Vasculitis- These are diseases that affect blood vessels. Subsequently, the pathological process often spreads to different organs and tissues.

There are a large number of different types of vasculitis, each of which is accompanied by damage to a certain type of vessel and its own specific symptoms.

The most common types of vasculitis:

• Urticarial vasculitis– a disease in which small vessels are damaged, mainly venules (small veins) and spots appear on the skin like urticaria.
• Allergic vasculitis– vascular damage due to various allergic reactions.
• Hemorrhagic vasculitis (Henoch-Schönlein disease) is a disease in which there is damage to the capillaries and small arteries.
• Periarteritis nodosa– a disease that primarily affects small and medium-sized vessels.
• Nonspecific aortoarteritis (Takayasu disease) is a disease that affects the aorta and the large arteries branching from it.
• Wegener's granulomatosis– vasculitis, which affects small vessels of the upper respiratory tract, lungs and kidneys.

• primary– develop as an independent disease;
• secondary– arise as a manifestation of another disease.

• Unable to determine root cause.It is not possible to identify the factor that initially led to the onset of the disease.
• Same development. As a result of one reason or another, immunity disorders occur and autoimmune reactions develop. Antibodies are produced, which, combining with various substances, form immune complexes. The latter settle on the walls of blood vessels and cause inflammation.
• Chronic course. All systemic vasculitis occurs over a long period of time. Exacerbations and remissions (improvement of condition) alternate.
• The same factors usually lead to exacerbations: administration of vaccines, various infections, hypothermia, prolonged exposure to the sun, contact with allergens.
• Damage to various organs and tissues: skin, joints, internal organs. Autoimmune processes develop throughout the body, but mainly in those places where there are large concentrations of blood vessels.
• For all types of vasculitis, medications that suppress the immune system help.

Anatomy of blood vessels

Types of arteries:

• elastic;
• muscular;
• mixed.

Type of arteries	Wall structure
Elastic. The aorta and other large vessels are structured according to the elastic type. Their task is to provide a constant flow of large amounts of blood under high pressure.	The inner layer is represented by endothelium, which makes up 20% of the wall thickness. These are the cells lining the lumen of the vessel from the inside. They ensure normal blood movement and prevent the formation of blood clots. Under the endothelium there is loose tissue connecting it to the middle layer. It is in it that cholesterol plaques form during atherosclerosis.
	The middle layer is represented by multilayer elastic membranes, in which there are holes - windows.
	The outer layer of elastic arteries is thin and consists of loose tissue and fibers. It is designed to protect the vessel from overstretching and rupture. The vessels and nerves supplying the artery pass through here.
Muscular. Arteries of the muscular type are also called distributive. Their walls contain muscle fibers, with the help of which the lumen of the vessel can quickly change. Muscle-type arteries can increase or restrict blood flow to a particular part of the body. Muscular arteries are large vessels that are branches of the aorta and supply blood to large areas of the body.	The inner layer of muscular arteries is practically no different from the elastic one. It consists of: endothelium; a layer of loose tissue underneath; membrane separating the inner layer from the middle one.
	The middle layer consists of muscle fibers that are arranged in a spiral and cover the entire vessel. By contracting, they reduce the lumen of the vessel and partially block the blood flow.
	The outer shell is a fabric with a large number of fibers. Nerves and blood vessels pass through it.
Mixed (muscular-elastic).	In structure they occupy a middle position between arteries of the muscular and elastic types. Their middle layer contains both fibers and muscle cells. Mixed-type arteries are small and medium-sized vessels. As their diameter decreases, the walls become thinner.
Arterioles	Arterioles are the smallest arteries that connect the arterial system to the capillaries. The wall of arterioles is very thin. It consists of the same layers as the wall of the arteries: The inner layer is the endothelium, located on a membrane film. The middle layer is muscle cells. They are arranged in two layers. The junction between the arteriole and the capillary is covered by one muscle cell: by contracting and relaxing, it regulates the flow of blood into the capillaries. There are spaces between the endothelial cells of arterioles. Therefore, hormones and other substances that enter the bloodstream can quickly act directly on muscle cells. The outer layer of arterioles consists of connective tissue and is very thin.
Capillaries	Capillaries are the final section of the bloodstream. These are the smallest vessels connecting arterioles to venules. Gas exchange between blood and tissues occurs in capillaries; here arterial blood turns into venous blood. Different organs have different numbers of capillaries. Their density is highest in the brain and heart. Normally, in a calm state, only 50% of the capillaries are active.

Allergic vasculitis

Causes of allergic vasculitis

• infections: staphylococci and other bacteria, viruses, fungi;
• chronic foci of inflammation in the body: tuberculosis, chronic cystitis, adnexitis, sinusitis, tonsillitis, etc.;
• frequent colds;
• taking certain medications: antibiotics, painkillers, sedatives, contraceptives, etc.;
• contact with certain chemicals(mostly occupational hazards);
• exposure to radiation, frequent exposure during radiation therapy for cancer;
• cardiovascular diseases: arterial hypertension, varicose veins, heart failure;
• some chronic diseases: obesity, type II diabetes mellitus, gout etc.

Manifestations of allergic vasculitis

Manifestations of allergic vasculitis depending on the form of the disease:

Description	Appearance of elements on the skin
Hemorrhagic vasculitis (Henoch-Schönlein disease) - see below, described separately.
Allergic arteriolitis of Rutera
There are many different types of skin rashes: blisters, red spots, spider veins, pustules, blisters, ulcers. Headache. Increase in body temperature, usually up to 37⁰C. Pain, inflammation in the joints.
Nodular necrotizing vasculitis
This form of the disease usually occurs chronically over a long period of time. There is always a significant deterioration in the patient's general condition. Red spots, hemorrhages, and nodules appear on the skin, which then ulcerate.
Erythema nodosum
The disease can occur in acute or chronic form. Small nodules and larger nodules form on the skin. The lesion is mainly localized on the anterior surface of the legs. There may be pain and inflammation in the joints.

Diagnosis of allergic vasculitis

Examination for allergic vasculitis:

Diagnostic method	What does it reveal?	How is it carried out?
General blood analysis	General clinical analysis. It is carried out in patients with suspected diseases. In allergic vasculitis, inflammatory changes are detected: acceleration of erythrocyte sedimentation; increase in the number of immune cells - leukocytes.	Blood is drawn from a finger or a vein, usually early in the morning.
Skin biopsy	The main method for diagnosing allergic vasculitis. The doctor takes a small piece of the patient's skin and sends it to the laboratory for examination under a microscope. After this, you can say exactly what pathological changes are occurring in the skin.	The doctor obtains a piece of skin using a special razor (a small piece of skin is removed, the procedure is almost painless) or a needle.
	Aimed at identifying specific antibodies and immune cells that are involved in the development of an allergic reaction.	For immunological studies, a small amount of blood is usually taken from a vein.

• identification of chronic foci that could contribute to the onset of the disease;
• identifying infections that could contribute to the onset of the disease;
• identification of complications from joints, heart, etc.

The examination program is drawn up individually by the doctor.

Treatment of allergic vasculitis

• glucocorticoids– adrenal cortex drugs that suppress the immune system;
• cytostatics– drugs that suppress the immune system;
• hemosorption and plasmapheresis– hardware methods for purifying blood from immune complexes and toxic substances (see below when describing periarteritis nodosa).

Urticarial vasculitis

Causes of urticarial vasculitis

Symptoms of urticarial vasculitis:

Diagnosis of urticarial vasculitis

Study	Description	How is it carried out?
General blood analysis	An acceleration of erythrocyte sedimentation is detected - a sign of an inflammatory process.	To perform a complete blood count, blood is usually taken from a finger or a vein.
Immunological studies	An increase in the concentration of antibodies and some other substances responsible for autoimmune inflammation is detected.	For testing, blood is usually taken from a vein.
General urine analysis	Finding blood and protein in the urine indicates kidney involvement.
Skin biopsy	It is the main, most informative method for urticarial vasculitis. This is the study of a fragment of a patient's skin under a microscope. Signs of inflammation and necrosis (tissue death) are detected.	The skin for examination is taken using a scraping, a needle, or a small fragment is cut off with a scalpel.

Treatment of urticarial vasculitis

• if these drugs are ineffective - glucocorticoids (drugs of adrenal hormones) and cytostatics (drugs that suppress the immune system).

Hemorrhagic vasculitis

Causes of hemorrhagic vasculitis

Factors provoking the development of hemorrhagic vasculitis:

• angina– inflammation of the tonsils caused by streptococcal bacteria;
• exacerbation of chronic inflammation of the tonsils(tonsillitis);
• pharyngitis– inflammation of the pharynx caused by infection;
• administration of certain vaccines and serums, to which the patient has intolerance;
• hypothermia.

Signs of hemorrhagic vasculitis

Group of symptoms	Description
General symptoms	increased body temperature; fever;
Skin lesions
Signs of joint damage (detected in 75% of patients)	Large joints are more often affected; there is pain and swelling; the intensity and duration of pain can vary greatly; impaired joint mobility (often associated with hemorrhage into the joint).
Signs of damage to internal organs	sharp stabbing or cramping pain in the abdomen; most often the pain is localized around the navel, sometimes in other parts of the abdomen; vomiting with blood; blood in the stool; with kidney damage - blood in the urine.

Diagnosis of hemorrhagic vasculitis

Study	What does it reveal?	How is it carried out?
General blood analysis	In a general blood test for hemorrhagic vasculitis, inflammatory changes are detected: increase in the number of leukocytes. The platelet count is within the normal range - this is a sign that the hemorrhages under the skin are not caused by a decrease in blood clotting.	For analysis, blood is taken from a finger or vein, usually in the morning.
Blood chemistry	an increase in the amount of immune proteins - immunoglobulins; an increase in the content of fibrinogen, a protein responsible for blood clotting.	For analysis, blood is taken from a vein on an empty stomach.
Blood clotting test.	Specific analyzes and tests aimed at studying blood clotting. All indicators are normal, and this helps to prove that hemorrhages under the skin are not caused by bleeding disorders.	For analysis, blood is taken from a finger or vein.
Immunological studies	Determination of the content of antibodies, immune complexes, and some other substances in the blood that are responsible for the autoimmune inflammatory process.	For analysis, blood is taken from a vein.
Skin biopsy	Examination of a skin fragment under a microscope.	Allows you to accurately determine the pathological process occurring in the tissue.

Treatment of hemorrhagic vasculitis

Periarteritis nodosa

Causes of periarteritis nodosa

• taking certain medications: antibiotics, painkillers, anti-tuberculosis, X-ray contrast agents;
• viral infections: hepatitis B, herpes, cytomegalovirus infection;
• genetic predisposition.

• development of autoimmune inflammation in the vascular wall, as a result of which it is destroyed, grows and increases blood clotting;
• blocking the lumen of blood vessels, as a result of which the blood supply to organs is disrupted;
• vascular thrombosis;
• aneurysms(thinning of the wall) and ruptures of blood vessels;
• heart attacks(death of tissue as a result of cessation of blood circulation) in internal organs, after which atrophy and scarring develop, functions are disrupted.

Symptoms of periarteritis nodosa

What does periarteritis nodosa look like in the photo?

Erythema (red spots)
Maculopapular rash (red spots and blisters)
Hemorrhages (bleedings)
Vesicles (bubbles)
Specific nodules along the vessels under the skin.
Necrosis (areas of dead skin).

Diagnosis of periarteritis nodosa

Treatment of periarteritis nodosa

Nonspecific aortoarteritis (Takayasu disease)

The disease, like other systemic vasculitis, is rare. Women get sick 3 to 8 times more often than men.

Causes of nonspecific aortoarteritis

• Autoimmune process. As with periarteritis nodosa, specific immune complexes are formed that cause damage to the vascular wall.
• Hereditary predisposition. The presence of certain genes increases the likelihood of developing the disease.

Manifestations of Takayasu's disease

• Initially, under the influence of immune cells, specific growths - granulomas - appear on the inner wall of the vessel.
• Subsequently, the inflammatory process gives way to scarring, and vascular sclerosis occurs.

All the symptoms described occur with a large number of other diseases. Therefore, during a direct examination, it can be difficult for a doctor to establish an accurate diagnosis. It is confirmed only after a complex of laboratory and instrumental studies.

Diagnosis of nonspecific aortoarteritis

Diagnostic method	Description
Ultrasound examination of blood vessels	Using an ultrasound sensor, the doctor can visualize large vessels, determine the thickness of their lumen, and detect existing narrowings.
Dopplerography	Dopplerography is an addition to ultrasound examination, allowing one to assess the intensity of blood flow in the vessels and, thus, judge its disturbances.
Duplex scanning	Combination of Dopplerography with classical ultrasound examination. Allows you to create the most complete picture of the lumen of large vessels and the intensity of blood flow in them.
Rheovasography	The older method of studying blood flow in vessels has today been almost completely replaced by Dopplerography. The body is exposed to high frequency current and the electrical resistance of the blood vessels is measured. Based on the data obtained, blood flow is assessed.
Ultrasound examination of the heart and kidneys	Allows to identify disorders in these organs caused by damage to large vessels.
Angiography	A study during which a radiopaque contrast agent is injected into the vessels, after which X-rays are taken. Gives an idea of ​​the degree of blockage of the lumen of blood vessels. Kidney angiography is often performed - it gives an idea of ​​​​the degree of disruption of blood flow in them. Coronary angiography (angiography of the coronary arteries of the heart) helps identify narrowing sites in the coronary arteries.
General blood analysis	With nonspecific aortoarteritis, inflammatory changes are detected in a general blood test: increase in the number of leukocytes; acceleration of erythrocyte sedimentation.
General urine analysis	A general urine test for aortoarteritis helps identify signs of kidney damage: protein impurities in the urine; admixtures of red blood cells.

Treatment of nonspecific aortoarteritis

Surgical treatment of nonspecific aortoarteritis

• significant impairment of blood flow in the kidneys;
• significant circulatory impairment in the brain;
• poor circulation in the extremities, gangrene.

Wegener's granulomatosis

Causes of Wegener's granulomatosis

Factors that play a role in its occurrence:

• various infectious diseases;
• autoimmune reactions.

Signs of Wegener's granulomatosis

• symptoms of upper respiratory tract damage;
• symptoms of lung damage;
• symptoms of kidney damage.

• Local: the lesion affects only the upper respiratory tract.
• Limited: the lesion involves the upper respiratory tract and lungs. In this case, the kidney vessels are not affected.
• Generalized: damage to the lungs, upper respiratory tract and kidneys is noted.

An accurate diagnosis is established after an examination.

Diagnosis of Wegener's granulomatosis

Type of study	Description
Rhinoscopy	Examination of the nasal cavity by an ENT doctor using a special instrument - a rhinoscope. The doctor examines the mucous membrane of the nasal cavity and assesses its condition.
Laryngoscopy	Examination of the larynx using a special device - a laryngoscope. It is carried out under anesthesia. The doctor examines the patient's laryngeal mucosa and assesses its condition.
Biopsy of the nasal mucosa	A fragment of the nasal mucosa is collected using special endoscopic equipment. The resulting material is then sent to the laboratory, where it is subjected to microscopy. A biopsy helps distinguish Wegener's granulomatosis from other nasal diseases, such as tumors, etc.
X-ray, X-ray tomography of the lungs	During an X-ray examination, a large number of small compactions are detected in the lungs. Can reveal small cavities with walls.
Computed tomography, magnetic resonance imaging of the lungs	They are more accurate compared to radiography methods. They help clarify the data obtained during an x-ray examination.
Electrocardiography (ECG)	Used for signs of heart damage. During the study, increased loads on the left ventricle and thickening of its wall are revealed.
Kidney ultrasound	During an ultrasound examination, the doctor assesses the condition of the kidneys and their vessels. The test helps distinguish Wegener's granulomatosis from other kidney diseases.
Kidney biopsy	Taking a piece of kidney tissue for examination under a microscope. It is carried out using a needle that is inserted through the skin.
General blood analysis	: increased erythrocyte sedimentation rate; increase in the total number of leukocytes; an increase in the number of leukocytes of a special type responsible for allergic reactions - eosinophils; anemia, decreased hemoglobin content in the blood; an increase in the number of platelets, which indicates an increased tendency to form blood clots.
Blood chemistry	Signs of an autoimmune inflammatory process: violation of the ratio of blood proteins, increase in the relative amount of immunoglobulins - proteins that are antibodies; Most often, the content of immunoglobulins of class A, E, M increases. Detection of rheumatoid factor, a substance that is a marker of rheumatism and other autoimmune diseases.
General urine analysis	For kidney damage: detection of protein in urine; detection of a small number of red blood cells.

Treatment of Wegener's granulomatosis

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Classmates

Inflammation of blood vessels.

Vasculitis is a syndrome rather than a disease, a general name for a group of diseases characterized by inflammation and destruction of the walls of blood vessels. Occurs in a number of autoimmune connective tissue diseases: rheumatoid arthritis, systemic lupus erythematosus, etc. Vasculitis can also occur in isolation, without damage to the connective tissue.

Typically, the disease affects several tissues or organs: the narrowing of damaged blood vessels disrupts the blood supply to the organs, causing the death of the tissues supplied to them. The disease can occur in any organ.

Depending on the occurrence, vasculitis is divided into two types: primary and secondary. Primary vasculitis occurs independently and is not accompanied by other diseases. Secondary vasculitis is a concomitant disease of other pathologies.

Primary vasculitis

Primary vasculitis falls primarily within the competence of rheumatologists, although the diagnosis and treatment of these diseases is impossible without the participation of doctors of other specialties: otorhinolaryngologists, ophthalmologists, neurologists, dermatologists, etc. Inflammation of the walls of blood vessels is an integral feature of these diseases, which is found in all patients without exception. .

Primary systemic vasculitides include:

• Nonspecific aortoarteritis (synonyms: “Takayasu’s disease”, “aortic arch syndrome”);
• Giant cell arteritis (synonyms: “temporal arteritis”, “senile arteritis”, “Horton’s disease”);
• Polyarteritis nodosa;
• Kawasaki disease;
• Wegener's granulomatosis;
• Microscopic polyangiitis;
• Eosinophilic angiitis and granulomatosis (synonym: “Churg-Strauss syndrome”);
• Cryoglobulinemic vasculitis;
• Henoch-Schönlein purpura (synonym: “hemorrhagic vasculitis”).

In all of these diseases, inflammation occurs in the wall of blood vessels, but the caliber of the affected blood vessels in different forms of vasculitis is not the same and varies from large arteries (1.0 cm in diameter or more) to the smallest arterioles, capillaries and venules, visible only under a microscope. The type of inflammation is also different. All this explains the extremely pronounced diversity of clinical manifestations of primary systemic vasculitis and their dissimilarity from each other.

Secondary vasculitis

Secondary vasculitis develops as an element of another disease and can be considered either as an optional manifestation or as a complication. An example is many infectious diseases: scarlet fever, typhus, meningitis, sepsis, as well as skin diseases such as psoriasis, etc.

Sometimes vasculitis can be one of the manifestations of a malignant tumor of a particular organ; in this case, vasculitis will also be secondary, since after successful surgical, radiation or chemotherapy treatment of the tumor, the accompanying vasculitis, as a rule, disappears without any special treatment.

Vasculitis has a large number of subtypes and classifications; they differ in severity, localization and etiology. Widespread or generalized damage to blood vessels is called systemic vasculitis. Some vasculitis affects only the skin without causing serious harm to other organs; others can cause irreparable damage to vital organs and, without proper treatment, lead to death.

The process can develop in any blood vessel. Diseases such as Henoch-Schönlein syndrome, erythema nodosum, periarteritis nodosum, giant cell arteritis and Takayasu arteritis are characterized by vasculitis limited to one or another blood vessel: veins, large arteries, small arteries or capillaries, or any specific vessel(s) , for example, the vessels of the head, legs or kidneys.

Causes of vasculitis

Vasculitis is an autoimmune disease and first of all it is necessary to normalize the immune response. Vasculitis is a self-sustaining autoimmune process in blood vessels, which is caused by the following main reasons:

1. infections: streptococci, staphylococci, salmonella, mycobacterium tuberculosis, hepatitis B and hepatitis viruses, cytomegalovirus (one of the most insidious viruses of the herpes family), parvoviruses, etc.;
2. allergies - drug, serum, post-vaccination vasculitis;
3. for connective tissue diseases, injuries, burns, exposure to ionizing radiation.

The source of infection or the cause of an auto-aggressive immune reaction, like all other causes, is usually located not in the vessels at all, but in a different place. Without solving these problems, the growth of vasculitis cannot be stopped. And problems with digestion, metabolism, as well as smoking, alcohol and chronic stress only worsen the situation.

Therefore, vasculitis is not a separate vascular disease, but an “SOS” signal for your entire body.

For example, the role of hereditary (genetic) predisposition to the development of systemic vasculitis is not fully understood: in several cases, the occurrence of vasculitis in members of the same family has been noted; Some genes have been identified that are found with a higher frequency among patients with systemic vasculitis than among other individuals.

It has been shown that if a kidney transplant is necessary for a patient with systemic vasculitis that has caused severe kidney damage, it is undesirable to use a donor organ obtained from close relatives, since genetic relatedness increases the risk of relapse of vasculitis in the transplanted kidney. However, in the vast majority of cases, vasculitis is not inherited from parents to children, and the risk of developing these diseases in offspring is minimal.

Risk factors that can cause the development of vasculitis include drug abuse, uncontrolled administration of vaccines and serums, excessive tanning and sun exposure, prolonged hypothermia. Sometimes the role of a “trigger” is played by physical trauma, psycho-emotional stress or alcohol consumption (sometimes even small doses of alcohol unexpectedly turn out to be capable of triggering the development of the disease).

Symptoms of vasculitis

The symptomatic picture varies depending on the location of vasculitis and concomitant disease.

When vasculitis affects the skin, a rash appears. In case of nerve damage, a person’s sensitivity is disrupted, from hypersensitivity to its complete loss. A disruption in the blood supply to the brain causes a stroke. Renal failure may develop due to renal vasculitis.

One of the most dangerous complications of vasculitis are heart attack and stroke, which most often have the most serious consequences for life.

Common symptoms of vasculitis may be lack of appetite, fatigue, weakness, fever, and pallor. Characterized by a constant low-grade fever that does not decrease while taking antibiotics. Body temperature may decrease on its own or when glucocorticoids are prescribed. Weight loss in some variants of vasculitis is a classic sign, and a significant decrease in body weight over a short period of time has not only diagnostic value, but is also evidence of disease activity.

Manifestations of vasculitis are nonspecific. These include fever, general weakness, loss of appetite and body weight, skin rashes, hemorrhages, joint pain, swelling, and swollen lymph nodes. In its course, vasculitis can masquerade as an infection, autoimmune diseases, neuritis, or tumor processes, which makes its diagnosis difficult.

Nodular vasculitis is characterized by muscle pain, weight loss, abdominal pain, nausea and vomiting, and mental disorders.

Wegener's granulomatosis affects the paranasal sinuses; In patients, purulent and bloody discharge comes out of the nose, the nasal mucosa becomes covered with ulcers, a cough may appear (sometimes with blood), shortness of breath, chest pain are observed, and kidney failure may develop. Giant cell arteritis causes fever, weakness, weight loss, severe headaches, and swelling in the temple area. Symptoms of nonspecific aortoarteritis are pain and weakness in the arms and legs, blurred vision, and fainting.

Behçet's syndrome is accompanied by recurring stomatitis, genital ulcers, and eye inflammation.

When systemic vasculitis is accompanied by arthritis, the disease usually begins acutely or subacutely. First, general symptoms of inflammation occur, and after a few weeks or months a period of generalization of the disease begins.

Joint lesions in systemic vasculitis manifest themselves:

• joint pain without visible changes in the joints;
• transient arthritis of large joints with a benign course and reverse development without residual changes;
• arthritis with symmetrical damage to the small joints of the hands and often a long or chronic course, but without joint deformation.

The main signs of disease progression, in which you need to immediately sound the alarm:

• the appearance of pain in the heart;
• intestinal bleeding;
• cerebrovascular accidents;
• blood in urine.

Kidney damage is one of the most common and prognostically unfavorable signs; it occurs in 20–40% of patients, depending on the form of vasculitis. Clinical symptoms of kidney damage appear at the height of the disease and already indicate pronounced changes. Various manifestations of the disease in the gastrointestinal tract, respiratory system and heart are also possible.

You should consult a rheumatologist if you have signs of an inflammatory process, such as fever, general weakness, weight loss not associated with a change in diet. Depending on the localization of the process in the arterial bloodstream, visual disturbances, muscle pain, and blood in the urine may occur.

Diagnosis of vasculitis

There are many syndromes in which inflammation occurs in the walls of arteries of one caliber or another. In addition, the affected area gives its own symptoms.

All this complicates the diagnosis of systemic vasculitis. Diagnosis (and especially treatment) of systemic vasculitis in most cases is difficult to implement in non-specialized medical institutions. And it is completely unacceptable and completely unjustified for patients to attempt to independently diagnose vasculitis and self-medicate.

As a rule, diagnosis is carried out in specialized centers based on numerous microscopic, immunological, chemical and instrumental research methods.

Diagnostic measures include complete blood and urine tests, vascular examination (angiography), X-ray examination methods, tomography, and biopsy.

The diagnosis is made on the basis of the entire complex of clinical signs, features of the development of the disease, data from many laboratory and instrumental studies; Moreover, the scope of the examination (the list of necessary diagnostic methods) is always determined individually for each patient.

Treatment of vasculitis

Now the diagnosis of vasculitis is more common than before.

Immunosuppressive medications may be continued for several years to achieve stable remission. At the second stage, the functioning of organs affected by systemic vasculitis is restored.

Therapy is prescribed based on the specific diagnosis and cause of vasculitis. Anticoagulants, antihistamines, corticosteroids, vitamin preparations, immunosuppressants, membrane stabilizers are often used; cytostatics and plasmapheresis may be used.

Systemic vasculitis is the most dangerous: its treatment is based on taking cytotoxic drugs, administering immunoglobulins, and performing plasmapheresis (blood purification in Wegener's syndrome). Also, treatment of hemorrhagic vasculitis requires taking drugs that reduce blood clotting and the permeability of vascular walls. Before prescribing a diet for vasculitis, sensitizing factors (causing immune system reactions) are determined.

It must be remembered that vasculitis is always a signal of serious problems in the functioning of the whole organism. Vasculitis should never be ignored. This disease, if left untreated or treated incorrectly, always progresses, leading over time to permanent disability or even premature death from heart failure. Therefore, to treat this disease, it is very important to make a correct diagnosis in time and prescribe the correct drug treatment that does not cause allergic reactions and side effects. Thanks to high-quality, adequate treatment, the life expectancy of patients increases significantly.

Important! Treatment is carried out only under the supervision of a doctor. Self-diagnosis and self-medication are unacceptable!

The term “” (synonyms: arteritis and angiitis) combines a group of diseases characterized by immunopathological inflammation of the walls of blood vessels of various etiologies, but of similar pathogenesis. Often accompanied by thrombosis of the lumen of blood vessels and the transition of inflammation to surrounding tissues.

Classification of vasculitis

Depending from etiology distinguish:

Primary. Occurring as an independent autoimmune disease.
Secondary. Resulting from the underlying disease.

Depending on the size and type of vessel:

Capillarites;
Arteritis;
Phlebitis;
Arteriolitis.

Often inflammation simultaneously or sequentially affects vessels of different types and sizes.

Depending on the localization of the process in the vessels:

Endovasculitis;
Mesovasculitis;
Perivasculitis;
Panvasculitis.

Relatively arterial lesions:

Endoarteritis;
Mesoarteritis;
Periarteritis.

The combined pathology of veins and arteries is called angiitis. Systemic vasculitis differs from segmental or regional vasculitis in generalized or multisystem damage to the arteries and vessels. With segmental vasculitis, a limited process is localized in one area of ​​the organ or in some area of ​​the vascular system.

The division of primary vasculitis occurs relatively vessel caliber.

Vasculitis affecting large vessels and the aorta:

Giant cell arteritis (synonyms: Horton's disease or senile, temporal arteritis);
Nonspecific aortoarteritis or Takayasu syndrome.

Vasculitis affecting medium and small vessels:

Periarteritis nodosa;
Allergic granulomatosis;
Systemic necrotizing vasculitis;
Wegener's granulomatosis;
Kawasaki syndrome;
Cutaneous leukocytoclastic angiitis and its necrotic-ulcerative type.

Vasculitis with damage to small vessels.

ANCA-associated vasculitis:

Thromboangiitis obliterans;
Eosinophilic granulomatosis in combination with polyangiitis;
Microscopic polyangiitis.

Small vessel vasculitis (immune complex):

Hemorrhagic;
Essential cryoglobulinemic;
Goodpasture's syndrome;
Hypocomplementary urticaria.

Vasculitis with damage to vessels of different sizes:

Cogan's syndrome;
Eosinophilic granulomatous vasculitis;
Behçet's disease.

Secondary vasculitis is classified depending on from the underlying disease:

Vasculitis in systemic connective tissue diseases:

Rheumatoid and rheumatic;
Lupus;
Pulmonary vasculitis in sarcoidosis.

Vascular damage in infectious diseases:

Syphilitic;
Septic;
Rickettsial;
Tuberculous.

Vasculitis associated with medications, for example, drug-induced, with oncological neoplasms - paraneoplastic, as well as with hypersensitivity - whey.

Causes

1. Viral and bacterial infections in both acute and sluggish chronic forms;
2. Medicinal and chemical agents such as vaccines, drugs, serums;
3. Genetic predisposition;
4. Physical factors, such as severe hypothermia, injury or burns, radiation exposure.

The causes of secondary vasculitis are the main diseases that provoke vascular inflammation:

1. Infections, be it viral hepatitis, scarlet fever, sepsis;
2. Rheumatic and systemic diseases: rheumatism, lupus erythematosus, dermatomyositis;
3. Tumors of malignant and benign nature;
4. Allergies;
5. Endocrine pathology, for example, diabetic microangiopathy;
6. Blood diseases.

Clinical manifestations of vasculitis

As autoaggression develops, symptoms appear that are characteristic of a certain type of vasculitis and the area of ​​its affection.

Hemorrhagic form of vasculitis can begin at any age, but is more common in children under 12 years of age. It occurs with manifestations of superficial vasculitis with damage to the capillaries of the gastrointestinal tract, joints, kidneys, and skin. The temperature reaches 38.8–390C. On the body, mainly on the distal surfaces of the extremities, near large joints and on the buttocks, symmetrically located hemorrhagic purpura (rash) appears. Depending on the location, articular, renal, abdominal and skin syndromes are distinguished. Joint changes are more common in adults. The systemic process is manifested by many symptoms: abdominal crises with melena, arthralgia, hematuria, and rarely, shortness of breath.

For allergic vasculitis characterized by a petechial rash, spider veins and many small yellowish-brown spots. The rashes often appear in the area of ​​the lower extremities and are accompanied by itching of varying intensity. In rare cases, trophic ulcers may form.

Symptoms giant cell arteritis– headache, fainting, fever, decreased vision, swelling in the temple corresponding to the lesion.

Behçet's disease accompanied by erosions and ulcers of the mucous membranes, most often the genitals and mouth, as well as serious damage to the eyes. Vesicles with transparent contents appear in the oral cavity, which then open, forming bright pink aphthae (erosions). Accompanied by stomatitis, pharyngitis, gingivitis and glossitis. Changes in the eyes - inflammation of the iris and ciliary body (iridocyclitis), inflammation of the cornea (keratitis), and so on.

For erythema nodosum Characterized by the formation of nodes of different sizes, shapes and numbers, localized on the legs. The color of the skin over the nodules can change like a passing bruise: from dark scarlet to bluish and greenish-yellow.

Systemic vasculitis with rheumatism it is generalized. In addition to skin rashes, such vasculitis affects the vessels of vital organs - lungs, liver, brain, heart and other organs.

Diagnostic methods

Physical examination.

Laboratory tests:

1. General blood test. Characterized by increased ESR, leukocytosis, eosinophilia;
2. Biochemistry. Indicators of globulin fractions are important, in particular gamma globulin, hematocrit (increased), C-reactive protein, protein fractions;
3. Immunological tests;
4. Blood test for HBsAg if viral hepatitis is suspected, causing vasculitis;
5. Conducting a number of other blood tests with certain indicators characteristic of the underlying disease that provoked vascular inflammation. For example, PCR test, determination of antistreptolysin-O titers.

Early active therapy with cytostatics and glucocorticoids provides 60 to 90% survival in the first five years from the onset of vasculitis. Without specific treatment, only 10% of patients have a 5-year survival rate.

Other instrumental methods:

Doppler ultrasound;
Bronchoscopy;
Angiography;
Body plethysmography.

An important diagnostic criterion is a biopsy of the skin or organ tissue, after which the biopsy is examined under a microscope to determine the nature of vascular damage.

Treatment options

Minimization or complete elimination of the effects on the body of intoxications, allergic, chemical factors that provoked the disease;
Refusal to use antibiotics and sulfonamides;
A diet high in proteins, carbohydrates and vitamins, especially vit. S and R;
Timely treatment of the underlying disease to prevent consequences in the form of thromboembolism, thrombosis or bleeding characteristic of vasculitis;
Prescription of cytostatics and glucocorticosteroids for immunosuppression;
Modern methods - plasmaphoresis, ultraviolet blood irradiation (UVR blood), heme oxygenation, plasma transfusion;
Parallel administration of antithrombotic and vasodilator drugs;
For mild cases, non-steroidal anti-inflammatory drugs are indicated;
Physiotherapy and spa treatment are not recommended.

Folk remedies in the treatment of vasculitis

Cowberry, calendula officinalis, burdock, snake knotweed, plantain, coltsfoot, and sweet clover have anti-inflammatory properties.

Black currants, cranberries, rose hips and rowan berries strengthen the walls of blood vessels.
Herbs that contain vitamin K can prevent or stop bleeding. These are stinging nettle, viburnum bark or shepherd's purse.

An effective medicine can be obtained by combining several herbs and preparing an infusion or decoction from them.

To relieve the symptoms of allergic vasculitis, a decoction of lingonberries, string and tricolor violet is suitable. Take 3 tablespoons of each and mix. Brew 2 tablespoons with 2 cups of boiling water. After an hour of infusion, adults can drink half a glass 4 times during the day, children - 2 times before meals.

Prognosis and possible complications

The prognosis is unfavorable in the absence of treatment and in the acute course of some types, for example, with fulminant hemorrhagic vasculitis or Wegener's granulomatosis.

Prevention

Vasculitis - what is this disease? Causes, types and forms of vasculitis (hemorrhagic, allergic, systemic, cutaneous, etc.), symptoms and diagnosis of the disease, photos

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The site provides reference information for informational purposes only. Diagnosis and treatment of diseases must be carried out under the supervision of a specialist. All drugs have contraindications. Consultation with a specialist is required!

There are no exact statistics on the incidence of vasculitis, but doctors note that the number of people with this pathology is increasing every year. This may be due to the deterioration of the environmental situation and the uncontrolled use of immunostimulating drugs. It has been established that children and the elderly are more susceptible to the disease. Men and women get sick equally often.

Different forms of vasculitis have their own characteristic symptoms. General manifestations of the disease: fever, skin rashes that do not disappear with pressure, joint pain, weight loss. From the initial focus, vasculitis can spread to other organs and tissues, with the kidneys most often affected.

Causes of vasculitis

• Microorganisms:
  • streptococci;
  • staphylococci;
  • typhoid bacillus;
  • Mycobacterium tuberculosis;

According to the latest data, the main role in the development of vasculitis is played by staphylococci and streptococci. This is proven by the presence of corresponding antigens in the blood of most patients.

Predisposing factors. The development of the disease is almost always preceded by situations that reduce immunity and disrupt the normal course of immune reactions:

• age – children and the elderly are most susceptible. These categories often exhibit immaturity or age-related decline in immunity;
• diseases associated with metabolic disorders - diabetes mellitus, atherosclerosis, gout, thyroid pathologies, hypertension, liver diseases;
• prolonged exposure to the sun;
• excessive mental stress;
• severe injuries and operations;
• work involving prolonged standing;
• lymphostasis – impaired lymph outflow;
• tendency to allergic reactions;
• chronic infectious foci - otitis media, adnexitis, sinusitis, tonsillitis.

Mechanism of disease development

2. Next, the vascular wall is infiltrated by immune cells, neutrophils. As a result of reactions, enzymes (myeloperoxidase, elastase, lysozyme, lactoferrin) and hydrogen peroxide are released through the neutrophil wall. These aggressive substances destroy the walls of blood vessels and cause inflammation.
3. The vascular wall becomes a target of attack by the immune system - specific antibodies begin to be produced that are aimed against the vascular endothelium.
4. Antiendothelial antibodies attack the vascular wall, making it more permeable and fragile.
5. Immune inflammation is often accompanied by the formation of blood clots that block the lumen of blood vessels.
6. Destruction of the vascular wall leads to its rupture and hemorrhage into the surrounding tissue.
7. Poor circulation results in the surrounding tissues not receiving enough oxygen and nutrients. This causes cell death and necrosis of individual tissue areas.

Types and forms of vasculitis. Classification of vasculitis

Classification of vasculitis by severity

Classification according to the root cause of the disease

Classification by size of affected vessels

Classification according to the type of vessels affected

Classification by location of affected vessels

The most common types of vasculitis and their symptoms

Damage to large vessels

Giant cell (temporal) arteritis is inflammation of large and medium-sized arteries. Granulomas form on the inner wall of the vessel - accumulations of lymphocytes and giant multinucleated cells that look like dense nodules. Individual segments of the temporal, ophthalmic and vertebral arteries are affected, and less commonly the arteries of the liver and intestines. Blood clots form at the affected sites, which can cause a stroke. Damage to the aorta is also possible, which can lead to ruptures. The disease develops in elderly people 50-90 years old with well-preserved immunity. The number of sick men and women is approximately the same.

Symptoms

• Temperature rises to 37.5-40 degrees.
• Signs of general intoxication are weakness, drowsiness, sweating, weight loss.
• Headache . Pain in areas corresponding to the affected arteries (usually in the temples).
• The skin over the affected vessels is reddened. Pressure on this area causes pain. Unevenly thickened arteries can be felt under the skin.
• Sharp pain in the masticatory muscles and tongue when chewing.
• Decreased or absent pulse in distant areas of the damaged artery.
• Impaired or partial loss of vision due to damage to the ophthalmic arteries. Visual impairment can be temporary or permanent.

Damage to medium-sized vessels

Periarteritis nodosa is an inflammation of the vascular wall of small and medium-sized arteries. Numerous nodular thickenings and microaneurysms (protrusions of the wall that appear as a result of its overstretching) are formed in them, which disrupt blood flow. In 75% of patients, internal organs are affected, in 25% the skin is affected. It is more often detected in men 30-60 years old. The cause of development has not been established.

Symptoms

2. Kawasaki disease

Kawasaki disease primarily affects medium-sized arteries. More often than others, the coronary arteries of the heart, as well as the mucous membranes of the nasopharynx, are affected. Thickenings form on the inner wall of the vessel - the lumen narrows and can become clogged with a blood clot. The vessel wall dissects, leading to the formation of aneurysms. Develops 1-3 weeks after suffering streptococcal or staphylococcal infections. Occurs in children 1-5 years old. Boys get sick more often than girls. In the Japanese, Kawasaki disease occurs 10-30 times more often than in European countries. The prognosis is favorable in most cases, recovery occurs in 6-10 weeks.

Symptoms

• Acute fever. Fever lasts 12-45 days.
• Redness of the conjunctiva.
• Dryness and redness of lips.
• Redness of the oral mucosa.
• Enlargement of the cervical lymph nodes is unilateral or bilateral.
• Severe redness of the fingers and toes due to dilated capillaries.
• Dense swelling of the feet and hands.
• Rash - small red dotted elements (resembling the rash of scarlet fever) are located on the torso, limbs and in the groin folds.
• "Raspberry" tongue. This symptom appears in the second week after the onset of fever.
• Peeling of fingers and toes. The skin comes off in sheets 2-3 weeks after the onset of the disease.

Damage to small vessels

Wegener's granulomatosis is a severe form of vasculitis associated with impaired immunity. Manifested by a runny nose, sore throat and cough. Small arteries, veins and capillaries are affected. Due to the accelerated division of cells, numerous granules are formed on their walls, and over time, necrosis of the inner choroid occurs. In 90% of patients, the ENT organs and lungs are affected. Men get sick 2 times more often than women. The average age of patients is about 40 years.

Symptoms
Symptoms increase gradually and without treatment the patient’s condition worsens.

2. Hemorrhagic vasculitis

Hemorrhagic vasculitis or Henoch-Schönlein disease is an inflammation of the blood vessels of the skin, which is further complicated by damage to the joints, gastrointestinal tract and kidneys. Mostly the smallest veins (venules) and capillaries are affected. Hemorrhagic vasculitis develops 1-3 weeks after an infectious disease. The main group of patients are children 4-8 years old, mostly boys.

Symptoms

• Acute onset with fever and severe intoxication. In adults, the onset is usually erased.
• Papular-hemorrhagic rash is characteristic of the skin form. Red elements rising above the skin. When pressed, the rash does not disappear. Over time, its color changes and darkens. When the rash disappears, small scars may remain.
• The nature of the rash is polymorphic. The following may be simultaneously detected on the patient’s body:
  • red spots;
  • papules - stripless small nodules;
  • blisters filled with bloody contents;
  • pustules with purulent contents;
  • necrosis – areas of necrosis;
  • telangiectasia - dilated blood vessels under the skin;
  • blisters are dense formations without a cavity inside;
  • ulcerations are deep defects of the epithelium.
• Symmetrical location of the rash. It is mainly localized on both legs and buttocks.
• Wave-like appearance of rashes. New rashes appear once every 6-8 days. The first waves of rash are always the most severe.
• Joint damage is characteristic of the articular form. Joint pain appears simultaneously with the rash or a few days later. Mainly the knee and ankle joints are affected. Pain, swelling and redness appear. These changes are reversible and disappear after a few days.
• Gastrointestinal phenomena. Occurs in the abdominal form of hemorrhagic vasculitis. If these symptoms appear, surgical supervision is required:
  • cramping abdominal pain;
  • nausea;
  • vomit;
• Kidney damage develops in patients with the renal form of vasculitis. Manifestations range from slight increases in protein and red blood cell levels in the urine to symptoms of acute glomerulonephritis:
  • oliguria – decrease in daily urine volume to 500 ml;
  • pale skin;
  • dyspnea;
  • pain in the lumbar region and headache;
  • swelling, especially typical on the face. The amount of “excess” water in the body can reach 20 liters;
  • increase in blood pressure to 180/120 mmHg.
• Necrotizing purpura is characteristic of the fulminant form of the disease. Foci of necrosis appear on the skin, emitting an unpleasant odor, ulcerations, and crusts of dried blood. With this course of the disease, the patient’s condition is serious and he requires emergency help.

Churg-Strauss syndrome is an inflammatory-allergic disease with the formation of necrotizing inflammatory granulomas in small and medium-sized vessels. The disease affects the respiratory, central and peripheral nervous systems, skin and joints. The age of patients is 15-70 years, women are sick somewhat more often than men.

In its development, Churg-Strauss vasculitis goes through several stages:

• lesions of the nasal mucosa - lasts several years;
• lung damage – lasts 2-3 years;
• systemic vasculitis affecting many organs (nervous system, skin, joints) has a chronic course.

• Allergic rhinitis - nasal congestion is the first sign of the disease.
• Proliferation of polyps in the nasal passages.
• Lung damage is associated with eosinophilic infiltration - the penetration of eosinophils into the mucous membrane of the respiratory tract. Severe coughing attacks, suffocation, hemoptysis, shortness of breath, and chest pain with deep breathing occur. Patients experience:
  • prolonged bronchitis with an asthmatic component;
  • bronchial asthma is a chronic disease manifested by narrowing of the airways and attacks of suffocation;
  • bronchiectasis - local dilation of the lumens of the bronchi;
  • eosinophilic pneumonia - inflammation of the lungs caused by the accumulation of eosinophils in the pulmonary alveoli;
  • pleurisy - inflammation of the layers of the pleura (the serous membrane covering the lungs).
• Heart damage is associated with the destruction of the coronary vessels that supply it. Manifested by pain in the heart area and cardiac arrhythmia (tachycardia or bradycardia). Patients develop:
  • myocarditis – inflammation of the heart muscle;
  • coronaritis – inflammation of the coronary vessels of the heart;
  • constrictive pericarditis - inflammation of the outer connective tissue membrane of the heart, in which fluid accumulates in its cavity, compressing the chambers of the heart;
  • lesions of the mitral and tricuspid valves;
  • Myocardial infarction – necrosis (death) of a section of the myocardium resulting from a disruption in the blood supply.
• Lesions of the nervous system are called “brain vasculitis.” Developing:
  • peripheral neuropathy – damage to peripheral nerves: optic nerve, spinal nerve roots (sciatica);
  • hemorrhagic stroke - bleeding in the brain caused by a ruptured vessel;
  • epileptic seizures – spontaneous attacks of convulsions;
  • emotional disorders.
• Rash on the skin of the lower extremities
  • hemorrhagic purpura - bleeding into the skin. Painful small red-purple spots with irregular edges;
  • erythema - redness of the skin;
  • urticaria - small blisters that rise above the skin;
  • subcutaneous nodules are hard, smooth formations.
• Joint damage. Migrating arthritis occurs, affecting several joints in succession. The ankle, knee, wrist and elbow joints are most often affected. Churg-Strauss syndrome is characterized by symmetrical joint damage.
• Kidney damage – damage to individual glomeruli. It is rare and has an unexpressed course. Pathology is indicated only by abnormalities in urine analysis.

Symptoms of vasculitis

• the first elements appear on the lower extremities, mainly on the legs;
• symmetrical location of the rash;
• tendency of rashes to edema, necrosis and hemorrhage;
• evolution and polymorphism of elements - over time, the rash changes shape or color;
• connection of the rash with a previous infection;
• the appearance of a rash due to allergic, autoimmune, rheumatic or systemic diseases.

Symptom	Mechanism of occurrence	Manifestations
Deterioration of general condition
Intoxication	Poisoning of the body with toxins that are formed when blood circulation is impaired.	Weakness, loss of appetite, drowsiness, loss of strength.
Headache	Effects of toxins on the central nervous system.	The intensity of pain depends on the number and location of damaged vessels. Intense pain occurs with systemic vasculitis and damage to cerebral vessels.
Weight loss	The result of metabolic disorders and decreased appetite.	Unreasonable weight loss of 0.3-1 kg monthly.
Temperature increase	The body's response to the presence of toxins that appear when blood circulation deteriorates.	In mild forms, the temperature rises slightly - up to 37.5 degrees, and in severe forms - up to 40. Fluctuations during the day are characteristic.
Skin rash
Stains	Areas of skin redness are associated with local expansion of capillaries and intense blood flow.	Red or bright pink elements that do not rise above the level of the skin.
Hemorrhagic purpura	Damage to the vascular wall leads to its rupture. Subcutaneous hemorrhage occurs. Irritation of nerve endings and aseptic (without the participation of microorganisms) inflammation leads to painful sensations in the area of ​​the rash.	Hemorrhages can look like spider veins or spots ranging in size from the head of a match to the size of a lentil grain. Purple spots with a diameter of 3-10 mm, with irregular edges. Over time, the rashes turn blue, then become yellowish due to the destruction of blood cells. When pressed, the rash does not disappear.
Hives	It is a manifestation of an allergic reaction. Histamine increases vascular permeability. The layers of skin become saturated with fluid, causing blisters to form. Irritation of the nerve endings of the skin causes itching and burning.	Blisters are pink or red colored elements without a cavity. These elements have irregular outlines.
Subcutaneous nodules and nodes of various sizes	They are formed when a limited area of ​​skin is infiltrated by eosinophils, which causes the proliferation of the epidermis and connective tissue. Poor circulation leads to necrosis in the center of the nodes.	Dense, painful, flat or semicircular, hard, bandless formations that rise above the level of the skin. The size ranges from a few millimeters to 1-2 cm. Necrosis may develop in the center of the nodules - the tissue turns black and is rejected.
Bubbles	Increased permeability of the vessel walls in a limited area leads to the release of fluid under the skin and the formation of blisters.	Formations larger than 5 mm filled with liquid contents. It may be clear or mixed with blood.
Erosions and ulcers	Defects of the epidermis and dermis that occur when tissue nutrition is disrupted and nodules disintegrate.	Superficial (erosion) or deep (ulcer) skin defects.
Damage to the nervous system
Mood swings	Emotional disorders are caused by toxins. They affect the cerebral cortex and the limbic system, which is responsible for managing emotions.	Sudden mood swings, causeless tantrums, depression.
Seizures	Intracranial hemorrhage or the formation of foci of synchronous impulses in the brain cause certain muscle groups to contract.	Uncontrolled contractions and relaxations of muscles throughout the body or individual groups.
Damage to nerve fibers	Neuropathy is damage to nerve fibers associated with impaired blood circulation. This leads to disruption of the sensitivity and motor function of the areas for which the damaged nerves are responsible.	Muscle weakness, often asymmetrical. Paresis (incomplete paralysis) of the muscles of the limbs. Increased or decreased sensitivity in the “glove” and “sock” type.
Hemorrhagic stroke	Hemorrhage in brain tissue due to destruction of the vessel wall. In this case, small and large hematomas are formed, disrupting the functioning of the brain.	Panic and impaired consciousness. Headache, increased breathing. Increased or slow heart rate. Dilated pupil, possible divergence of the eyeballs. Violations of muscle tone - paresis of the limbs, asymmetrical muscle tone of the face.
Lung damage
Prolonged bronchitis with an asthmatic component	The penetration of eosinophils into the bronchial mucosa leads to its swelling and inflammation.	Prolonged paroxysmal cough with a small amount of sputum. The asthmatic component is manifested by difficult and noisy exhalation. When a bacterial infection occurs, the temperature rises and purulent sputum is released when coughing.
Bronchial asthma	Non-infectious inflammation of the bronchi during vasculitis makes them very sensitive to various allergens. Bronchospasm sharply limits the access of air to the lungs.	Attacks of suffocation, during which inhalation becomes short and exhalation becomes difficult, prolonged and noisy. Loud whistling wheezing can be heard from the side.
Eosinophilic pneumonia	Non-infectious pneumonia is associated with chronic infiltration by eosinophils.	Fever, weakness, shortness of breath, night sweats. Cough accompanied by scanty secretion of clear sputum.
Pleurisy	Inflammation of the pleura is caused by poor circulation. It is accompanied by the accumulation of fluid between the layers of the pleura, which leads to compression of the lung.	Slight increase in temperature, pain when taking a deep breath. Shortness of breath and shallow breathing.
Bronchial or pulmonary hemorrhage	Associated with rupture of the vessel wall or destruction of the infiltrate.	Bleeding may be minor and may appear as streaks of blood in the sputum. When a large vessel ruptures, a significant amount of blood is released from the respiratory tract.
Bronchiectasis	Expansion and deformation of the bronchi with prolonged eosinophilic infiltration and circulatory disorders	When a blood vessel is damaged, pulmonary hemorrhage develops. During exacerbations, a cough occurs with a large amount of purulent sputum, discharged after a night's sleep. Cyanosis (blue discoloration) of the extremities, shortness of breath, general malaise, fever.
Visual impairment
Optic nerve damage	Malnutrition of the optic nerve leads to its atrophy.	Progressive loss of vision, which can lead to complete blindness. Visual impairment can be unilateral or bilateral.
Protrusion of the eyeball - exophthalmos	Granulomatosis of the orbit of the eye. At the initial stage, cells capable of phagocytosis grow. Subsequently, the granulomas are replaced by connective tissue, pushing the eye outward and downward.	Swelling and redness of the tissues of the eye. Difficulty moving the eyeball.
Respiratory system lesions
Long-term rhinitis, sinusitis and sinusitis	Increased vascular permeability leads to swelling of the mucous membrane and inflammation, which gives rise to allergic rhinitis.	Prolonged runny nose. Mucous discharge mixed with blood. Dry crusts in the nose. Smell disorders. Recurrent nosebleeds. Swelling in the area of ​​the bridge of the nose and one half of the face.
Destruction of the nasal septum and the walls of the maxillary sinus	Malnutrition and proliferation of granulation tissue leads to the destruction of cartilage and bone.	Prolapse of the nasal bridge Difficulty in nasal breathing, purulent mucous discharge mixed with blood.
Kidney damage
Decreased kidney function	The deterioration of kidney function is associated with disruption of the blood vessels that provide nutrition to the glomerular apparatus.	Pain in the lumbar region, swelling, fever, dry mouth. Decreased urine volume. With minor damage, protein and red blood cells may appear. With massive damage to the kidney tissue, the urine may become cloudy or acquire a reddish tint due to the admixture of blood.
Acute and chronic renal failure	Massive damage to the kidney tissue leads to the fact that they lose the ability to perform their function.	General weakness, swelling, itching, high blood pressure, sleep disturbances. An increase and then a decrease in the amount of urine produced.
Joint damage
Arthritis	Damage to the vessels of the joint capsule leads to the release of additional fluid into the joint cavity. It causes swelling of the joint, which is accompanied by pain.	The knee joints are usually the first to be affected. They become red and swollen, and the swelling spreads to surrounding areas. A rash may appear on the skin over the joints. No joint deformation is observed. The pain is quite severe and can deprive a person of the ability to move. After a few days, the inflammation spreads to neighboring joints, and the pain in the primary site decreases. In most cases, the changes are reversible. They go away on their own, without treatment.
Gastrointestinal lesions
Abdominal pain	Damage to the vessels of the intestine and mesentery leads to impaired blood circulation. Multiple hemorrhages into the intestinal wall and peritoneum provoke swelling and non-microbial inflammation. In this case, sensitive nerve endings are irritated and acute pain occurs, which can simulate an attack of appendicitis.	Severe paroxysmal pain in the abdomen, which has the nature of colic. Often localized in the navel area. It intensifies 20-30 minutes after eating.
Digestive disorders	Damage to the intestinal vessels impairs its function. May lead to atrophy and destruction of the intestinal wall and intestinal perforation.	Patients experience nausea and vomiting. Frequent, watery stools in small portions, sometimes mixed with blood.

Diagnosis of vasculitis

The doctor conducts an examination, studies the presence and nature of the rash. During a conversation with the patient, the doctor finds out:

• how long ago the first symptoms of the disease appeared;
• whether the disease was preceded by infections;
• is there a tendency to allergies;
• whether individual sensitivity to drugs was observed;
• are there any chronic diseases that are foci of chronic infection;
• Are there any complaints of runny nose, cough, pain in the abdomen, joints or lower back?

Type of study	The essence of the study	Signs of vasculitis revealed by this study
Clinical blood test	A study that allows you to evaluate various indicators of peripheral blood that indicate changes in the body - the number and ratio of blood elements, erythrocyte sedimentation rate.	An increase in ESR levels is a common, but not specific sign of vasculitis. Shift of the leukocyte formula to the left.
Coagulogram	Determination of blood clotting.	The patient exhibits signs of intravascular activation of the blood coagulation process An increase in the level of fibrinogen (a protein that ensures blood clotting) over 4 g/l. Inhibition of fibrinolysis - the process of dissolving blood clots slows down. Paracoagulation products are detected. This means that there are bacterial components in the blood that cause increased blood clotting. Increased spontaneous platelet aggregation - red blood cells change in such a way that the process of blood clots increases. D dimers above 500 ng/ml are detected. These are large fragments of fibrin breakdown, indicating the active formation of blood clots in vessels damaged by vasculitis.
C-reactive protein test	The detection of C-reactive protein in the blood indicates an inflammatory or autoimmune process in the body.	Detection of CRP over 80-100 mg/l indicates the presence of the disease. The higher the score, the more severe the degree of vasculitis. However, this indicator increases significantly in the acute period of bacterial infections, and therefore is nonspecific.
Immunological studies
Determination of the level of immunoglobulin in the blood	Study of venous blood serum for the level of immunoglobulins, which indicate a dysfunction of the immune system. Exceeding the norm indicates excessive immune activity.	IgA over 2.5 g/l - indicates acute vasculitis. IgM over 3 g/l – mixed form with kidney damage. IgE over 100 IU/l – wave-like course of vasculitis. IgG over 16 g/l – predominant damage to the skin and joints.
Circulating immune complexes (CIC) in the blood	Determination in blood serum of complexes consisting of antibodies, antigen and complement components. The study allows us to assess the degree of progression of autoimmune diseases.	Identification of CEC over 75 standard units. U/L confirms the presence of vasculitis.
Analysis for antibodies to the cytoplasm of neutrophils ANCA	Determination of these antibodies in blood serum by indirect immunofluorescence.	The detection of these antibodies indicates an immune attack on immune cells - neutrophils, which is typical for systemic vasculitis.
Urine examination
Clinical urine analysis	Study of the physicochemical properties of urine.	Indicates kidney damage red blood cells in urine more than 3 in the field of view. increased protein level over 0.033 g/l. cylinders in the renal form of vasculitis - normally they should not be present.
Other types of research
Angiography (vascular examination)	X-ray examination of blood vessels after the introduction of contrast agents into the blood.	In damaged vessels, segmental narrowing, dilation, or complete blockage of the vessel by a thrombus is detected. When small-caliber capillaries are affected, angiography is not very informative.
Chest X-ray	X-ray examination to evaluate changes in the chest organs.	If the lungs are affected, they can be detected Signs of inflammation of the bronchi and lung tissue; Large or small infiltrates; Cavities in lung tissue; An accumulation of fluid between the layers of the pleura, compressing the lung tissue.
Biopsy (for abdominal vasculitis)	Removing a small piece of tissue from a damaged area of ​​the intestine.	When the gastrointestinal tract is damaged, the following are detected: Infiltrates consisting of granulocytes and IgA deposits; Immune complexes in tissue.
MRI	Study of internal organs using the phenomenon of nuclear magnetic resonance.

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