Hemosiderosis: development, localization, symptoms, diagnosis, treatment. Hemosiderosis of the skin of the legs and other parts of the body: diagnosis and treatment Hemosiderosis of parenchymal organs

Hemosiderosis is a disease belonging to the group of pigmentary dystrophies. It is characterized by the accumulation of excess amounts of hemosiderin, an iron-containing pigment, in the tissues of the body.

Skin manifestations of hemosiderosis

Causes and risk factors

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

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

hemolytic anemia;
poisoning with hemolytic poison (quinine, lead, sulfonamides);
leukemia;
multiple blood transfusions;
cirrhosis of the liver;
Rhesus conflict;
infectious diseases (relapsing fever, malaria, brucellosis, sepsis);
decompensated heart failure;
chronic venous insufficiency;
diabetes;
dermatitis;
eczema.

Some experts believe that in pathological mechanism Hereditary predisposition and immune system disorders play an important role in the development of hemosiderosis.

Forms of the disease

According to the degree of spread of the pathological process, the following are distinguished:

general (generalized) hemosiderosis - it is caused by intravascular (endovascular) hemolysis of red blood cells that occurs against the background of any systemic processes. Hemosiderin is deposited in the spleen, red bone marrow, liver, as a result of which they acquire a rusty, brown color;
local (local) hemosiderosis - develops as a result of extravascular (extravascular) hemolysis. The accumulation of hemosiderin can be observed both in small areas of the body (in the area of hematomas) and within an organ (for example, the lung).

According to the characteristics of the clinical course, the following are distinguished:

hemosiderosis of the skin (ocher dermatitis, purpuric angiodermatitis, lichenoid pigmentary dermatitis, senile hemosiderosis, annular telangiectatic purpura of Majocchi, Schamberg's disease);
pulmonary idiopathic hemosiderosis (brown induration of the lungs).

Pulmonary hemosiderosis progresses and leads to disability in patients. It can be complicated by massive pulmonary hemorrhages, leading to rapid death.

In some cases, hemosiderin deposition causes dysfunction of the affected organ and the development of structural changes in it. This form of hemosiderosis is called hemochromatosis.

Symptoms

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

Pulmonary idiopathic hemosiderosis is diagnosed mainly in children and young people, characterized by periodically occurring pulmonary hemorrhages of varying severity, increasing respiratory failure and persistent hypochromic anemia.

In the acute phase of the disease the following are observed:

dyspnea;
pain in chest;
cough with bloody sputum;
pale skin;
icterus sclera;
cyanosis of the nasolabial triangle;
weakness;
dizziness;
increase in body temperature.

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

The cutaneous form of hemosiderosis occurs more often in men over 40 years of age. The course is chronic and benign. Appear on the skin of the forearms, hands, legs and ankles dark spots brick red color. Over time, the color of the rash elements changes to yellowish, dark brown or brown. Damage to internal organs does not occur in the cutaneous form of hemosiderosis, and the general condition does not suffer.

Diagnostics

Diagnosis of hemosiderosis is based on the characteristic clinical signs of the disease, data from laboratory and instrumental examination methods. Appointed general analysis blood, serum iron concentration is determined.

If hemosiderosis is suspected, a desferal test is performed. To do this, deferoxamine is injected intramuscularly, and then the iron content in the urine is determined. The test is considered positive if a portion of urine contains more than 1 mg of iron.

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

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

For hemosiderosis of the lungs, the following is also carried out:

spirometry;
microscopic examination of sputum;
lung perfusion scintigraphy;
chest x-ray;
bronchoscopy.

Treatment

Therapy for pulmonary hemosiderosis begins with the administration of corticosteroids. If it is ineffective, patients are prescribed immunosuppressants and undergo plasmapheresis sessions. In some cases, it is possible to achieve stable remission after removal of the spleen (splenectomy). In addition, symptomatic therapy is carried out with the prescription of bronchodilators, hemostatics and other drugs (depending on the manifestations of the disease).

Treatment of cutaneous hemosiderosis consists of local application of corticosteroid ointments. Angioprotectors, calcium preparations, rutin, and ascorbic acid are also prescribed. In severe cases of the disease, the use of deferoxamine and PUVA therapy is indicated.

Possible complications and consequences

The most common complications of pulmonary hemosiderosis:

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

Forecast

The prognosis for pulmonary hemosiderosis is serious. The disease progresses and leads to disability in patients. It can be complicated by massive pulmonary hemorrhages, leading to rapid death.

With the cutaneous form of hemosiderosis, the prognosis is favorable.

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

Prevention

Prevention of disorders of hemosiderin metabolic processes consists in timely treatment hematological, vascular and infectious diseases, prevention of chemical or drug intoxication, blood transfusion complications.

HEMOSIDEROSIS (haemosiderosis; Greek, haima blood + sider iron + -osis) - excessive formation of hemosiderin and its deposition in tissues, observed in a number of diseases and due to various reasons. Among them, there are endogenous ones, for example, massive destruction of red blood cells, increased absorption of iron in the intestine, and exogenous ones, for example, with frequent blood transfusions. G. can be local or general in nature.

The body has a fairly constant supply of iron under normal conditions in the form of two protein complexes - ferritin and hemosiderin. Ferritin is a water-soluble compound, the molecule of which consists of a protein part (apoferritin) and colloidal strands of ferric iron. Hemosiderin is a water-insoluble yellow-brown pigment; its protein part is identical to apoferritin. Hemosiderin, unlike ferritin, also contains inorganic compounds phosphorus, sulfur, nitrogen and non-protein organic substances. There is an idea about the transformation of ferritin into hemosiderin [Shoden, Stegeron (A. Shoden, P. Sturgeron)].

It has been established that iron levels are maintained by the regulation of absorption, and not by the process of active excretion. Every day, 0.5 mg of iron is excreted in feces (by cells of the exfoliating intestinal epithelium), 0.2 mg in urine, and 0.5-1.5 mg in women during menstruation. These small losses are compensated by iron absorption. Iron absorption occurs mainly through the mucous membrane of the duodenum.

Food products contain iron in quantities many times higher than required. However, the magnitude intestinal absorption iron depends little on its content in the products entering the intestines.

Conrad, Weintraub, Crosby (M.E. Conrad, L.R. Weintraub, W.H. Crosby) using radioactive iron showed that iron absorption occurs in two phases: the entry of iron from the intestinal lumen into the mucous membrane and the movement of iron from the mucous membrane into the blood plasma and fabrics. According to M. S. Wheby's hypothesis, iron absorption consists of three phases: penetration into the mucous membrane from the intestinal lumen, penetration from the intestinal mucosa into the plasma, and iron deposition in the mucous membrane. Penetration of iron into the mucous membrane from the intestinal lumen occurs faster than from the mucous membrane into the plasma. However, when the body's need for iron increases, its entry into the plasma accelerates and iron in this case is not deposited in the form of a reserve.

It has been shown that 80% of the iron adsorbed by the intestinal mucosa quickly passes into the plasma and combines with the transport protein transferrin. Next, the iron bound to transferrin is taken up by red blood cell precursors and used again for the synthesis of hemoglobin. Weintraub (1965) was able to identify the dependence of the intensity of intestinal absorption of iron on the level of hemoglobinogenesis, but the mechanism of the quantitative relationship between these two processes remains unclear. The remaining 20% of absorbed iron is fixed in the tissue by iron-sensing protein. If the body's need for iron increases, this bond weakens and the iron passes into the plasma, and the receptor protein again fixes the iron with a new intake of food. If the need for iron in the body is small, then most of the adsorbed metal is fixed in the form of hemosiderin and ferritin in intestinal cells. Since the latter quickly desquamate (usually after 3-4 days), the iron fixed in them is released into the intestinal lumen.

If there is an abnormality in iron absorption, such as, for example, with hemochromatosis (see), hemosiderin is deposited in the organs. The pathogenesis of these disorders is not completely clear; It is indisputable, however, that in the intestine the absorption of iron does not depend on its reserves in the body.

Rice. 24. Accumulation of hemosiderin (blue) in the epithelium of convoluted tubules of the kidneys in secondary hemosiderosis (Perls stain; x 120). Rice. 25. Hemosiderosis of the liver (hemosiderin - blue; Perls stain): a - in liver and Kupffer cells (X 400); b - diffuse hemosiderosis in thalassemia (X100). Rice. 26. Alveolar macrophages with hemosiderin ( brown color) with essential pulmonary hemosiderosis (X400).

Hemoglobin of destroyed erythrocytes is fixed by reticular, endothelial and histiocytic cells of the spleen, liver, kidneys (color. Fig. 24 and 25), bone marrow, lymph nodes, where it is preformed into hemosiderin grains, causing these organs to become rusty. Brown.

Methods and techniques for detecting hemosiderosis

To assess iron reserves, complexones are used, which bind and remove ferric iron from the body. The most commonly used complexon is desferal (syn. deferoxamine), which complexes with the iron of iron-containing proteins - ferritin and hemosiderin (but not with the iron of hemoglobin and iron-containing enzymes). It forms a stable complex with ferric iron and is excreted by the kidneys in the form of ferrioxyamine (see Complexons). The introduction of desferal does not significantly affect the release of other metals and trace elements.

Desferal test: 500 mg of the drug is administered intramuscularly to the patient once and for 6-24 hours. After the injection, urine is collected and the amount of iron is determined. The test is considered positive if the iron content in the urine is more than 1 mg. Based on the data from the desferal test, it is possible to decide on the need for complexone therapy to remove excess iron from the body, as well as the advisability of treatment with iron preparations when iron reserves are depleted. The desferal test is used as a diagnostic test in patients with thalassemia; Using this test, you can exclude iron deficiency anemia (a common misdiagnosis in patients with thalassemia).

To identify G., the level of serum iron is also examined (if it decreases, iron supplements are prescribed) and the degree of blood saturation with transferrin. A reliable diagnostic criterion is the detection of iron in a liver biopsy, in a bone marrow treponate using the Perls method (see Perls method), as well as counting the number of sideroblasts in a bone marrow aspirate.

Diagnostic value

In areas of hemorrhage, with extravascular destruction of red blood cells, local hemorrhage occurs. General hematopoiesis is observed in various diseases of the hematopoietic system (anemia, some forms of leukemia), intoxication with hemolytic poisons, some infectious diseases (relapsing fever, brucellosis, malaria, etc.), and frequent blood transfusions. etc. Rarely general G. manifests itself as hereditary disease- hemochromatosis (see). The latter is characterized by the deposition in tissues, in addition to hemosiderin, of another iron-containing pigment - hemofuscin, as well as lipofuscin.

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

Treatment

Treatment measures are carried out primarily in relation to the underlying disease. In addition, bloodletting is used, which is especially effective for diffuse G. accompanying idiopathic hemachromatosis. Bloodletting in a volume of 500 ml is equivalent to the removal of 200 mg of iron. However, in case of iron-refractory anemia, this method, which requires constant and systematic blood transfusions, is not justified [R. M. Bannerman]. In the treatment of secondary hepatitis (complications of liver cirrhosis), the drug diethylenetriamine penta-acetate [McDonald, Smith (R. A. McDonald, R. S. Smith)] is effective; however, its injections are painful and sometimes cause side effects. The introduction of desferal into the wedge and practice has opened up new opportunities in the treatment of G. of various origins. Desferal is usually administered 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 [F. Wohler] on the use of desferal for a year or more in patients with idiopathic hemochromatosis. The main criterion determining the duration of treatment is the excretion of iron in the urine; if daily iron excretion does not exceed 1.0-1.5 mg, deferoxamine injections are stopped. From other to lay down. agents, you can specify complexing compounds - thetacine-calcium (see) and pentacine (see).

Essential pulmonary hemosiderosis (color. Fig. 26 and 27) occupies special place, because it is fundamentally different in etiology, pathogenesis and clinical picture from hemochromatosis. Deposits of hemosiderin are found only in the lungs, which is reflected in its old names - brown induration of the lungs, essential brown induration of the lungs, pulmonary stroke, congenital bleeding into the lungs (see Idiopathic pulmonary hemosiderosis).

Bibliography: Dolgoplosk N. A. and Skaldina A. S. A case of essential hemosiderosis of the lungs, Vestn, rentgenol, i radiol., No. 1, p. 88, 1971, bibliography; Martynov S. M. and Sheremeta N. A. About transfusion hyperhemosideroses and hemochromatosis in leukemia, hemoblastosis and aplastic anemia* in the book: Sovrem. Problem, hematol. and overflow, blood, ed. A. E. Kiseleva et al., c. 38, p. 243, M., 1966; Fainshtein F. E. et al. The use of desferal 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.

Hemosiderin is a characteristic pigment that is deposited due to the breakdown of red blood cells, including when their metabolism is disrupted. When hemosiderin begins to be deposited in large quantities, a disease called hemosiderosis occurs.

Hemosiderosis begins to occur, as a rule, as a result of other concomitant diseases, which are mainly associated with circulatory disorders, but can also have an independent form.

The disease occurs for two main reasons:

Endogenous. Characterized by extensive destruction of red blood cells and excessive absorption of iron.
Exogenous. Occurs due to blood transfusion.

The human body requires a regular supply of iron from external sources, but in quantities not exceeding the recommended ones, approximately 15 mg per day. In case of constant excess of the amount of incoming iron, this is fraught with its abnormal accumulation in tissues (hemosiderosis), which leads to various serious diseases.

In adults, iron accumulation in the body does not exceed 5 grams. If the human body experiences an excess of iron, then hemosiderin accumulates in the tissues of the brain and other organs. This abnormal accumulation contributes to the development of a number of other diseases.

Other reasons for the rapid accumulation of hemosiderin in the brain are:

Acute infectious diseases (brucellosis, malaria);
Chemical and toxic poisoning;
Abnormal effects of various medicines, due to their overuse(sorbifer, maltofer);
Systematic blood transfusion;
Genetic diseases (enzymopathy, hemoglobinopathy);
Systematic blood transfusions;
Circulatory disorders;
Autoimmune diseases.

Classification

Hemosiderosis has 2 forms of development:

Local

This pathology is characterized by extravascular destruction of red blood cells or so-called extravascular hemolysis in places where hemorrhage occurred. In this case, red blood cells are deprived of hemoglobin and transform into pale round bodies.

Once released, hemoglobin and the remainder of the red blood cells are taken up by other cells (leukocytes, endothelium and epithelium) and are initially generated in the cytoplasm into hemosiderin.

In areas of excessive blood accumulation, hemosiderin is deposited. In areas where there is no oxygen, hematoidin crystals begin to settle. Depending on the conditions of occurrence, hemosiderosis occurs in a specific area of tissue or an entire organ (hemosiderosis of the lungs, liver, brain).

General

Has a characteristic excess of iron due to intravascular hemolysis or abnormal absorption of iron from food. Hemosiderin is deposited, as a rule, in the bone marrow, liver and other organs. In this case, the pigment does not have the property of destroying parenchymal cells, as a result of which the functions of the organs are not damaged.

Occurs in diseases such as anemia, leukemia, brucellosis, malaria and others. If an excess of iron occurs, in which tissue begins to be damaged, resulting in a decrease in the functionality of organs, this leads to the disease hemochromatosis.

There are also 3 types of hemoteriosis as independent diseases:

Essential pulmonary.

This disease is hereditary. It is characterized by pathology of the lung tissue, resulting in frequent hemorrhage into this tissue, as well as the development of pulmonary sclerosis. When diagnosed, hemosiderin has a distinct brown color. The disease is characterized by extensive pathological symptoms of the lungs, such as persistent cough with pain and frequent bleeding, shortness of breath, nausea and malaise.

Hemochromatosis.

This disease is also hereditary and is manifested by a disorder of iron metabolism with abnormal accumulation in the tissues and organs of the patient. Iron tends to accumulate in almost all human organs, as a result of which it provokes diseases such as heart failure, diabetes, arthritis, and cirrhosis of the liver. Symptoms are pronounced and manifest themselves in the form of weakness, fatigue, low blood pressure, joint diseases and heart failure.

Skin hemosiderosis

Given pathological disease characterized by the deposition of hemosiderin in the dermis. Hemosiderin in the brain and tissues of other organs, due to hemorrhages, begins to be deposited in the skin, as a result of which characteristic pigment spots with a diameter of 0.5 - 3 cm, yellow or brownish, begin to appear on the skin. Symptoms manifest as external skin rashes, with internal organs the person is completely fine

Symptoms largely depend on what type of disease the patient has (skin, pulmonary, etc.). However, in many cases the symptoms may be similar or appear to varying degrees. It is also worth saying that the disease can occur in completely different ways, so each person experiences the symptoms of the disease individually.

The most common symptoms of hemosiderosis are:

Coughing up blood (usually a pulmonary type of illness);
Shortness of breath;
Accelerated heartbeat, as well as pain in the heart and internal organs.
Change in skin color;
Pulmonary infarction and also abnormal changes in the liver or lung;

Childhood hemosiderosis usually occurs at the age of 6-7 years. Symptoms in children are largely similar to those in adults and manifest themselves as shortness of breath, even in a calm state, and characteristic general weakness. The cough may also be accompanied by blood, although, as a rule, not with such characteristic discharge.

The temperature also begins to rise strongly, up to 39.5 degrees. This symptomatology tends to last about 7 days and then gradually weaken

Several specialists are involved in the examination and diagnosis of hemosiderosis. These specialists are a dermatologist (cutaneous hemosiderosis), a pulmonologist, an infectious disease specialist, a hematologist and others.

A specialist, regardless of the form of the disease, begins to carry out the following procedures:

General blood analysis;
Determination of serum iron;
The ability to bind iron in the body.
Biopsy of bone marrow and other tissues to detect hemosiderin

For diagnostic purposes, the following techniques can be used:

Radiography
Magnetic resonance imaging and;
Bronchoscopy.

Also, the specialist must carry out the so-called desferal test, during which the patient is repeatedly administered 500 mg of desferal. After that, urine is collected from 6 to 24 hours and the amount of iron in it is determined. As a rule, a blood test shows low hemoglobin levels and a low number of red blood cells.

Video

Hemosiderosis is a pathology in which the level of hemosiderin (hemoglobin pigment) in the tissues of the body exceeds.

Due to the variety of types, causes and complex clinical picture, this disease is studied by doctors in the field of pulmonology, dermatology, hematology, immunology and other medical disciplines.

Hemosiderin is a brown pigment, the main component of which is iron oxide.

It is formed in the biological process of fermentation (breakdown) of hemoglobin and subsequent synthesis in sideroblasts (nucleated cells).

Normally, the body of each person contains approximately 4-5 g of this iron-containing pigment.

Excessive accumulation of it can lead to structural changes inside the body.

Reasons for its accumulation

The pathogenesis of hemosiderosis depends on the type of disease - general (over the entire surface of the organs) or local (with the formation of foci).

The etiology of general hemosiderosis is not fully understood, but there are many hypotheses, including the following:

heredity;
immune pathologies;
congenital disorder of metabolic processes.

It is noted that hemosiderin deposition in the lungs is observed in patients with decompensated heart pathologies.

Cutaneous hemosiderosis can occur either independently or as a consequence of any other pathologies.

The secondary form of the disease can occur due to the following pathologies:

hematological diseases (leukemia, hemolytic anemia);
infections (sepsis, malaria, syphilis, brucellosis, typhoid);
diseases of the endocrine glands (diabetes mellitus, hypothyroidism);
vascular disorders (hypertension, chronic venous insufficiency);
dermatitis, eczema, neurodermatitis, pyoderma;
violation of skin integrity (trauma, erosion);
intoxication with pesticides, metals;
Rhesus conflict.

In addition, the following factors may influence the onset of the disease:

hypothermia;
chronic fatigue;
stressful situations, nervous tension;
overdose of drugs (NSAIDs, diuretics, Paracetamol, Ampicillin).

Types of disease and their symptoms

Hemosiderosis is classified according to the etiological principle, location and extent of spread. The clinical picture of the disease depends on these factors.

Depending on the etiology, there are two types of hemosiderosis:

primary - the causes of occurrence are not fully understood;
secondary - develops against the background of certain diseases and external provoking factors.

In the first case, the skin and lungs are affected, in the second - the area of the kidneys, liver, spleen, bone marrow, salivary and sweat glands.

The classification of hemosiderosis by location and extent of spread is presented in this table:

Varieties of nosological forms:

Lungs

Idiopathic pulmonary hemosiderosis is characterized by periodic hemorrhages into the alveoli. In this case, blood cells are broken down, forming hemosiderin.

The pigment is attacked by alveolar macrophages (killer cells), which provokes its deposition in spaces connective tissue. As a result, compaction is noted, and then the replacement of organic tissue with connective tissue.

Main symptoms of the disease:

cough accompanied by sputum;
expectoration of blood;
respiratory failure combined with shortness of breath;
pain in the chest area;
pallor;
change in color of the skin, mucous membranes and membranes of the eyes (sclera);
the appearance of cyanosis in the nasolabial area;
general malaise, weakness, decreased ability to work;
elevated temperature;
loss of appetite;
cardiopalmus;
hypotension (low blood pressure);
increase in the size of the liver and spleen;
hypochromic anemia, up to the last degree of severity.

Brown induration of the lungs is a serious disease that is diagnosed in rare cases. This pathology in most cases occurs in children, less often in young people.

This pathology is characterized by periods of remissions and exacerbations. During remissions, the clinical picture appears weakly or disappears. After each exacerbation, the remission intervals become shorter.

Skin

Hemosiderosis of the skin is a pathology caused by the accumulation of iron-containing pigment in the layers of the dermis.

This is what it looks like in the photo:

Clinical characteristics - changes in the skin due to rashes or age spots up to 3 cm in size.

General symptoms:

foci of pigmentation are most often observed in the legs (on the shins or ankles), as well as in the forearms and hands;
variations in the color of spots - from brick color (with fresh formations) to brown, dark or yellow tones in old rashes;
mild skin itching may occur;
nodules, pathechia (tiny flat spots), lichenoid papules (pimples, balls) or plaques may form on the affected areas.

This disease is more often diagnosed in mature men (30-60 years old).

A chronic form of the pathology is usually observed. In this case, the condition of the patients is assessed as satisfactory, no organ damage is noted.

Internal organs

Hemosiderosis with damage to internal organs has a severe form. The accumulation of glandular pigment occurs in hepatocytes (the main cells of the liver).

Hepatic hemosiderosis is of two types:

hereditary primary (or idiopathic);
secondary.

In the first case, this is a consequence of impaired metabolism, in which hemosiderophages of the gastrointestinal tract capture iron. In this case, uncontrolled absorption and deposition of hemosiderin occurs in the liver.

In the secondary form, the pathology is caused by a number of external or internal causes. For example, poison intoxication, cirrhosis, etc.

Main symptoms:

compaction of the organ with subsequent increase in size;
pain on palpation;
the appearance of portal hypertension, ascites (signs of cirrhosis);
icteric color of the sclera of the eyes and skin;
increase in spleen volume;
the appearance of age spots on the hands, armpits, face;
with a prolonged course, the development of diabetes mellitus may occur;
with severe damage, the possibility of acidosis or coma is noted.

At laboratory research Signs of nephrotic syndrome may be detected, which indicate the deposition of hemosiderin in the renal parenchyma.

Clinical manifestations of renal hemosiderosis:

swelling of the eyelids and lower extremities;
cloudiness and decreased amount of urine;
aversion to food;
pain in the lumbar region;
feeling of malaise, weakness;
dyspepsia (indigestion).

This pathology requires immediate medical intervention before the onset of renal failure, which can be fatal.

Somewhat less often, pigment deposits are observed in the bone or brain, heart, etc. This occurs when macrophages attack hemorrhages surrounding organs.

Heart damage is considered very dangerous, which often ends in severe cardiovascular pathologies or death.

Diagnostic methods

The initial appointment with a primary care physician includes a questioning, history taking, and examination of the patient for signs of illness.

Diagnosis of hemosiderosis is carried out using the following methods:

How is the treatment carried out?

Treatment is prescribed by a specialist after establishing the diagnosis and the cause of the disease. To completely get rid of pathology in medicine, it is customary to use an integrated approach.

Table medicines, capable of normalizing hemosiderin metabolism and reducing its harmful effects on organs:

In addition to taking medications, the patient may be prescribed the following procedures:

PUVA therapy;
plasmapheresis;
oxygen inhalation;
cryoprocedure.

Complications and consequences

In most cases, the prognosis for treating the pathology is favorable.

The exception is the advanced stages of pulmonary hemosiderosis, which is fraught with the following complications:

organ infarction;
internal bleeding;
pneumothorax with phases of relapse;
disorders of the right region of the heart;
pulmonary hypertension and development of cor pulmonale;
chronic form of respiratory failure.

Prevention measures

Rules for the prevention of hemosiderosis:

Prevention of diseases that can cause increased destruction of red blood cells.
Correct dosage of iron supplements when treated with them.
It is necessary to periodically check for the presence of vascular pathologies.
Weight, cholesterol and blood pressure levels should be monitored.
It is important to promptly consult a doctor at the first signs of infection or skin pathology.

Clinically, hemosiderosis of the skin is characterized by pigment spots 0.1-3 cm in diameter or more from yellow to dark brown; At the same time, small, persistently dilated vessels - telangiectasia, pinpoint hemorrhages - petechiae, and areas of atrophy - are usually observed. The tourniquet symptom (petechiae at the site of compression by the tourniquet) and cupping test (petechiae at the site of cupping) are often positive, which indicates a decrease in capillary resistance. Depending on the nature of the rashes, their location and localization, several forms of skin hemosiderosis are distinguished: Schamberg's disease (see); ring-shaped telangiectatic purpura of Majocchi - isolated, circular, small-spotted rashes with atrophy, located mainly around the hair follicles; senile reticular hemosiderosis of the skin - small purpuras and pigmentation on the back of the hands and extensor surfaces of the forearms; lichenoid purpuric and pigmentary dermatitis Gougerot-Blum [distinguished by the presence of lichenoid (small flat) papules, areas of atrophy are absent]; ocher-yellow dermatitis of the legs, usually accompanying varicose ulcers of the legs. The prognosis is favorable. When fresh hemorrhages stop, skin hemosiderosis slowly reverses.

Treatment: ascorbic acid 0.25 g 3 times a day, rutin 0.05-0.1 g 3 times a day, diphenhydramine 0.03-0.05 g 3 times a day, calcium supplements (10% calcium chloride solution according to 1 tablespoon 3 times a day, calcium gluconate 0.5 g 3 times a day). Treatment is carried out for 3-4 weeks, depending on clinical picture.

Hemosiderosis

Hemosiderosis is a disease of the group of pigmentary dystrophies, characterized by excessive accumulation of the iron-containing pigment hemosiderin in the tissues of the body. There are local forms of the disease (cutaneous and pulmonary hemosiderosis) and general (with the deposition of hemosiderin in the cells of the liver, spleen, kidneys, bone marrow, salivary and sweat glands). Diagnosis of hemosiderosis is based on determining the iron content in the blood plasma, the total iron-binding capacity of the blood, as well as the pigment content in biopsy samples of tissues and organs. Depending on the clinical picture, treatment of hemosiderosis includes drug therapy(glucocorticoids, cytostatics, angioprotectors, vitamin C), in some cases plasmapheresis, local PUVA therapy.

Hemosiderosis

Hemosiderosis is a disorder of the exchange of the hemoglobinogenic pigment hemosiderin with its local or systemic deposition in tissues. Hemosiderin is an iron-containing intracellular pigment formed during the enzymatic breakdown of hemoglobin. Hemosiderin synthesis occurs in sideroblast cells. Along with other hemoglobin derivatives (ferritin, bilirubin), hemosiderin is involved in the transport and deposition of iron and oxygen, and the metabolism of chemical compounds. Normally, hemosiderin is found in small quantities in the cells of the liver, spleen, bone marrow, and lymphatic tissue. Under various pathological conditions, excessive formation of hemosiderin can occur with the development of hemosiderosis. Studying the epidemiology of hemosiderosis is difficult due to great variety forms of this disorder.

Depending on the prevalence of the pathological process, local (local) and generalized (general) hemosiderosis are distinguished. Local hemosiderosis is the result of extravascular hemolysis, i.e., extravascular destruction of red blood cells. Local hemosiderosis can develop both in foci of limited hemorrhages (hematomas) and within an entire organ (lung, skin). Generalized hemosiderosis is a consequence of intravascular hemolysis - intravascular destruction of red blood cells in various common diseases. In this case, hemosiderin is deposited in the cells of the liver, spleen and bone marrow, giving the organs a brown (“rusty”) color.

Independent forms of hemosiderosis include:

hemosiderosis of the skin (Schamberg's disease, annular telangiectatic purpura of Majocchi, senile hemosiderosis, lichenoid pigmentosa and purpuric angiodermatitis, ocherous dermatitis, etc.)
idiopathic pulmonary hemosiderosis (brown induration of the lungs)

In the case when the deposition of hemosiderin is accompanied by structural changes in tissues and dysfunction of the organ, they speak of hemochromatosis. Due to the variety of causes and forms of hemosiderosis, immunology, dermatology, pulmonology, hematology and other disciplines are studying it.

Causes of hemosiderosis

The etiology of pulmonary hemosiderosis is not entirely clear. Assumptions have been made regarding hereditary predisposition, the immunopathological nature of the disease, congenital disorders structures of the wall of pulmonary capillaries, etc. It is known that patients with decompensated cardiac pathology (cardiosclerosis, heart defects, etc.) are more susceptible to the development of pulmonary hemosiderosis.

Cutaneous hemosiderosis can be primary (without previous skin lesions) or secondary (occurs against the background of skin diseases). The skin is predisposed to the development of primary hemosiderosis endocrine diseases(diabetes mellitus), vascular pathology (chronic venous insufficiency, hypertonic disease). Dermatitis, eczema, neurodermatitis, skin trauma, and focal infection (pyoderma) can lead to secondary accumulation of hemosiderin in the layers of the dermis. Hypothermia, overwork, and taking medications (paracetamol, NSAIDs, ampicillin, diuretics, etc.) can provoke the onset of the disease.

Pulmonary hemosiderosis

In the acute phase of the disease, patients experience moist cough with the release of bloody sputum. The consequence of prolonged or profuse hemoptysis is the development of severe iron deficiency anemia, pallor of the skin, icterus of the sclera, complaints of dizziness, and weakness. The progressive course of pulmonary hemosiderosis is accompanied by the development of diffuse pneumosclerosis, reflected by shortness of breath and cyanosis. Periods of exacerbation are accompanied by pain in the chest and abdomen, arthralgia, and fever. Objective data are characterized by dullness of percussion sound, the presence of moist rales, tachycardia, arterial hypotension, spleno- and hepatomegaly.

During periods of remission, complaints are not expressed or absent, however, after each subsequent attack, the duration of clear intervals, as a rule, is reduced. In patients with chronic hemosiderosis, cor pulmonale often develops; Severe infarction-pneumonia and recurrent pneumothorax often occur, which can cause death. Idiopathic pulmonary hemosiderosis can be combined with hemorrhagic vasculitis, rheumatoid arthritis, systemic lupus erythematosus, glomerulonephritis, Goodpasture's syndrome.

Skin hemosiderosis

Hemosiderosis of the skin has a chronic course (from several months to several years), and is more common in older men. General state patients with cutaneous hemosiderosis remains satisfactory; internal organs are not affected. The disease must be distinguished from atypical forms lichen planus, pseudosarcoma and Kaposi's sarcoma.

Diagnosis of hemosiderosis

Depending on the form of hemosiderosis, its diagnosis can be carried out by a dermatologist, pulmonologist, infectious disease specialist, hematologist and other specialists. In addition to the physical examination, a general blood test, determination of serum iron, and total iron-binding capacity of the blood are performed. To identify hemosiderosis, tissue biopsy data (skin, liver, lung, bone marrow) are of greatest importance, histological examination of which reveals hemosiderin deposition. A desferal test is used as a diagnostic test - determining the amount of iron in the urine after intramuscular injection 500 mg deferoxamine. If the urine contains more than 1 mg of iron, the test is considered positive.

For pulmonary hemosiderosis, chest x-ray, CT scan, lung perfusion scintigraphy, microscopic examination of sputum, and spirometry are additionally performed. Carrying out bronchoscopy with the collection of lavage water makes it possible to detect siderophages and red blood cells in the lavage fluid.

Treatment of hemosiderosis

Treatment for skin hemosiderosis includes local use corticosteroid ointments, cryotherapy, taking ascorbic acid, routine, calcium supplements, angioprotectors. For severe skin manifestations hemosiderosis resort to PUVA therapy and the prescription of deferoxamine.

Forecast and prevention of hemosiderosis

Idiopathic pulmonary hemosiderosis is a difficult to diagnose disease with serious prognosis. The progressive course of the pathology leads to disability of the patient, the development of life-threatening complications - massive pulmonary hemorrhage, respiratory failure, pulmonary hypertension. The course of skin hemosiderosis is favorable. The disease is largely a cosmetic defect and tends to gradually resolve.

Prevention of hemosiderin metabolic disorders can be facilitated by timely treatment of skin and general infectious, vascular, hematological and other diseases, prevention of blood transfusion complications, and exclusion of drug and chemical intoxications.

Hemosiderosis - treatment in Moscow

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Hemosiderosis: development, localization, symptoms, diagnosis, treatment

Hemosiderosis is a metabolic disorder caused by an excess content of the pigment hemosiderin in the body's cells. Hemosiderin is formed as a result of the biochemical breakdown of hemoglobin under the influence of endogenous enzymes. This substance is involved in the transportation and storage of some chemical substances and connections. Accelerated breakdown of red blood cells, excessive absorption of hemosiderin in the intestine, disruption of metabolic processes in the body lead to excessive formation of pigment and the development of hemosiderosis.

Hemosiderosis has several equivalent names: pigmentary hemorrhagic dermatosis, chronic pigmentary purpura, capillaritis. This dystrophic pathology can occur in various forms Oh:

Local or local, associated with damage to the skin and lungs,
General or generalized, in which hemosiderin accumulates in the liver, spleen, kidneys, bone marrow, salivary and sweat glands.

Various forms of pathology are manifested by similar clinical signs: a red or brown hemorrhagic rash, hemoptysis, anemia, and general asthenia of the body. The disease most often develops in men in adulthood. In children, the pathology is extremely rare.

Hemosiderosis is a blood and metabolic disease that is difficult to treat. This is not just a cosmetic defect, but serious problem, causing dysfunction of internal organs and systems.

Diagnosis and treatment of pathology is carried out by doctors of various specialties: hematologists, dermatologists, pulmonologists, immunologists. Patients are prescribed glucocorticosteroids, cytostatic and angioprotective drugs, multivitamins, and plasmapheresis.

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

hemosiderin deposits in tissues (idiopathic pulmonary hemosiderosis)

General hemosiderosis is the result of intravascular hemolysis and significant deposition of hemosiderin in the internal organs. Hepatocytes of the liver, cells of the spleen and other internal organs are predominantly affected. Excess pigment makes them brown or “rusty.” This occurs in systemic diseases.

The following nosological forms are distinguished:

Essential pulmonary hemosiderosis,
Hereditary hemochromatosis,
Cutaneous hemosiderosis,
Hemosiderosis of the liver,
Idiopathic hemosiderosis.

In turn, cutaneous hemosiderosis is divided into the following forms: Schamberg disease, Majocchi disease, Gougerot-Blum disease, ocher dermatitis.

Causes

The etiology of the disease is not fully understood. Hemosiderosis is a secondary condition caused by pathological processes existing in the body.

The disease develops in individuals who have:

Hematological problems - hemolytic anemia, leukemia,
Infectious diseases - sepsis, brucellosis, typhoid, malaria,
Autoimmune processes and immunopathologies,
Endocrinopathies - diabetes mellitus, hypothyroidism,
Congenital defects and anomalies of the vascular wall,
Vascular pathologies - chronic venous insufficiency, hypertension,
Heart failure in the stage of decompensation or cirrhosis of the liver,
Intoxication syndrome,
Rhesus conflict.

Frequent blood transfusions, hereditary predisposition, skin diseases, abrasions and wounds, hypothermia, taking certain medications, and excessive consumption of iron in food are of great importance in the development of pathology.

Symptoms

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

In the skin form, the rash lasts for months and years and is accompanied by itching of varying intensity. The pigment spots are clearly defined, have a reddish color and remain on the skin even with pressure.

Pulmonary hemosiderosis is characterized by the appearance of shortness of breath at rest, anemia, a wet cough with bloody discharge, a rise in temperature to febrile values, an increase in signs of respiratory dysfunction, and hepatosplenomegaly. Exacerbations after a few days are replaced by remission, in which the hemoglobin level normalizes, and Clinical signs gradually disappear.

Pulmonary hemosiderosis

Idiopathic pulmonary hemosiderosis – severe chronic pathology, the main pathomorphological links of which are: repeated hemorrhages in the alveoli, breakdown of red blood cells and a significant accumulation of hemosiderin in the pulmonary parenchyma. As a result, patients develop persistent pulmonary dysfunction.

hemosiderin deposits in the alveoli of the lungs

Symptoms acute form diseases are:

Productive cough and hemoptysis,
Pale skin
Scleral injection,
brokenness,
Dyspnea,
Chest pain,
Arthralgia,
Temperature rise
Cardiopalmus,
Drop in blood pressure
Hepatosplenomegaly.

Remission is characterized by the absence of complaints and pronounced clinical symptoms. During this period, patients remain able to work. Over time, exacerbations of pathology occur more often, and remission becomes shorter.

IN severe cases The chronic course of hemosiderosis is manifested by symptoms of cor pulmonale, pneumonia, pneumothorax and can be fatal.

Brown induration of the lungs - serious disease, rarely diagnosed during life. Autoantibodies are formed in the blood of patients in response to exposure to a sensitizing antigen. An antigen-antibody complex is formed, and autoallergic inflammation develops, for which the lungs become the target organs. Pulmonary capillaries expand, red blood cells penetrate from the vascular bed into the lung tissue, and hemosiderin begins to be deposited in it.

Skin hemosiderosis

Skin hemosiderosis - dermatological disease, in which pigment spots and various rashes appear on the skin of patients. The appearance of areas of pigmentation and petechiae is caused by the accumulation of hemosiderin in the dermis and damage to the capillaries of the papillary layer.

The spots on the skin vary in color and size. Fresh rashes are usually bright red, while older ones are brownish, brown or yellow. Spots up to three centimeters in size are localized on the lower extremities, hands and forearms. Petechiae, nodules, papules, and plaques often appear on the affected skin. Patients complain of slight burning and itching.

In the patient's dermis, the structure of the endothelium of the capillaries changes, and the hydrostatic pressure in them increases. Plasma leaves the vascular bed, and red blood cells are excreted along with it. The capillaries dilate, clumps of hemosiderin are deposited in the endothelium, histocytes and endothelial cells are affected, and perivascular infiltration develops. This is how the process of hemosiderin deposition occurs in the skin. In patients in clinical analysis blood usually reveals thrombocytopenia and impaired iron metabolism.

Hemosiderosis of the skin can occur in various clinical forms, among which the most common are: Majocchi disease, Gougerot-Blum, orthostatic, eczematid-like and itchy purpura.

Schamberg's disease

Schamberg's disease deserves special attention. This is quite common autoimmune pathology chronic course, characterized by the appearance of red dots on the skin, similar to the mark of a regular injection. Circulating immune complexes are deposited in the vascular wall, autoimmune inflammation of the endothelium develops, and intradermal petechial hemorrhages appear. Hemosiderin in large quantities accumulates in the papillary layer of the dermis, which is clinically manifested by the appearance of symmetrical brown spots on the skin. They come together and form plaques or entire areas that are yellow or brown. Bright red rashes appear along the edges of such plaques. In patients, petechiae and hemorrhages the size of a pea are also present on the skin, which merge with each other and form large lesions. Over time, the plaques in the center atrophy. The general health of the patients remains satisfactory. The prognosis of the pathology is favorable.

Cutaneous hemosiderosis, unlike pulmonary and general hemosiderosis, can be easily corrected. Patients feel well and recover quickly.

Hemosiderosis of internal organs

Systemic or generalized hemosiderosis develops in the presence of massive intravascular hemolysis of red blood cells. The disease is characterized by damage to internal organs and has a severe clinical course. Patients with general hemosiderosis complain of bad feeling, their skin color changes, and frequent bleeding occurs.

Hemosiderosis of the liver can be idiopathic or primary, as well as secondary. Hemosiderin is deposited in hepatocytes. The liver enlarges and thickens, becomes painful on palpation, ascites, hypertension, jaundice of the skin and sclera, splenomegaly, pigmentation of the hands, face and armpits occur. IN terminal stage if left untreated, acidosis develops. The patient falls into a coma.
Kidney hemosiderosis is characterized by the appearance of brown granules in the parenchyma of the organ. Patients develop clinical signs of nephrosis or nephritis. Protein is found in the urine, and increased lipid levels are detected in the blood. The main symptoms of kidney hyposiderosis are: swelling of the feet, legs and eyelids, weakness, lack of appetite, cloudiness in the urine, lower back pain, dyspepsia. If treatment is not started in time, severe complications will arise - kidney failure, which often ends in the death of patients.

hemosiderosis of the liver (left) and kidneys (right)

Systemic hemosiderosis poses a danger to the life of patients, making it miserable and short. Damage to internal organs often ends in the development of serious consequences.

Diagnostics

After listening to patient complaints, collecting anamnesis and conducting a general examination, specialists move on to laboratory and instrumental research methods.

In a clinical laboratory, blood is taken for a general analysis, serum iron and total iron-binding capacity are determined.
A biopsy of the affected tissue and histological examination of the biopsy is of great importance for making a diagnosis.
The desferal test allows you to determine hemosiderin in the urine after intramuscular injection"Desferala."
Dermatoscopy of the rash area - microscopic examination of the papillary layer of the dermis.

Among additional methods The most common diagnostic tests are the following:

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

Treatment

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

Eat right, exclude food allergens, spicy and fried foods, smoked foods, alcohol from your diet;
Avoid injuries, hypothermia, overheating and overexertion;
Timely identify and sanitize foci of chronic infection in the body;
Treat concomitant diseases;
Do not use cosmetics which can cause allergies;
Fight bad habits.

Drug therapy consists of prescribing medications to patients:

Local and systemic corticosteroids - Prednisolone, Betamethasone, Dexamethasone and drugs based on them,
Anti-inflammatory drugs - Ibuprofen, Indomethacin,
Disaggregants - “Aspirin”, “Cardiomagnyl”, “Acetylsalicylic acid”,
Immunosuppressants - “Azathioprine”, “Cyclophosphamide”,
Angioprotectors - “Diosmina”, “Hesperidin”,
Antihistamines - “Diazolina”, “Suprastina”, “Tavegila”,
Nootropic drugs - “Piracetam”, “Vinpocetine”, “Maxidol”,
Multivitamins and polyminerals - ascorbic acid, rutin, calcium supplements.

Symptomatic correction includes long-term use of iron supplements, hemostatic agents, multivitamins, bronchodilators, and oxygen therapy. Patients undergo extracorporeal hemocorrection: hemosorption, plasmaphoresis, cryoprecipitation, blood therapy. In severe cases, splenectomy and blood transfusions give good results.

Traditional medicine used to strengthen the vascular wall and reduce the manifestations of hemosiderosis: infusion of mountain arnica and hazel bark, decoction of thick-leaved bergenia.

Prevention

Hemosiderosis - chronic illness, characterized by alternating exacerbation and remission. After proper treatment and stabilization of the patient’s condition, it is necessary to observe preventive actions, preventing a new exacerbation. These include spa treatment, proper nutrition And healthy image life.

Preventive measures to prevent the development of hemosiderosis:

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

Skin hemosiderosis treatment with folk remedies

General hemosiderosis is a secondary condition, etiologically associated with diseases of the blood system, intoxications, infections, and autoimmune processes. Possible causes of excessive hemosiderin deposition include hemolytic anemia, leukemia, cirrhosis of the liver, infectious diseases (sepsis, brucellosis, malaria, relapsing fever), Rh conflict, frequent blood transfusions, poisoning with hemolytic poisons (sulfonamides, lead, quinine, etc. .). The etiology of pulmonary hemosiderosis is not entirely clear. Assumptions have been made regarding hereditary predisposition, the immunopathological nature of the disease, congenital disorders of the structure of the wall of the pulmonary capillaries, etc. It is known that patients with decompensated cardiac pathology (cardiosclerosis, heart defects, etc.) are more susceptible to the development of pulmonary hemosiderosis. Cutaneous hemosiderosis can be primary (without previous skin lesions) or secondary (occurs against the background of skin diseases). Endocrine diseases (diabetes mellitus) and vascular pathology (chronic venous insufficiency, hypertension) predispose to the development of primary hemosiderosis of the skin. Dermatitis, eczema, neurodermatitis, skin trauma, and focal infection (pyoderma) can lead to secondary accumulation of hemosiderin in the layers of the dermis. Hypothermia, overwork, and taking medications (paracetamol, NSAIDs, ampicillin, diuretics, etc.) can provoke the onset of the disease.

Idiopathic pulmonary hemosiderosis is a disease characterized by repeated hemorrhages into the alveoli with subsequent deposition of hemosiderin in the pulmonary parenchyma. The disease mainly affects children and young people. The course of pulmonary hemosiderosis is characterized by pulmonary hemorrhages of varying intensity, respiratory failure and hypochromic anemia. In the acute phase of the disease, patients develop a wet cough with the release of bloody sputum. The consequence of prolonged or profuse hemoptysis is the development of severe iron deficiency anemia, pallor of the skin, icterus of the sclera, complaints of dizziness, and weakness. The progressive course of pulmonary hemosiderosis is accompanied by the development of diffuse pneumosclerosis, reflected by shortness of breath and cyanosis. Periods of exacerbation are accompanied by pain in the chest and abdomen, arthralgia, and fever. Objective data are characterized by dullness of percussion sound, the presence of moist rales, tachycardia, arterial hypotension, spleno- and hepatomegaly. During periods of remission, complaints are not expressed or absent, however, after each subsequent attack, the duration of clear intervals, as a rule, is reduced. In patients with chronic hemosiderosis, cor pulmonale often develops; Severe infarction-pneumonia and recurrent pneumothorax often occur, which can cause death. Idiopathic pulmonary hemosiderosis can be combined with hemorrhagic vasculitis, rheumatoid arthritis, systemic lupus erythematosus, glomerulonephritis, and Goodpasture's syndrome.

In the cutaneous version of hemosiderosis, deposition of iron-containing pigment occurs in the dermis. Clinically, the disease is characterized by the appearance on the skin of a hemorrhagic rash or pigment spots with a diameter of 0.1-3 cm. Fresh rashes have a brick-red color; old ones become brown, dark brown or yellowish in color. Most often, pigmented lesions are localized on the skin of the ankles, legs, hands, and forearms; Sometimes the rash is accompanied by mild itching. In areas of skin lesions, petechiae, nodules, lichenoid papules, telangiectasia, and rusty-colored plaques may appear. Hemosiderosis of the skin has a chronic course (from several months to several years), and is more common in older men. The general condition of patients with cutaneous hemosiderosis remains satisfactory; internal organs are not affected. The disease should be distinguished from atypical forms of lichen planus, pseudosarcoma and Kaposi's sarcoma.

The first-line drugs used for the treatment of pulmonary hemosiderosis are glucocorticosteroids, but they are effective only in half of the cases. A method of combined treatment with immunosuppressants (azathioprine, cyclophosphamide) in combination with plasmapheresis has been proposed. In addition, symptomatic therapy is used: iron supplements, hemostatic agents, blood transfusions, bronchodilators, oxygen inhalations. In some cases, remission of the disease occurs after splenectomy. Treatment of skin hemosiderosis includes local use of corticosteroid ointments, cryotherapy, ascorbic acid, rutin, calcium supplements, and angioprotectors. For severe skin manifestations of hemosiderosis, they resort to PUVA therapy and the prescription of deferoxamine (desferal).

The information provided in this section is intended for medical and pharmaceutical professionals and should not be used for self-medication. The information is provided for informational purposes only and cannot be considered official.

Treatment of skin diseases with folk remedies

Skin diseases are usually associated with great physical discomfort. Often many of them have very unsightly external manifestation. Therefore, such illnesses often bring enormous psychological suffering to patients.

Treatment of skin diseases depends on correct diagnosis

Today, in the fight against such diseases, they are successfully used Newest technologies. However, we should not forget about proven folk remedies that have helped more than one generation. Treatment of skin ailments with herbs and ointments prepared only from natural ingredients can be an effective addition to complex drug therapy.

Simple home remedies successfully help get rid of boils, scabies, pustules, calluses, warts and wounds. Known folk recipes, which can heal skin diseases such as eczema, psoriasis, lichen, cheilitis, lupus, dermatitis, trophic ulcers, seborrhea and many others.

Lichen

Lichen ruber versicolor is popularly treated with red beets. Fresh root vegetables are grated and applied to the affected areas. Cover the top of the mass with cellophane film. The compress is changed as the beets dry. The procedures are carried out daily until the signs of the skin disease completely disappear.

Lichen planus is treated with church incense. To do this, 50 g of this resin is mixed with 40 ml of aloe juice and three tablespoons of garlic juice. Whisk all the ingredients into a homogeneous mass, and gradually add the raw yolk from one chicken egg to it. Apply the product to the affected skin daily. Store in a cool place.

Ringworm that appeared after nervous stress, they treat like this. Mix: rice starch (25 grams), zinc oxide (5 grams), petroleum jelly (15 grams). The mass is thoroughly mixed and 1 g of salicylic acid is added. Lubricate the ringworm with this ointment three times a day.

Ringworm caused by pulmonary tuberculosis (lichen scrofulous) is treated with this remedy. 100 grams of honey are mixed with 100 grams of salt. The salt should completely dissolve, after which the affected skin is generously lubricated with this composition and left for 30 minutes.

Pityriasis versicolor is treated like this. The stems of celandine are twisted in a meat grinder and mixed in a 1:1 ratio with sugar (sand). The mass is placed in gauze and placed in a three-liter glass jar. Pour milk cheese there at the rate of: for two glasses of vegetable-sugar mass - 2.5 liters fermented milk product. Infuse the product for at least three weeks. Next, pour the composition into a new jar and close the lid. Take this product before meals. Soon the skin will clear up.

Lichen squamosus can be cured the following means. Mix tar with fish oil in a ratio of 1:3. Apply this ointment to the affected areas of the body and cover or bandage with gauze. Ringworm is successfully treated with naphthalone. Brown ointment made from crude oil is also used to lubricate sore areas.

Eczema

This skin disease is popularly treated with this remedy. Every day during the day they drink pure lemon juice in accordance with the following treatment regimen: on the 1st day - from 5 fruits, on the 2nd day - from 10 fruits, 3 - from 15 fruits and continue the course, adding 5 lemons each time until their number will reach 25 fruits. After this, the amount of juice is reduced to reverse order. After drinking the juice, rinse your mouth thoroughly. The skin will gradually clear up.

Internally for eczema, you should drink a decoction of buckthorn root, string, elderberry flowers, St. John's wort and yarrow. All herbs are taken in equal proportions. The course of treatment is long - at least 8 months.

For eczema on the scalp traditional healers They suggest treatment with the following remedy. Ginger root, several nutmegs and galangal root are passed through a meat grinder. The mixture is poured with half a liter of high-quality vodka. They insist. To do this, the product is placed in a dark and warm place for a day. The prepared tincture is applied to the affected skin and applications are made.

The affected areas of the skin should be lubricated three times a day with this ointment. Grind the elecampane root into powder and mix it with butter. At the same time, the proportion is maintained at 1:2.

Skin hemosiderosis - treatment with folk remedies

Hemosiderin is a yellow-brown, granular, iron-containing pigment formed from the breakdown of hemoglobin. Hemosiderin staining, or hemosiderosis, is a medical term used to define the condition of iron overload. Improper functioning of red blood cells causes the body to store excess iron in organ tissues. The increase in hemosiderin in the intercellular fluid leads to a brown change in the color of skin pigments. This iron overload can cause damage to organ tissue and can lead to serious complications.

Treatment of hemosiderosis is aimed at reducing the effects of the underlying disease, which leads to further iron deposition. Frequent phlebotomy or blood thinning may help in some cases to relieve iron overload. In folk medicine, leeches and herbal infusions are used to cleanse the blood. But it is worth noting that this disease has several different forms, which are treated differently. Therefore, visiting a doctor is mandatory.

Scabies

Mix sulfur and birch tar 4:1. Add crushed laundry soap and Vaseline to the mixture. Thoroughly grind the mass until smooth. Lubricate and rub it into areas affected by scabies mites for 5 days.

This oil helps cure scabies at home. 200 g of garlic are peeled and chopped. Pour in 400 ml of mustard oil. This composition is boiled over fire for 5 minutes. Let it sit and strain through a strainer. Lubricate areas of the body affected by scabies mites throughout the day.

Scabies is popularly treated with euphorbia (euphorbia) juice. Apply mite-affected skin with it daily. Wash off the juice after 30 minutes.

Dermatitis, neurodermatitis, diathesis, scrofula, bedsores

Oak bark is crushed or purchased at a pharmacy (200 g). Fill it with 1.5 liters of boiling water. Boil and let sit for two hours. The strained product is used for baths or compresses for skin diseases. The decoction has an anti-inflammatory and healing effect, relieves itching, pain and irritation, cleanses skin covering when peeling.

For dermatitis, you can use celandine juice. At the same time, it is diluted with cold boiled water 1:2. Applications are made to the affected skin. Soak a bandage or cotton wool in the extract and apply to the skin for no more than 10 minutes.

Neurodermatitis ethnoscience advises to treat this way. Melted lard (40 grams) or pharmaceutical Vaseline is heated to melt. Allow to cool slightly and pour in 50 ml of aloe juice. Mix the composition and add 30 drops of fir oil to it. Apply the prepared ointment to itchy and inflamed areas.

Diathesis is treated with such an ointment. Mix birch tar and petroleum jelly in equal proportions. Apply ointment to the affected areas. Every evening they take a bath of pine branches and currants.

For scrofula in children they do herbal baths from oak bark, string, chamomile, marsh wild rosemary or birch buds. Internally drink an infusion of hop fruits or a decoction of viburnum branches.

Bedsores are treated as follows. The towel is soaked in a soda solution. For one glass of warm boiling water, take one dessert spoon of powder. Dissolve. Change the towel every 4 hours. The wounds will soon be cleared of pus and heal.

Boils, pustules, lupus, warts, calluses and other skin problems

Purulent wounds, abscesses, and pustules can be treated with fresh carrots chopped on a fine grater. The pulp is applied to the sore spot on a sterile napkin or gauze and bandaged. The bandage is changed periodically until complete healing. For the same purpose, you can use black radish, white cabbage, aloe.

Skin affected by lupus erythematosus is treated with ointment from birch buds. It is prepared as follows. A glass of (faceted) kidneys is crushed and mixed with hot rendered lard. It will require no more than 500 grams. Next, place the mixture in a hot oven and simmer it in it for four hours. After this, the drug is cooled and the rash on the face is smeared with it. This medicine is also taken orally, dissolving it in milk.

Warts are treated with the juice of celandine, dandelion, and calendula. You can apply the juice to the affected skin throughout the day. Tea tree oil is also used to get rid of warts.

Calluses can be successfully treated with such grated potatoes. The pulp is tied to the sore spot and covered with cellophane. Secure everything with a bandage and leave it overnight. The callus will soften and can be removed using a pumice stone or a special pedicure grater.

Preventive measures

It must be remembered that to prevent skin diseases it is important to follow the following rules.

Strictly perform daily hygiene procedures.
Use only high-quality cosmetic products that meet all standards and regulations.
Maintain your immunity at the proper level.
Avoid stress and don't be nervous.
Eat well and take vitamins.
Inspect and treat internal organs in a timely manner.

Take care of yourself and be healthy!

I was always afraid to take such drugs in the summer, especially since my skin is light and there are a lot of moles and freckles, because I spend a lot of time in the sun... The doctor explained something to me about pigment spots that can appear due to a reaction to the sun, but L- qing compared to similar drugs more safe. Has anyone else tried it?

Lyubov Molchanova, what drugs are you talking about? The synthetic fluoroquinolone antibiotic that you mention acts against bacteria.

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