flow, and that there was where he should begin to study.

L, the test is perfectly available Rationale is whether urine hemosiderin is a biomarker of a venous problem (in CNS in our case). According to Zamboni it is. In principle hemosiderin should not be in urine if Fe metabolism is working correctly.
I wonder why this is not included in large studies as Buffalo´s. Perhaps it was. Or perhaps there are other medical reasons I ignore. The fact is that this element emerges from Zamboni´s work very strongly. I am kind of surprised why it is so absent or hidden in the talks.
For sure more clarification and help are needed on this