Phase images were used to enhance the effect of the local hemosiderin build-up.

Treatment for hemosiderin focuses on limiting the effects of the underlying disease leading to continued deposition.

Within cells, iron is stored in a protein complex as ferritin or hemosiderin.

The iron within deposits of hemosiderin is very poorly available to supply iron when needed.

Iron is also stored as a pigment called hemosiderin in an apparently pathologic process.

Subsequent hemosiderin deposition can occur in a reticular distribution.

The end product of the digestion of the red blood cells is an iron-storage complex known as hemosiderin.

Near the borders of the lesion, deposits of hemosiderin and hemorrhage is often found.

The characteristic brown coloration results from hemosiderin deposition into the osteolytic cysts.

Another aspect is that iron, which composes hemosiderin, emits light of several wavelengths when stimulated.

The bilirubin is then converted into hemosiderin, a golden brown color, which accounts for the color changes of the bruise.

Red blood cell extravasion and deposition of hemosiderin that follows clinically appears as hyperpigmentation.

On laboratory examination of the urine, breakdown products of red blood cells (hemoglobin and hemosiderin) may be identified.

This results in red cells breaking down, with iron containing hemosiderin possibly contributing to the pathology of this entity.

Stainable marrow hemosiderin is increased.

In this case they are fibers of asbestos coated with an iron-rich material derived from proteins such as ferritin and hemosiderin.

As ferritin accumulates within cells of the reticuloendothelial system, protein aggregates are formed as hemosiderin.

Around 30% of the iron in the body is stored as ferritin or hemosiderin in the spleen, the bone marrow and the liver.

White blood cells called macrophages engulf (phagocytose) the hemoglobin to degrade it, producing hemosiderin and biliverdin.

The tissue remnant usually includes fibrous tissue and signs of old infarction with hemosiderin deposition identified histologically.

Alveolar macrophages (dust cells) ingest the red blood cells, and become engorged with brownish hemosiderin.

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.

This differentiates melanin from common hemosiderin which are larger, chunky and refractile and range in color from green to yellow or red-brown.

Brown induration is fibrosis and hemosiderin pigmentation of the lungs due to long standing pulmonary congestion (chronic passive congestion).

The tubule cells of the proximal tubule slough off with the hemosiderin and are excreted into the urine, producing a "brownish" color.

The staining is due to the presence of haemosiderin.

The haemoglobin is converted into haemosiderin inside cells in the organ.

In the lung, the haemosiderin cells are known as heart failure cells.

Coffee ground vomiting is due to haemolysis of the red blood cells causing haemosiderin deposits.

They are visible on MRI scanning due to the presence of haemosiderin.

Hemosiderin or haemosiderin is an iron-storage complex.

Over time, haemosiderin released from red blood cells trapped in the skin is released causing a brown discolouration of the skin.

The deposition of iron in the lungs, occurring in the form of haemosiderin, is the defining characteristic of this illness.

They consist of fibrous tissue with haemosiderin and calcium deposits, and probably form due to scarring at sites of small perivascular haemorrhages.

In general, the term haemosiderosis is used to indicate the pathological effect of iron accumulation in any given organ, which mainly occurs in the form of haemosiderin.

Haemosiderosis is haemosiderin deposition within cells, while haemochromatosis is haemosiderin within cells and interstitium.

As they increase, the iron which is initially stored as ferritin is deposited in organs as haemosiderin and this is toxic to tissue, probably at least partially by inducing oxidative stress.

Impaired venous drainage from the foot in varicose veins may sequentially result in brown haemosiderin discolouration to the ankle and foot, varicose stasis dermatitis and finally venous ulcers.

Idiopathic pulmonary haemosiderosis (or idiopathic pulmonary hemosiderosis; IPH) is a lung disease of unknown cause that is characterized by alveolar capillary bleeding and accumulation of haemosiderin in the lungs.

Phase images were used to enhance the effect of the local hemosiderin build-up.

Treatment for hemosiderin focuses on limiting the effects of the underlying disease leading to continued deposition.

Within cells, iron is stored in a protein complex as ferritin or hemosiderin.

The iron within deposits of hemosiderin is very poorly available to supply iron when needed.

Iron is also stored as a pigment called hemosiderin in an apparently pathologic process.

Subsequent hemosiderin deposition can occur in a reticular distribution.

The end product of the digestion of the red blood cells is an iron-storage complex known as hemosiderin.

Near the borders of the lesion, deposits of hemosiderin and hemorrhage is often found.

The characteristic brown coloration results from hemosiderin deposition into the osteolytic cysts.

Another aspect is that iron, which composes hemosiderin, emits light of several wavelengths when stimulated.

The bilirubin is then converted into hemosiderin, a golden brown color, which accounts for the color changes of the bruise.

Red blood cell extravasion and deposition of hemosiderin that follows clinically appears as hyperpigmentation.

On laboratory examination of the urine, breakdown products of red blood cells (hemoglobin and hemosiderin) may be identified.

This results in red cells breaking down, with iron containing hemosiderin possibly contributing to the pathology of this entity.

Stainable marrow hemosiderin is increased.

In this case they are fibers of asbestos coated with an iron-rich material derived from proteins such as ferritin and hemosiderin.

As ferritin accumulates within cells of the reticuloendothelial system, protein aggregates are formed as hemosiderin.

Around 30% of the iron in the body is stored as ferritin or hemosiderin in the spleen, the bone marrow and the liver.

White blood cells called macrophages engulf (phagocytose) the hemoglobin to degrade it, producing hemosiderin and biliverdin.

The tissue remnant usually includes fibrous tissue and signs of old infarction with hemosiderin deposition identified histologically.

Alveolar macrophages (dust cells) ingest the red blood cells, and become engorged with brownish hemosiderin.

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.

This differentiates melanin from common hemosiderin which are larger, chunky and refractile and range in color from green to yellow or red-brown.

Brown induration is fibrosis and hemosiderin pigmentation of the lungs due to long standing pulmonary congestion (chronic passive congestion).

The tubule cells of the proximal tubule slough off with the hemosiderin and are excreted into the urine, producing a "brownish" color.