Shambling disease - cosmetic defect or serious illness? Gemosiderosis: Symptoms and treatment of gemosiderosis of the skin of the feet treatment of folk remedies

Hemosiderosis is a violation of exchange processes in the body, which is explained by excessive content in pigment tissue cells called hemosiderer. This pigment is formed as a result of the decay of hemoglobin, on which endogenous enzymes affect. Hemosiderin takes part in the delivery of some chemicals to the tissues. To the development of such a disease as hemosiderosis, certain violations in the body are given, among which: its excessive absorption in the intestine, failures in metabolic processes, too the intensive process of destruction of red blood cells.

Hemosiderosis is not the only designation for this pathology. Also, the disease is called a pigment hemorrhagic, chronic pigment purple.

Hemosiderosis can be local, affecting only skin and lungs, and may be generalized. In the latter case, the pigment begins in an excessive amount to accumulate in the liver, in the bone marrow, kidneys, in sweat and salivary glands, as well as in other internal organs.

At the same time, regardless of the form of the disease, it is manifested by the same symptoms, among which: hemorrhagic skin rashes (rash has a reddish tint), heaming, chronic fatigue syndrome. Most often from the hemosiderosis suffer from men of older. Children of this pathology are practically not subject to.

Treat hemosiderosis is very difficult, since this disease is not just a defect of appearance. Its reasons are broken in global disorders of metabolic processes in the body, which lead to a failure in the functioning of all internal organs.

Doctors of various profiles can identify and treat hemosiderosis: dermatologists, pulmonologists, immunologists, hematologists. In this case, the patient is prescribed hormonal steroid drugs, cytostatics, angioprotectors, vitamin and mineral complexes, plasmapheresis.

When hemolysis (the destruction of blood red blood cells and the release of hemoglobin) outside the vascular channel in any organ or hematoma, hemosiderosis develops. Excessive pigment content at a certain portion of the body does not lead to the fact that the tissues are damaged, but if they have already been exposed to sclerotic changes, the body work will be broken.

Hamosiderin deposits in tissues (idiopathic pulmonary hemosiderosis):

In case of intravascular hemolysis, general hemosiderosis is developing, which is accompanied by massive sediments of hemosiderin in the internal organs. More often, the rest of the liver and spleen cells suffer, but other internal organs may be affected. They change their light to darker, as a lot of pigment accumulates in them. Most often, total hemosiderosis develops against the background of systemic lesions of the body.

Also distinguish several more forms of hemosiderosis:

Pulmonary essential.

Hereditary.

Dermatological. This form of hemosiderosis is represented by such pathologies as: Maockey's disease, hidden dermatitis, Geuzo-Blum's disease, Shambling's disease.

Hepatic.

Idiopathic.

Until now, the causes of the development of hemosiderosis are not fully disclosed. Hemosiderosis is not a major disease, and a secondary state that develops against the background of the violations already available in the body.

In the risk group for the development of hemosiderosis, the following persons consist:

People with blood diseases and blood formation systems (leukemia, hemolytic anemia).

People with infectious diseases: with sepsis, brucellosis, malaria, typhoid.

People suffering from autoimmune pathologies, from violations in the work of the immune system.

People with diseases of the vascular wall.

Patients with vascular pathologies: with chronic venous insufficiency, p.

People with body intoxication.

Women in the body of which develops a rhesus conflict.

Hemosiderosis may occur in people who often perform blood transfusions. Also in the risk group are people with hereditary predisposition to this violation. Increase the likelihood of the development of hemosiderosis Dermatological diseases, wounds and abrasions on the skin, the supercooling of the body, the reception of a number of drugs, as well as the excessive intake of iron along with food.

The symptoms of the hemosiderosis are largely determined by the location of the lesion. Manifests pathology unexpectedly for a person, but has a smooth development.

If the hemosiderosis is striking the skin, then rashes can be maintained on it for several months and even years. At the same time, a person suffers from a skin itch, which can be very intense. Pigmentation has a stain shape with clear boundaries. The spots themselves are painted red, when pressed on the skin, they do not disappear.

With the pulmonary hemosiderosis of the patient begins to pursue shortness of breath, which occurs even at rest. A person suffers a wet cough, during which a bloody spree is distinguished. The body temperature rises to high marks, the symptoms of respiratory failure are growing, the liver and spleen increase in size, signs of anemia appear. A few days later, relief occurs, while the hemoglobin level in the body comes back to normal.

The hemosiderosis of the lungs is a disease with an unexplained etiology. It has a severe chronic course. At the same time, repeated hemorrhages in the alveoli often occur in the patient, and the erythrocytes fall into the pulmonary parenchyma. In parallel, a significant amount of hemosiderine is distinguished. All these pathological processes lead to the fact that the lungs are starting worse and worse to cope with their main function.

Symptoms of the hemosiderosis of the lungs in the acute stage of the disease:

Increase the spleen and liver in size.

When the acute stage of the disease remains behind, the person begins to feel satisfactory. At this time, he is able to perform his work, lead a full-fledged lifestyle. However, as the disease progressing is progressing, recurrences occur more and more often, and the quiet period becomes all shorter.

If hemosiderosis has a difficult course, the patient develops a pulmonary heart, pneumothorax. Even the death of man is possible.

After opening, a rowing lung induration is found in a number of patients, which is rarely diagnosed during a person's life. In the blood of such patients, autoantibodes are formed, which are spike of antibodies and antigens. This leads to the development of an inflammatory response that is localized in the lungs, since it is their tissue that becomes a target for attack by autoantibodies. Small vessels that permeate lung parenchyma are expanding. Of these, red blood cells are emerging, which disintegrate directly in the pulmonary fabric, which leads to an excess accumulation of hemosiderin.

With damage to the skin on them, rashes that have dark color appear. They are formed due to excessive accumulation of pigment in skin cells, against the background of the destruction of capillaries that permeate its puff layer.

The intensity of the rash color may vary, the same applies to their size. The reappearing rashes have a more rich color, which is close to red. The rashes that exist on the skin for quite a long time, on the contrary, pale, becoming brown or yellowish. Spots are located on hand and legs, on brushes and forearms. Their size can be achieved 3 cm. Also on the skin are often formed nodules, plaques, papules and pethihi. Patients may indicate itching and burning skin.

In the capillaries, penetrating the dermis, the pressure increases. This leads to the fact that the plasma containing erythrocytes begins to be selected through them. They are destroyed that hemosiderine deposits entails. When conducting a clinical analysis of blood, a decrease in platelet levels and anemia will be detected.

Most often, the skin shape of the hemosiderosis proceeds in the form of orthostatic, eczema-like and itchy purple, or in the form of Majorca's disease.

Shamberman's disease

Shambling disease refers to frequent autoimmune disorders, which has a chronic course. At the same time, on the human body, red-made rashes appear, resembling a trace of the injection. In the vascular walls, immune complexes begin to be postponed, which lead to the development of an autoimmune inflammatory process in the inner layers of the dermis. For this reason, the skin is covered with small hemorrhages. As the hemosiderine layer accumulates in her papilla, the stains increase in size, bring brown color. In the future, they merge, forming large plaques, bored with a bright red rim.

As the disease progressing, the plaques merge with each other and begin to atrophy. In this case, the general well-being of a person does not suffer.

In general, dermatological hemosiderosis is well treatment, which differs from the hemosiderosis of other localizations. Patient recovery occurs fairly quickly.

Gemosiderosis of internal organs

With expressed intravascular hemolysis, erythrocytes in the patient develops generalized or systemic hemosiderosis. The internal organs suffer, their performance is disturbed, which affects human well-being.

With the hemosiderosis of the liver Pigment deposition occurs in hepatocytes. The disease can develop as independent pathology, or as being a consequence of other violations in the body, and often the cause of hemosiderosis is not possible to find out. At the same time there is an increase in the liver in size, which becomes apparent even when pressed to the area where it is located. As the disease progresses in the abdominal cavity, the ascitic fluid occurs, blood pressure increases, the skin becomes yellow, the spleen increases in the sizes, on the hands, under the mouse and on the face there are pygmentation areas. If the treatment is absent, then the patient develops acidosis and it flows into someone.

In the hemosiderosis of the kidneys They are covered with brown granules. The disease proceeds by the type of jade or nephrosis. The urine detects the protein component, the level of lipids in the blood increases. A person notes the swelling of the lower extremities, painful sensations in the field of the lower back, disappears the desire to take food, develop diversual disorders. In the absence of adequate and timely therapy, which often becomes the cause of death.

Hemosiderosis of the liver (left) and kidneys (right):

In addition, the accumulation of hemosiderine can occur in the brain, in the spleen and in other internal organs. All these states are conjugate with severe violations from the affected systems, which often ends with a fatal outcome.

The systemic flow hemosiderosis is a disease that is associated with the threat of a person's life.

To clarify the diagnosis, insufficiently standard examination of the patient.

After its implementation, it is necessary to appoint the following studies:

Blood fence on overall analysis with the definition of serum iron and the overall blood ability to bind iron.

Biopsy of body tissues followed by histological examination of the material taken.

Referral test. This study makes it possible to detect hemosidererine in the urine for which the patient is injected into the injection of the drug Descivity. Cross make intramuscularly.

Microscopic examination of the patient's demes in the presence of rashes on the skin.

Auxiliary research methods are:

Passage of X-ray examination.

Passage of CT and scintigraphy.

Performance of bronchoscopy.

Performing spirometry.

The study of sputum under the microscope and the execution of its bacteriological sowing.

Gemosiderosis therapy requires the following recommendations:

Compliance with diet with refusal of alcoholic beverages. Mandatory from the menu you need to remove all products that can provoke an allergic reaction.

It is important to avoid hypothermia, injuries, an organism overheating, as well as mental and physical overvoltage.

All diseases must be treated in a timely manner.

Chronic foci of infection needs to be eliminated.

It is important to be from the use of cosmetics, which can cause.

All bad habits must be forgotten.

Medicine therapy involves the use of the following medicines:

Reception and local application of hormonal steroid drugs, including: prednisone, betamethasone, dexamethasone.

Reception of drugs to reduce the inflammatory reaction: indomethacin and ibuprofen.

Reception of disagrement: aspirin, cardiomagnet.

Reception of drugs with immunosuppressive action: Azatioprine, cyclophosphane.

Receiving angioprotectors: Diosmin, Heperidin.

Reception Nootropov: Piracetam, Vinpocetin, Maxidol.

Reception of drugs against allergies: Suprastin, Tueva, diazoline.

Reception of vitamins and minerals: vitamin C, routine, calcium.

Also, the patient can be appointed iron preparations, preparations for stopping bleeding, bronchopholics. It is possible to conduct oxygen therapy. Also patients are sent to hemosorption, cryoprecipitation, cryotherapy and plasmapheresis. Sometimes the blood transfusion is required, or the removal of the spleen.

Prevention of hemosiderosis

Hemosiderosis is a disease that often exacerbates. Provided that a person gets quality treatment, recurrences will happen less often, but for this you need to comply with preventive measures, including: proper nutrition, passage of treatment in specialized sanatoriums, conducting a healthy lifestyle.

To prevent the development of hemosiderosis, you need to adhere to the following recommendations:

Do not engage in the self-treatment of infectious diseases, and in a timely manner for medical help.

Maintain the health of the vessels.

Control blood pressure, monitor its weight and cholesterol.

Minimize the risks of intoxication of the body.

Education: In 2013, the Kursk State Medical University was completed and a diploma degree was received. Two years later, the ordinite was completed in the specialty "Oncology". In 2016, graduate school was passed in the National Medical and Surgery Center named after N. I. Pirogov.

Hemosiderosis is a disease related to a group of pigment dystrophy. It is characterized by accumulation in the tissues of the body of an excessive amount of hemosiderin - iron-containing pigment.

Skin manifestations of hemosiderosis

Causes and risk factors

Hemosidererin is formed in the process of cleavage of hemoglobin molecules under the action of certain enzymes in sideroblast cells. Normally, a slight amount of hemosiderine is contained in lymphoid tissue, bone marrow, spleen and liver cells. With an increase in the synthesis of hemosiderin, its excess is deposited in the cells of other tissues.

General hemosiderosis is always a secondary pathology, the development of which is due to autoimmune processes, intoxications, infections or blood diseases. The most frequent causes of hemosiderosis are:

hemolytic anemia;
hemolytic poisoning of hemolytic poison (quinine, lead, sulfonamide);
leukemia;
multiple hemotransphus;
cirrhosis of the liver;
resh conflict;
infectious diseases (return typhus, malaria, brucellosis, sepsis);
decompensated heart failure;
chronic venous insufficiency;
diabetes;
dermatitis;
eczema.

Some specialists believe that in the pathological mechanism of development of the hemosiderosis, the hereditary predisposition and disorder of the immune system play an important role.

Forms of the disease

According to the degree of propagation of the pathological process, it is allocated:

general (generalized) hemosiderosis - to it causes an emerging (endovascular) hemolysis of erythrocytes against the background of any systemic processes. Gemosiderin is postponed in a spleen, red bone marrow, liver, as a result of which they acquire a rusty, brown coloring;
local (local) hemosiderosis - develops as a result of an outcast (extravascular) hemolysis. The accumulation of hemosiderine can be observed both in small areas of the body (in the hematomas region) and within any organ (for example, light).

According to the characteristics of the clinical flow, allocate:

skin hemosiderosis (hidful dermatitis, purpurous anchodermatitis, lichenoid pigment dermatitis, senile hemosiderosis, ring-shaped teleangectatic Purple Maockey, Shambling disease);
pulmonary idiopathic hemosiderosis (bright lung induration).

Pulmonary hemosiderosis progresses and leads to disability of patients. It can be complicated by massive pulmonary bleeding, driving fast death.

In some cases, the deposition of hemosiderin becomes the cause of the violation of the function of the affected body and the development of structural changes in it. This form of hemosiderosis is called hemochromatosis.

Symptoms

The clinical picture of the hemosiderosis depends on the form of the disease.

Pulmonary idiopathic hemosiderosis is diagnosed mainly in children and young people, characterized by periodically emerging pulmonary bleeding of various degrees of severity, increasing respiratory failure and resistant hypochromic anemia.

In the acute phase of the disease observed:

dyspnea;
pain in the chest;
cough with a branch of blood wet;
pallor skin;
scler's characterity;
cyanosis of the nasolabial triangle;
weakness;
dizziness;
increase body temperature.

During the period of remission, clinical manifestations of the disease are very weakly pronounced or completely absent. After each period of exacerbation of the idiopathic pulmonary hemosiderosis, the duration of the remission period decreases.

The skin shape of the hemosiderosis occurs more often in men over 40 years old. Current chronic benign. On the skin of the forearms, brushes, legs and ankles appear pigment spots of brick-red. Over time, the color of the elements of the rash changes to the yellowish, dark brown or brown. The damage to the internal organs during the skin form of the hemosiderosis does not occur, the general state does not suffer.

Diagnostics

The diagnosis of hemosiderosis is based on the characteristic clinical signs of the disease, data of laboratory and instrumental methods of the survey. A general blood test is assigned, the concentration of serum iron is determined.

If hemosiderosis is suspected, a desperval sample is carried out. For this, deferoxamine is injected intramuscularly, and then the iron content in the urine is determined. The sample is considered positive if the urine portions contain over 1 mg of iron.

To confirm the diagnosis, the puncture biopsy of the bone marrow, lung, liver or skin, followed by histological examination of the resulting tissue.

General hemosiderosis is always a secondary pathology, the development of which is due to autoimmune processes, intoxications, infections or blood diseases.

In the hemosiderosis of the lungs also carry out:

spirometry;
microscopic sputum examination;
perfusion scintigraphy of the lungs;
chest radiography;
bronchoscopy.

Treatment

Therapy of the pulmonary hemosiderosis begins with the appointment of corticosteroids. In case of its ineffectiveness, patients prescribe immunosuppressants and plasmapheresis sessions. In some cases, it is possible to achieve a resistant after removal of the spleen (splenectomy). In addition, symptomatic therapy is carried out with the appointment of bronchoditics, hemostatic and other drugs (depending on the manifestations of the disease).

Treatment of skin hemosiderosis is the local application of corticosteroidal ointments. Angioprotectors, calcium, rutin, ascorbic acid are also prescribed. With a serious course of the disease, the destination of deferoxamine, the PuU-therapy is shown.

Possible complications and consequences

The most frequent complications of the hemosiderosis of the lungs:

recurrent pneumothorax;
pulmonary bleeding;
lung infarction;
expansion and hypertrophy of the right heart departments;
pulmonary hypertension;
chronic respiratory failure.

Forecast

The outlook for the pulmonary hemosiderosis is serious. The disease progresses and leads to disabled patients. It can be complicated by massive pulmonary bleeding, driving fast death.

Under the skin form of the hemosiderosis, the forecast is favorable.

Pulmonary idiopathic hemosiderosis is diagnosed mainly in children and young people.

Prevention

Prevention of violations of hemosiderin exchange processes is the timely treatment of hematologic, vascular and infectious diseases, preventing chemical or drug intoxication, hemotransphusion complications.

Gemosiderosis (haemosiderosis; Greek, Haima Blood + Sider iron + -osis) - excess form of hemosidere and its deposition in tissues observed under a number of diseases and caused by various reasons. Among them are distinguished endogenous, for example, massive destruction of red blood cells, increased absorption of iron in the intestines, and exogenous, for example, with frequent hemotransphuses. G. May be local, as well as to be general.

The body has a rather permanent state of iron in the form of two protein complexes - ferritin and hemosiderin. Ferrine - water-soluble compound, a molecule to-ryo consists of protein part (apotheferritin) and colloid threads of trivalent iron. Hemosiderine - water-insoluble yellow-brown pigment; Its protein is identical to apotheferritin. As part of hemosiderin, in contrast to ferritin, there are both inorganic compounds of phosphorus, sulfur, nitrogen and non-protected organic substances. There is an idea of \u200b\u200bthe transformation of ferritin into hemosiderin [Shoden, Sturgeron (A. Shoden, P. Sturgeron)].

It has been established that the iron level is maintained by regulating suction, not the process of active selection. Every day with the fee is allocated (cells of the lunishing intestinal epithelium) 0.5 mg of iron, with urine - 0.2 mg, in women during menstruation of 0.5-1.5 mg. These small losses are compensated by the absorption of iron. Iron absorption occurs in the main mucous membrane of the duodenum.

In food products, iron is contained in quantities, many times greater than the need for it. However, the magnitude of the intestinal absorption of iron depends little on the content of it in the products entered into the intestines.

Konrad, Weintraub, Crosby (M. E. Conrad, LR WEINTRAUB, WH CROSBY) With the help of radioactive iron, showed that the absorption of iron is carried out in two phases: the flow of iron from the lumen of the intestine into the mucous membrane and the movement of iron from the mucous membrane in blood plasma and Fabrics. According to Webi hypothesis (M. S. Wheby), the absorption of iron is consisted of three phases: penetration into the mucous membrane from the intestinal lumen, penetration from the intestinal sheath in the plasma, deposition of iron in the mucous membrane. The penetration of iron into the mucous membrane of the intestinal lumen is faster than from the plasma mucous membrane. However, when the need for the body in the gland increases, its admission to the plasma is accelerated and iron in this case is not postponed in the form of stock.

It is shown that 80% of iron adsorbed by the intestinal mucosa quickly passes into the plasma and is connected to the transport protein-transferin. Next, the iron associated with transferrin is captured by erythrocyte precursors and is used again for the synthesis of hemoglobin. Weintrauba (1965) managed to identify the dependence of the intensity of the intestinal absorption of iron from the level of hemoglobingenesis, but the mechanism of quantitative communication between these two processes remains unexplained. The remaining 20% \u200b\u200bof the attempted iron is fixed in the tissue by perceiving with iron protein. If the body's need is increasing in the gland, this connection weakens and iron passes into the plasma, and the protein perceived again fixes the iron with a new food intake. If the need for iron in the body is small, then most of the adsorbed metal is fixed in the form of hemosidere and ferritin in intestinal cells. Since the latter are quickly descaming (usually after 3-4 days), the iron fixed in them is highlighted in the intestinal lumen.

With anomalies of iron absorption, as, for example, with hemochromatosis (see), hemosidere is postponed in organs. The pathogenesis of these disorders is not clear; Undoubtedly, however, that in the intestine absorption of iron does not depend on its reserves in the body.

Fig. 24. The accumulation of hemosiderine (blue) in the epithelium of the convinced kidney tube during the secondary hemosiderosis (painting by perrsha; x 120). Fig. 25. Hemosiderosis of the liver (hemosiderer - blue; Person's coloring): A - in hepatic and coupper cells (x 400); B - diffuse hemosiderosis under thalassemia (X100). Fig. 26. Alveolar macrophages with hemosiderin (brown) with essential pulmonary hemosiderosis (x400).

The hemoglobin of destroyed red blood cells is fixed by reticular, endothelial and histiocytic cells of the spleen, liver, kidneys (china. Fig. 24 and 25), bone marrow, lymph, nodes, where it is informed in the grain of hemosiderin, why these organs become rust-brown.

Methodology and technique of detecting hemosiderosis

In order to estimate iron reserves, complexones are used that bind and remove the trivalent iron from the body. Most often used the desferre (XI. Deferoxamine), which is complexed with iron-containing proteins - ferritin and hemosiderine (but not with hemoglobin iron and iron-containing enzymes). It forms a stable complex with trivalent glands and is allocated by the kidneys in the form of ferroxyamine (see complexions). The administration of the presverine does not significantly affect the allocation of other metals and trace elements.

Descharical sample: An intramuscularly 500 mg of the drug and for 6-24 hours are once in a patient. After injection, they collect urine, in which the amount of iron is determined. The sample is considered positive if the iron content in the urine is more than 1 mg. Based on the data of the design sample, it is possible to address the need for therapy with complexes to remove excess iron from the body, as well as about the feasibility of treatment with iron drugs during iron reserves. The desperial test is used as a diagnostic test in patients with thalassemia; With the help of this sample, it is possible to exclude iron deficiency anemia (frequent erroneous diagnosis of patients with thalassemia).

To identify G., the level of serum iron is also investigated (with decreasing it - iron preparations are prescribed) and the degree of blood saturation with transferrin. Reliable diagnostic criterion is the detection of iron in the liver bioptate, in the bone marrow treponate according to the PERSK method (see Pershov method), as well as counting the number of sideroblasts in the bone marrow aspirate.

Diagnostic value

In the foci of hemorrhages, during the introduction of the destruction of the red blood cells, the local G. Total is observed in various diseases of the blood formation system (anemia, some forms of leukemia), intoxication by hemolytic poisons, some infectious diseases (return title, brucellosis, malaria, etc.), frequent hemotransphuses etc. Rarely the common city is manifested as a hereditary disease - hemochromatosis (see). For the latter, the deposition in the tissues, in addition to hemosiderin, the other iron-containing pigment is hemopuscin, as well as lipofuscin.

G. is often a complication of liver cirrhosis [Powell, Williams (L. W. Powell, R. Williams)], diabetes. In experimental removal of the pancreas, the animals observed generalized G. Hemosiderosis detected in patients with hemoglobinopathies (see), with iron-refractory anemia (see).

Treatment

Therapeutic measures are carried out primarily in relation to the underlying disease. In addition, blewements are used, which are particularly effective in diffuse G., accompanying idiopathic hemakhromatosis. Blooding in a volume of 500 ml is equivalent to remove 200 mg of iron. However, with iron-refractory anemia, this method, requiring constant and systematic blood transfuses, is not justified [Bannerman (R. M. Bannerman)]. In the treatment of secondary G. (complications of the liver cirrhosis), the drug dietilenemine-acetate [Mac Donald, Smith (R. A. McDonald, R. S. Smith)], but the injection of it is painful and sometimes cause side effects. Introduction to the wedge, the practice of desferla discovered new opportunities in the treatment of various origin. Refieme is usually injected intramuscularly at a dose of 1-3 g per day. The duration of one course of treatment is at least 3 weeks. There are instructions [Weller (F. Wohler)] on the use of the presverine during the year and more in patients with idiopathic hemochromatosis. The main criterion that determines the duration of treatment is the release of iron with urine; If the daily excretion of iron does not exceed 1.0-1.5 mg, the injections of the deferoxamine are stopped. From others to leap. Facilities include the complexing compounds - thetacin calcium (see) and pentatin (see).

Essential pulmonary hemosiderosis (color. Fig. 26 and 27) occupies a special place, since it is fundamentally different in etiology, pathogenesis and clinic from hemochromatosis. Hemosiderine deposits are discovered only in the lungs, which affected its old names - brown lung induration, essential brown lung induration, pulmonary stroke, congenital bleeding into the lungs (see idiopathic hemosiderosis of the lungs).

Bibliography: Dolflosk N. A. and Skaldina A. S. The case of an essential hemosiderosis of the lungs, Vestn, X-ray, and radiol., No. 1, p. 88, 1971, bibliogr.; Martynov S. M. and Sheremete N. A. On transfusion hypergemide-roses and hemochromatozes for leukemia, hemoblastosis and aplastic anemia * in the book: Sovr. Probl, hematol. and overflow, blood, ed. A. E. Kiseleva et al., C. 38, p. 243, M., 1966; Finenestein F. E. et al. Application of presveron and some data on hemosiderosis in hypo- and aplastic anemia, Probl< гематол. и перелив, крови, т. 13, № 8, с. 31, 1968, библиогр.; Хуцишвили Г. Э. Десферал-тест в диагностике гемосидероза у больных гемоглобинопатиями, Лаборат, дело, № 9, с. 660, 1971* библиогр.; Blood and its disorders, ed. by R. M. Hardisty a. D. J. Weatherall, Oxford, 1974; Bothwell Т. H. a. Finch C. A. Iron metabolism, Boston, 1962; Clinical symposium on iron deficiency, ed., by L. Hallberg a. o., L.- N. Y., 1970; Iron metabolism, ed. by F. Gross, B., 1964; Mac Donald R. A. Hemochromatosis and hemosiderosis, Springfield, 1964, bibliogr.; Roberts L. N., Montes-s o r i G. a. P a 11 e r s o n J. G. Idiopathic pulmonary hemosiderosis, Amer. Rev. resp. Dis., v. 106, p. 904, 1972.

L. A. Danilina.

Which is accumulated in the blood due to the decay of erythrocytes, which are blood cells carrying oxygen to the tissues and internal organs. The duration of their life is 120 days, after which they disintegrate. Therefore, the destruction of erythrocytes occurs in good condition. But if too many blood cells breaks down, an excessive accumulation of hemosiderine pigment in the blood occurs. More information about the reasons, symptoms, features of diagnosis and treatment of this pathology further in the article.

Causes of pathology

Hemosiderer is a substance that, with an excess accumulation in the body, causes the development of the disease under the name of hemosiderosis. Two groups of causes of this pathology are distinguished: exogenous and endogenous. In the first case, the impact of external factors on the body is noted. In the second case, the disease is developing due to the violation of the inner environment of the body.

Endogenous factors that lead to increased hemosiderrine deposit include:

acute inflammatory diseases of infectious origin - malaria, brucellosis;
toxic poisoning;
the influence of some medicines;
excessive receipt of iron into the body with medicines containing it ("sorbifer", "Malto");
blood transfusion with an incompatible group or rhesus factor.

Among the greatest attention is given inheritance. There are some genetic diseases in which excessive hemosiderine deposition arises in the brain, liver and other internal organs. This is, first of all, such pathologies:

thalassemia - a violation of the synthesis of one of the chains of hemoglobin;
sick-shaped cell anemia - congenital violation of the form of red blood cells;
enzymopathy - a group of diseases in which there are not enough enzyme for the formation of hemoglobin;
membranopathy is congenital violations of the structure of red blood cells.

Separately distinguish autoimmune diseases, as the cause of the development of hemosiderosis.

Forms of the disease

Hemosiderine is a substance that can accumulate both everywhere in the body, in almost all internal organs, and is isolated, that is, in some particular place. In the first case, they talk about generalized, or general form of the disease. In the second case, local, or local, hemosiderosis develops.

The emergence of general hemosiderosis occurs against the background of any systemic pathology. Then hemosiderine accumulates in the brain, liver and other organs. With local form, the pigment is assembled in localized parts of the human body. For example, in the cavity of the tubular organ or in the hematoma.

Depending on the cause of development, two more disease groups are distinguished:

primary - the reasons for this form are still not clarified;
secondary - develops against the background of other diseases.

The following pathological conditions may appear as the main reasons for the secondary hemosiderosis:

leukemia - malignant bone marrow damage;
cirrhosis of the liver;
infectious diseases;
skin diseases: pyodermia, eczema, dermatitis;
hypertension with a heavy flow;
frequent blood transfusions;
hemolytic anemia.

In fact, the reasons for the development of secondary hemosiderosis is much more, therefore only the main ones are presented in the previous section.

Risk factors for the development of the disease

Separately, the factors that directly do not lead to increased hemosiderine deposit, but increase the risk of this pathological state. These include:

constant supercooling of the body;
chronic stress;
excessive physical exertion;
uncontrolled towing diuretic preparations, paracetamol, some antibiotics.

What bodies are amazed during the hemosiderosis?

Hemosiderine is a pigment that can accumulate in almost any domestic organ. But most often lesion is observed:

liver;
kidney;
spleen;
skin;
bone marrow;
salivary or sweat glands;
brain.

Skin hemosiderosis: manifestations

The most vivid manifestations has accumulation of hemosiderine in the skin. Practically, all patients with the main symptom is the formation of spots of dark brown on the legs. Typically, pigmentation sites have a large diameter, but sometimes there are small, practically point rashes. In some patients, it arises due to the lesion of the capillaries of the skin.

The shade of rashes can be different: from the color of red brick to dark brown or yellow. In addition to the stains, other elements of the rash appear: nodules, papulas, plaques. The patient worries the itching of the affected skin.

Liver hemosiderosis: symptoms

The deposition of hemosiderine in the hepatic tissue is manifested primarily by increasing the size of the organ. This leads to stretching the capsule surrounding the liver. The patient feels like a stupid pain to the right under the edge. With a significant increase, the abdominal asymmetry occurs and the on the right. Palpation of belly in these departments is also painful.

With a long-lasting process, the liver function is gradually violated. This is manifested by an increase in the abdomen because of the accumulation of liquids in it, varicose veins of the stomach and esophagus, hemorrhoids, the yellowing of the skin and the scool, hemorrhagic rash.

Kidney Gemosiderosis: Symptoms

The accumulation of pigment in the kidneys not only leads to changes in the urine, but also to certain clinical manifestations. Hemosiderine strikes the renal tubules and the gloves, which leads to a violation of blood filtering and the exit of it protein, carbohydrates. As a result, hypoproteinemia is developing - a decrease in the concentration of protein in the blood.

The patient complains about the appearance of edema. First, they arise on the face, and in the running cases cover the whole body. The patient is concerned with general weakness and fatigue.

Long-term damage to the kidney function leads to a violation of the functions of other organs and systems.

Beaming brain

The deposition of hemosiderin in the brain has very variable clinical manifestations. It all depends on what kind of department is localized defeat.

The accumulation of hemosiderine causes the death of nerve cells, the destruction of the myelin shell of the nerves. Often in patients with hemosiderosis of the brain there is a preceding hemorrhage into a parenchyma, tumor removal, hemorrhagic strokes.

Typical clinical manifestations of accumulation of hemosiderin in the brain are considered:

violation of equilibrium - Ataxia;
worsening hearing in the type of neurosensory hearing loss;
psyche disorders;
dysarthria - Violation of speech;
motor disorders.

Diagnostics

The diagnosis of hemosiderosis should be comprehensive. Often, the coordinated work of doctors of different specialization are necessary: \u200b\u200ba dermatologist, a neurologist, a pulmonologist, infectiousnessist and others. It all depends on what predominantly the organ is amazed.

The diagnostic search begins with a detailed painting of the patient about its complaints, their development in the dynamics, the presence of preceding diseases. Only after that additional methods of examination are prescribed.

Regardless of the form of the disease, such diagnostic methods are assigned:

The overall blood test is determined by a reduced amount of erythrocytes and hemoglobin.
Determination of the presence of hemosiderin in the urine.
Determine iron levels in blood serum.
Analysis on the binding capacity of iron in the body.
Biopsy of the affected area of \u200b\u200bfabric with histological examination to detect hemosidery deposits.

Only histological examination of the bioptate allows you to make a diagnosis of hemosiderosis with one hundred percent confidence. When studying a piece of fabric under a microscope, macrophages with hemosiderin are found, since it is these cells first "eat" an extra pigment.

Also, depending on which the defeat of which organ suspects the doctor, he appoints such methods of examination:

magnetic resonance imaging brain;
computer tomogram;
ultrasound procedure;
radiography;
bronchoscopy.

Another effective laboratory diagnostic method is a desperial test. It is introduced to the patient 500 mg of presverial. At least after 6 hours and a maximum of a day after the injection of the drug, the patient is assembled and the amount of iron in it is investigated.

Treatment of the disease

Since at the present stage, the most attention is paid to the autoimmune flow of hemosiderosis, drugs from the corticosteroid group are considered priority drugs. They oppress the immune system, thereby reducing the production of antibodies against their own erythrocytes. These funds include "dexamethasone", "prednisone". But glucocorticoids help only 40-50% of cases. In the absence of their effectiveness, the patient is prescribed cytostatics ("Methotrexate", "Azatioprin").

Also prescribed drugs that improve tissue trophics, cell metabolism, increasing the flow of oxygen to them. These drugs include:

Venotonics. They increase the elasticity of vascular walls, improve blood flow in brain tissues - "Detralex", "Doppeoplez".
Vitamins of Group V. Improve the conductivity of the nerve impulse, the state of the fabric.
Vitamin C increases the strength of the vascular wall.
Angioprotectors. They have a similar vitamin with the effect - "Ethalizila", "Vinkamin".
Nootropics. Improve the blood flow in the brain and accelerate the metabolism of cells - "cerebrolysis", "phenibut".
Neuroleptics. It is prescribed symptomatically in the presence of mental disorders in the patient - "aminazin".

In the hemosiderosis of the kidneys and the significant impairment of their functions are prescribed plasmapheres or hemodialysis.

Thus, excess accumulation of hemosidere is a serious pathological condition. It requires the highest possible diagnosis and timely treatment, since in advanced cases, hemosiderosis leads to severe violations of the functions of the internal organs. Often these violations are irreversible.

hemolytic anemia;
hemolytic poisoning of hemolytic poison (quinine, lead, sulfonamide);
leukemia;
multiple hemotransphus;
cirrhosis of the liver;
resh conflict;
infectious diseases (return typhus, malaria, brucellosis, sepsis);
decompensated heart failure;
chronic venous insufficiency;
diabetes;
dermatitis;
eczema.

Some specialists believe that in the pathological mechanism of development of the hemosiderosis, the hereditary predisposition and disorder of the immune system play an important role.

Forms of the disease

According to the degree of propagation of the pathological process, it is allocated:

general (generalized) hemosiderosis - to it causes an emerging (endovascular) hemolysis of erythrocytes against the background of any systemic processes. Gemosiderin is postponed in a spleen, red bone marrow, liver, as a result of which they acquire a rusty, brown coloring;
local (local) hemosiderosis - develops as a result of an outcast (extravascular) hemolysis. The accumulation of hemosiderine can be observed both in small areas of the body (in the hematomas region) and within any organ (for example, light).

According to the characteristics of the clinical flow, allocate:

skin hemosiderosis (hidful dermatitis, purpurous anchodermatitis, lichenoid pigment dermatitis, senile hemosiderosis, ring-shaped teleangectatic Purple Maockey, Shambling disease);
pulmonary idiopathic hemosiderosis (bright lung induration).

Pulmonary hemosiderosis progresses and leads to disability of patients. It can be complicated by massive pulmonary bleeding, driving fast death.

Symptoms

The clinical picture of the hemosiderosis depends on the form of the disease.

In the acute phase of the disease observed:

dyspnea;
pain in the chest;
cough with a branch of blood wet;
pallor skin;
scler's characterity;
cyanosis of the nasolabial triangle;
weakness;
dizziness;
increase body temperature.

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Diagnostics

To confirm the diagnosis, the puncture biopsy of the bone marrow, lung, liver or skin, followed by histological examination of the resulting tissue.

General hemosiderosis is always a secondary pathology, the development of which is due to autoimmune processes, intoxications, infections or blood diseases.

In the hemosiderosis of the lungs also carry out:

spirometry;
microscopic sputum examination;
perfusion scintigraphy of the lungs;
chest radiography;
bronchoscopy.

Treatment

Possible complications and consequences

The most frequent complications of the hemosiderosis of the lungs:

recurrent pneumothorax;
pulmonary bleeding;
lung infarction;
expansion and hypertrophy of the right heart departments;
pulmonary hypertension;
chronic respiratory failure.

Forecast

The outlook for the pulmonary hemosiderosis is serious. The disease progresses and leads to disabled patients. It can be complicated by massive pulmonary bleeding, driving fast death.

Under the skin form of the hemosiderosis, the forecast is favorable.

Pulmonary idiopathic hemosiderosis is diagnosed mainly in children and young people.

Prevention

Etiology

Since such a notch in children and adults can be primary and secondary, then the predisposing factors will differ.

In the first case, pathogenesis and ethiology of hemosiderosis remain completely uncalled, but clinicians put forward several assumptions, including:

genetic predisposition;
immunopathological nature of pathology;
congenital disorders of metabolic processes.

As for the secondary hemosiderosis, then as possible reasons can be:

hemolytic anemia;
leukemia;
liver damage with cirrhosis;
the flow of some diseases of infectious nature is to include sepsis and returning typhus, malaria and brucellosis;
frequent hemotransphus;
poisoning chemicals and poisons. Most often, sulfonamides, lead and quinine are as provocateurs;
flow of diabetes and other metabolic disorders;
malignant arterial hypertension;
venous insufficiency in chronic form;
dermatitis and neurodermatitis;
eczema and pyodermia;
any disorders of the integrity of the skin.

It is possible to provoke a demonstration of a disease:

prolonged supercooling of the body;
physical overwork;
stress and nervous overvoltage;
the uncontrolled reception of some groups of drugs, in particular diuretics, nonsteroidal anti-inflammatory agents, as well as paracetamol and ampicillin.

Not the last place in the formation of such a pathological process occupy:

an excess of iron in the body - this can be achieved by consuming products or medicines, which includes a large amount of this substance;
procedure of blood transfusion, especially if it is performed several times a week. In such cases, they say about the occurrence of transfusion hemosiderosis;
increased absorption of hemosiderrine by the organs of the digestive system;
violation of the metabolism of hemosidere;
supercooling of the body.

Classification

According to the degree of prevalence of the pathological process, there is:

generalized or general hemosiderosis - Forms against the background of a system process. In such situations, the hemosidemin accumulates in the spleen and liver, as well as in the Red bone marrow, which they change their color and become rusty or brown;
local, focal or local hemosiderosis It is characterized in that the accumulation of iron-containing intracellular pigment can be carried out both in small areas of the body, for example, in the hematoma zone and in the cavity of one of the internal organs. Most often it is noted in light tissues.

According to the etiological factor, the hemosiderosis happens:

primary - reasons for today remain unknown;
secondary - develops against the background of the flow of any of the above ailments.

It is worth attributed to independent types of disease.

skin hemosiderosis;
idiopathic light hemosiderosis, which in the medical sphere is called the buoy of purple lungs.

In cases of skin lesions, the disease may occur in several variations, which is divided into:

shambherg disease;
ring-shaped teleangectatic purple of Maokki;
senile hemosiderosis;
lihenoid pigment or purple anchodermit;
chicken dermatitis.

The secondary form of pathology also has its own classification:

liver hemosiderosis;
kidney hemosiderosis;
bone marrow hemosiderosis;
hemosiderosis of the spleen;
hemosiderosis with lesions of salivary or sweat glands.

Symptomatics

The clinical picture of such a disease in children and adults is directly dictated by a variety of its flow.

Thus, idiopathic hemosiderosis of lungs is represented by such manifestations:

productive cough, i.e. with the release of sputum;
hemochking;
breath;
increasing temperature values;
pain syndrome with localization in breast;
skin pallor;
icleric acid;
syushia of the nasolabial triangle;
strongest dizziness;
weakness and decrease in working capacity;
lack of appetite;
cardiac rhythm;
lowering blood pressure;
simultaneous change in the volume of liver and spleen to the biggest side.

Against the background that drowned income induration is a heavy illness, a similar diagnosis during a person's life is rarely established.

The skin hemosiderosis is primarily expressed in the occurrence of pigment stains having brown and in the overwhelming majority of cases localized the lower legs. In addition, the symptoms of such a variation of the illness also includes:

the emergence of hemorrhagic rash or small pigment spots, which in diameter range from one millimeter to 3 centimeters;
involvement in the pathology of the heads, forearms and brushes;
shading variability - they can be brick-red, brown, dark brown or yellowish;
minor skin itching;
the formation of petechy, nodules, dyeing patechs and plaques and plaques on problem areas.

The hemosiderosis of the liver is expressed in:

an increase in the size and density of the affected organ;
soreness in palpation of the projection of this body;
accumulate a large amount of fluid in the peritoneum;
increase blood tone;
the jaggility of the skin, visible mucous and scool;
pigmentation of the upper extremities, face and axillary depression.

In cases of involvement in the pathological process, the kidney will be marked by the presence:

the ethnicity of the lower limbs and the age;
disgust for food;
clouding Urin;
pain in the area of \u200b\u200bthe belt;
general weakness and breakdown;
dyspepsia.

All the above symptoms are appropriate to the child and adult.

Diagnostics

Since hemosiderosis is primarily characterized by a change in blood composition, it is quite natural that the basis of diagnostics will be laboratory studies.

In the event of characteristic symptoms, it is worthwhile for help from the therapist, which will conduct the manipulation of primary diagnostics and will prescribe general surveys, and if necessary, will send a patient for additional advice to other specialists.

The first step in establishing the correct diagnosis is directed to:

study of the history of the disease - to search for pathological factors leading to secondary hemosiderosis;
familiarization with the history of human life - to establish possible sources of the primary form of illness;
the most careful physical examination of the patient, which must necessarily include the study of the condition of the skin, palpation of the front wall of the abdominal cavity, measurement of the pulse and blood pressure;
detailed patient survey - to compile a complete symptomatic picture of the disease.

Laboratory studies are based on:

general blood analysis;
blood biochemistry;
PCR tests;
general analysis of urin;
the optic sample;
microscopic studies of sputum.

The most valuable diagnostics are tool procedures:

biopsy affected segment, i.e. skin cover, liver, kidney, light, bone marrow, etc.;
spirometry;
bronchoscopy;
scintigraphy;
radiography of the sternum;
CT and MRI.

Treatment

It is possible to cure such a disease using conservative therapy techniques used for any embodiment.

Treatment of hemosiderosis includes:

receiving glucocorticoids;
the use of immunosuppressants and iron preparations;
implementation of plasmapheresis;
use of medicines to relieve symptoms;
inhalation of oxygen;
cryotherapy;
vitamin therapy;
reception of drugs containing calcium and angioprotectors;
PuU-therapy - with skin hemosiderosis.

Surgical intervention in therapy is not applied.

Possible complications

Idiopathic hemosiderosis of lungs and other varieties of the disease, in the absence of therapy, are fraught with the formation of such consequences:

infarction easy
light hypertension;
internal hemorrhages;
recurrent pneumothorax;
chronic respiratory failure;
light heart syndrome;
hypochromic anemia.

Views

Local hemosiderosis develops as a result of emerging hemolysis in a lesion focus - in the organ or hematoma. Excess pigment accumulation does not cause tissue damage. If there are sclerotic changes in the organ, its function is broken.

The total hemosiderosis is the result of intravascular hemolysis and a significant deposit of hemosiderin in the internal organs. Gepatocytes of the liver, cells of the spleen and other internal organs are most affected. Excess pigment makes them brown or "rust". This happens in systemic diseases.

Separate nosological forms allocate:

Essential pulmonary hemosiderosis
Hereditary hemochromatosis
Skin hemosiderosis
Liver hemosiderosis
Idiopathic hemosiderosis.

In turn, skin hemosiderosis is divided into the following forms: Shambling disease, Maikki disease, Geuzo-Blum's disease, hidden dermatitis.

The reasons

The etiology of the disease is not fully clarified. Gemosiderosis is a secondary state caused by pathological processes available in the body.

The disease develops in persons having:

Hematological problems - hemolytic anemia, leukemia,
Infectious diseases - sepsis, brucellosis, typhoid, malaria,
Autoimmune processes and immunopathology,
Endocrinopathy - diabetes, hypothyroidism,
Congenital defects and abnormal walls,
Vascular pathology - chronic venous insufficiency, hypertensive disease,
Heart failure in the stage of decompensation or cirrhosis of the liver,
Intoxication syndrome
Rhow conflict.

Of great importance in the development of pathology have frequent hemotransphus, hereditary predisposition, skin diseases, abrasions and wounds, hulings of the body, receiving some medicines, excessive consumption of iron to food.

Symptomatics

The clinical picture of the hemosiderosis is determined by the location of the lesion. The disease begins suddenly and develops gradually.

At the skin shape, the rash is held for months and years and accompanied by itching of various intensity. Pigment stains are clearly limited, have a reddish color and remain on the skin even when pressed.

The pulmonary hemosiderosis is characterized by the appearance of shortness of shortness of breath, anemia, a wet cough with a bloody separated, temperature rise to febrile values, an increase in signs of respiratory dysfunction, hepatosplegegaly. The exacerbations later replaced by remission, in which the level of hemoglobin is normalized, and the clinical signs gradually disappear.

Light hemosiderosis

Idiopathic hemosiderosis of the lungs is a heavy chronic pathology, the main pattomorphological links of which are: repetitive hemorrhages in the alveoli, the collapse of the erythrocytes and a significant accumulation of hemosiderin in the pulmonary parenchyma. As a result, patients are formed persistent pulmonary dysfunction.

The symptoms of the acute form of the disease are:

Productive cough and hemoptia
Skin pallor
Injecting Scler,
Breaking
Dyspnea,
Chest pain,
Arthralgia,
Temperature rise
Heart palpitations,
Full blood pressure
Hepatosplegegaly.

Remissance is distinguished by the lack of complaints and severe clinical symptoms. During this period, patients retain performance. Over time, exacerbation of pathology occurs more and more often, and remission becomes shorter.

In severe cases, the chronic course of hemosiderosis is manifested by the symptoms of the pulmonary heart, pneumonia, pneumothorax and can endally end.

Brown lung induration - severe disease, rarely diagnosed in life. In the blood of patients, autoantibodes are formed in response to the impact of sensitizing antigen. The antigen antibody complex is formed, and autoameric inflammation is developing, for which the targets are becoming lungs. The pulmonary capillaries are expanding, the red blood cells penetrate from the vascular bed into the pulmonary tissue, gemiderine begins to postpone.

Skin hemosiderosis

Skin hemosiderosis is a dermatological disease, in which pigment spots and various rashes appear on the skin of patients. The appearance of sections of pigmentation and petechs is due to the accumulation of hemosidere in the dermis and the defeat of the capillaries of the papillary layer.

The specks on the skin have spilled color and size. Fresh rashes are usually painted in brightly red, and those who havetented - in brownish, brown or yellow. Spots of up to three centimeters are localized on the lower extremities, on brushes and forearms. On the affected skin, petechia, nodules, papulas, plaques are often arisible. Patients complain of insignificant burning and itching.

The patient's derma changes the structure of the endothelium of capillaries, the hydrostatic pressure increases in them. Plasma comes out of the vascular bed, and with it, red blood cells are displayed. The capillaries are expanding, gemiderine's boulders are postponed in the endothelium, histocytes and endotheliocytes are affected, perivascular infiltration develops. This is how the process of deposition of hemosiderin in the skin. In patients in clinical analysis of blood, thrombocytopenia and infringement of iron exchange are usually found.

Skin hemosiderosis may occur in various clinical forms, among which are the most common: myokki disease, geuceo-bluum, orthostatic, eczematid-like and itchy purple.

Shamberman's disease

Special attention deserves shamberman's disease. This is a fairly common autoimmune pathology of the chronic flow, characterized by the appearance on the skin of red dots, similar to the trail from the usual injection. In the wall of the vessels, circulating immune complexes are deposited, autoimmune inflammation of the endothelium develops, intradermal petechial hemorrhages appear. The hemosidererin in large quantities accumulates in the nipple layer of the dermis, which is clinically manifested by the appearance on the skin of symmetric brown spots. They combine and form plaque or whole areas of yellow or brown. At the edges of such plaques, bright red rashes appear. Patechia and hemorrhages are also present in the skin on the skin, which merge among themselves and form large foci. Over time, plaques in the center are atrophy. The overall health of patients remains satisfactory. Pathology favorable forecast.

Skin hemosiderosis, unlike the pulmonary and general, is well amenable to correction. Patients feel satisfactorily and quickly restored.

Gemosiderosis of internal organs

Systemic or generalized hemosiderosis develops in the presence of massive intravascular hemolysis of erythrocytes. The disease is distinguished by the damage to the internal organs and has a severe clinical course. Patients with a common hemosiderosis complain about poor well-being, they change the skin color, frequent bleeding occurs.

Gemosiderosis of the liver It happens idiopathic or primary, as well as secondary. Hemosiderine is postponed in hepatocytes. The liver increases and compacted, becomes painful during palpation, ascites occurs, hypertension, the yellowness of the skin and the scool, splenomegaly, the pigmentation of the hands, face and the armpits. In the terminal stage, as the absence of treatment, acidosis develops. The patient flows into anyone.
Gemosiderosis of the kidneys It is characterized by the appearance of brown granules in a parenchym of the organ. The patients develop a clinic of nephrotica or jade. In the urine, protein is found in the blood - an increased lipid content. The main symptoms of the kidney hypostendine are: swelling stop, legs and eyelids, weakness, lack of appetite, the appearance of muti in the urine, pain in the lower back, dyspepsia. If it does not start the treatment in time, severe complications will emerge - renal failure, which often ends with the death of patients.
Gemosiderine can be postponed in the brain, spleen and other organs, accumulate in macrophages and endothelium of vessels. This leads to the development of hazardous diseases, severe complications and even a deadly outcome.

Systemic hemosiderosis is a danger to the life of patients, making it unhappy and short. The defeat of the internal organs often ends with the development of serious consequences.

Diagnostics

After listening to the complaints of patients, the collection of history and the general inspection, experts go to laboratory and instrumental research methods.

In the clinical laboratory, blood takes on a general analysis, the serum iron and the overall iron binding ability are determined.
The biopsy of the affected tissues and histological examination of the biopsyat is of great importance for diagnosis.
The desperial sample allows you to determine the hemosidere in the urine after the intramuscular injection of "Refimer".
Dermatoscopy of the rash area is a microscopic study of the papillary layer of the dermis.

Among the additional diagnostic methods, the following are the following studies of the lungs:

radiographic
tomographic
scintigraphic
bronchoscopic
spirometric,
microscopic and bacteriological examination of sputum.

Treatment

Treatment of hemosiderosis begins with the fulfillment of general medical recommendations:

It is easy to eat, eliminate food allergens from dietary, sharp and fried dishes, smoked, alcohol;
Avoid injuries, supercooling, overheating and overvoltage;
Timely identify and sanitize the organisms of chronic infection in the body;
Treat concomitant diseases;
Do not use cosmetics that can provoke allergies;
Fight bad habits.

Medical therapy consists in prescribing patients with medicinal preparations:

Local and systemic corticosteroids - "prednisolone", "betamethazone", "dexamethasone" and drugs based on them,
Anti-inflammatory drugs - "ibuprofen", "indomethacin",
Disagregantes - "Aspirin", "Cardiomagnet", "acetylsalicylic acid",
Immunosuppressants - "Azatihodn", "Cyclophosphane",
Angioprotectors - "Diosmin", "Heperididin",
Antihistamine - "Diazolina", "Supratin", "Tueguil",
Nootropic drugs - Piracetama, Vinpocetina, "Maxidol",
Polyvitamins and polymininerals - ascorbic acid, routine, calcium preparations.

Symptomatic correction includes long-term use of iron preparations, hemostatic agents, polyvitaminins, bronchoditics, oxygen therapy. Patients conduct an extracorporeal hemocorrection: hemosorption, plasmophoresis, cryopritation, criteriapia. In severe cases, splenectomy and blood transfusions give good results.

The funds of traditional medicine used to strengthen the vascular wall and reduce the manifestations of hemosiderosis: infusion from the mountain arnica and the bark of the hazel, the decoction of the Tolstole Badan.

Prevention

Hemosiderosis is a chronic disease characterized by changing exacerbation and remission. After the competent treatment and stabilization of the state of the patients, preventive measures must be observed, warning a new exacerbation. These include spa treatment, proper nutrition and healthy lifestyle.

Preventive measures to prevent the development of hemosiderosis:

Timely and adequate treatment of acute infectious and dermatological pathologies,
Solving problems with vessels,
Control body mass, cholesterol and blood pressure,
Exclusion of poisoning and intoxication.