Immune complexes. Circulating Immune Complex (CIC)

Circulating immune complexes in plasma is evidence of the presence of various inflammatory processes. Thanks to such research, you can find out about the presence of autoimmune diseases and monitor their activity. A doctor can prescribe such a diagnosis if it is impossible to diagnose the patient for certain reasons, but he suspects the presence of autoimmune viral, fungal and other diseases. Analysis of circulating immune complexes is carried out among both adults and children. The study can be performed as a separate procedure or in a group with other blood tests.

CEC are components that begin to be produced by the human body and are formed in the blood as a response to exposure to foreign bodies. Such complexes usually include antigens, antibodies and other elements. If a person does not have an appropriate reaction and the production of the central nervous system is disrupted, then this indicates that a malfunction has occurred in the patient’s body immune system. The main task of such components is to recognize and remove harmful bodies and allergens from the body as quickly as possible. After the CECs have completed their function, they are usually destroyed by phagocytes.

Circulating immune complexes can form not only directly in the blood, but also in the liver. When they are no longer needed, they are removed from the body. If a person is very sick or infected with an infectious disease, then the level of components increases significantly. In this case, they begin to be deposited on the liver and eventually form a dense film, which provokes the formation of an inflammatory process. If such a lesion was not noticed on early stage, this can lead to the spread of inflammation to other internal organs abdominal cavity. Often such changes can lead to cancer. The normal content of CEC in plasma should be 30-90 IU/ml.

When and why is research performed?

The test is usually used to diagnose general state patient. This is necessary before undergoing a major operation, during pregnancy, if there is oncological diseases. Through such diagnostics it is possible to detect the presence in the body immune pathology or severe allergic reaction.

Chronic infections that are in the human body may not manifest themselves on the external plane and are not accompanied by bright severe symptoms, but are easily detected by circulating immune complex assays. Such diagnostics make it possible to monitor the development of glomerulonephritis and adjust its treatment. In case of damage to the immune system, a blood test is the best way to monitor the trend of development or cessation of the disease.

Quite often, only such a blood test will allow the doctor to obtain full picture the course of all allergic and viral processes in the body. The analysis is carried out more than once. If the diagnosis is part of a study of the state of the immune system, then the analysis will have to be repeated several times. During the treatment period, the patient does not need to follow a diet or resort to additional measures preparation for analysis. The process of donating blood can be quite painful, but these sensations disappear immediately after the procedure.

The doctor may prescribe such a diagnosis in several cases. Often the cause is an autoimmune pathology in the patient. If a person suspects arthritis, lupus, polymyositis, vasculitis or scleroderma, then this is a reason to conduct a diagnosis. She will be able to confirm or refute the diagnosis. Often such a blood test is prescribed to patients with joint syndromes, defeats cartilage tissue and blood vessels, kidney or liver dysfunction. This analysis is an integral part of the diagnosis when examining the immune system.

Increased rate in patients

In addition to the fact that circulating immune complexes are created by the human body, they are also destroyed by it. Phagocytes begin to influence those bodies that have already fulfilled their protective function and destroy them. But if the patient has an autoimmune disease, this means that either the body produces too many antibodies at one time, or they are not destroyed after they have completed their task.

If the CEC produces too much, then they lose all their properties. As a result, the human body contains many elements that cannot protect it and at the same time provoke inflammatory processes. Unused or excess circulating immune complexes begin to deposit on human organs. The kidneys suffer the most. They are covered with a layer of elemental cells, and their function is hampered. Inflammation begins, which can lead to the progression of diseases, tissue destruction or partial atrophy of the organ.

Formation of antibodies necessary process which must occur in the body. When excess content complexes and disruption of their functioning, viruses and allergens can enter the body, which nothing can resist. At that time human body especially susceptible to various diseases. Even the simplest ARVI can cause serious damage and transform into another disease.

With an increased content of complexes in the blood, the formation of not only inflammatory processes, but also tumors is observed in the human body. Such diseases and neoplasms can lead to the development of pathologies and serious damage to the immune system and all internal organs. In order to conduct the study, you need to take a test of your blood, which will then be combined with C1q elements. The result will depend on how able the plasma cells are to interact with the C1q components.

Reducing the level of elements

A decrease in the number of CECs entails deviations and tissue destruction. Insufficient production of elements provokes diseases of the immune system, since now the body cannot independently protect itself from harmful factors from the outside. If complexes an insufficient amount, then this leads to their accumulation on individual bodies. Substances lose their basic functions and grow on the tissues of the body, while destroying it. This occurs due to cell breakdown and a decrease in the density of vascular walls. As a result, the content of CEC in tissues increases and phagocytes can no longer break them down.

CECs can be found not only independently in the patient’s plasma, but also in association with red blood cells. These links, in excess or deficiency, do not have a destructive effect and do not cause significant harm to the body, therefore, during the study, attention is paid exclusively to the presence of components directly in the patient’s blood.

The level of elements can be checked by reaction to substances C3d and C1g. If the indicators are significantly reduced, then this indicates damage to the gene that is responsible for the transformation of protein elements in the body. A reduced value indicates the presence of an allergic disease, vasculitis or autoimmune lesion. Often this indicator means the presence of hepatitis, HIV, infectious arthritis or endocrit.

Like autoimmunity (page 25), the formation of antigen-antibody complexes or immune complexes (ICs) is normal physiological process, aimed at protecting the body from potentially pathogenic influences. However, under certain conditions, IR can play important role in the development of rheumatic diseases. Classic manifestations of the immune complex process associated with impaired clearance and deposition of IR in tissues are vasculitis, nephritis and arthritis, which are among the leading forms of organ pathology in many cases. rheumatic diseases. In rheumatic diseases, the development of immune complex pathology is associated with the following factors: 1. Disruption of the mechanisms of normal clearance of immune complexes from bloodstream: a) genetically determined (p. 81), or acquired pathology of the complement system, leading to disruption of the process of inhibition of immune precipitation and solubilization of antigen-antibody complexes, which promotes the circulation of complexes with a more pronounced inflammatory potential and the possibility of their deposition in target organs; b) congenital or acquired impairment of erythrocyte clearance of immune complexes due to pathology of CR1 erythrocyte receptors; Recently, a violation of the expression of CR1 receptors on the erythrocytes of patients with antiphospholipid syndrome was shown (p. 13): c) blockade functional activity Fc receptors of mononular phagocytic cells localized in the liver and spleen. 2. Overproduction of circulating immune complexes with a certain structure and charge, which have the ability to bind to charged biomolecules of target organs. Recently, it was shown that in SLE, the formation of anti-DNA containing IR expressing idiotypes 0-81 correlates with SLE activity and the development of diffuse proliferative nephritis with subendothelial deposits. Overproduction of IR containing IgM and IgG RF correlates with the development of rheumatoid vasculitis. Cryoprecipitating immune complexes can play a particularly important pathogenetic role (p. 95).

In general, in systemic rheumatic diseases, autoimmune and immune complex pathological processes are in close relationship, which is determined by a common genetic predisposition to impaired immunoregulation and weakened clearance of immune complexes and similar mechanisms of inflammation and tissue destruction mediated by autoantibodies and immune complexes.

Clinical significance of determining circulating immune complexes (CIC).

To determine the CEC, it is advisable to use several methods based on different principles, 1. C1q binding method.

Changes in the concentration of CEC, determined by the C1q binding method, correlate with the articular index in RA and, in some cases, with the activity of the pathological process in SLE. However, this method may produce false-positive results due to the production of antibodies to C1q, especially when used for the detection of solid-phase immobilized CEC C1q.

2. Method using Raji cells.

Until recently, this method was considered as the most sensitive way to detect CEC.

TO The disadvantages of this method include the possibility false positive results due to binding

With antilymphocyte antibody cells. (p. 103), often present in serums patients with SLE. This method is sometimes used to assess disease activity in systemic necrotizing vasculitis and sarcoidosis.

3. Method of precipitation of immune complexes with polyethylene glycol.(PEG method).

The simplest and most commonly used clinical practice method for determining CEC: an increase in the concentration of CEC according to this method correlates with the inflammatory and immunological activity of the process in SLE, RA. seronegative arthropathy. The disadvantages of the method include its insufficient high sensitivity, difficulties in quantitatively assessing the content of CEC in terms of aggregated gammaglobulin, dependence of the results on the concentration of IgG in the serum. 4. IgA-containing CECs.

Detection of IgA-containing immune complexes correlates with hematuria in ankylosing spondylitis, in which IgA nephropathy can develop. IgA-fibronectin complexes are most characteristic of IgA nephropathy, while they are not detected in ankylosing spondylitis. The formation of C1q-binding immune complexes and IgA-containing immune complexes correlates with seropositivity, disease activity, and the development of vasculitis in RA. 5. Composition of circulating immune complexes. Exogenous or endogenous antigens can be found in the CEC - yersinia in yersinia arthritis, HBsAg in urticarial vasculitis and nodular periarteritis, DNA - for SLE. Antibodies to Borrelia burgdorferi are present in the CEC in seronegative patients with Lyme borreliosis.

It is assumed that in autoimmune diseases, in which it is rarely possible to detect any autoantigen in the immune complexes, the formation of idiotipantiidiotypic immune complexes, the production of which is associated with polyclonal B-cell activation, is of primary importance.

LITERATURE.

Nasonov E.L. Immune complexes in rheumatic diseases. Results of science and technology. Immunology Series, Volume II, 1984, pp. 104-158; Nasonov E.L., Sura V.V. The relationship between autoimmune and immune complex pathologies: current state problems Therapist. archive, 1984, No.10, pp. 4-10. Nasonov E. L. Methodological aspects of determining circulating immune complexes using polyethylene glycol. Therapist. archive, 1987, No.4, pp. 38-45; Davies K.A. Immune complexes and disease. Eur. J. Int. Med. 1992; 3:95-108.

INTERMITTING HYDRATHROSIS

A rare disease characterized by recurrent accumulation of fluid in a joint at regular intervals. Usually the disease is idiopathic in nature, but sometimes a similar pathology develops with RA, ankylosing spondylitis, or Reiter's syndrome. It differs from palindromic rheumatism (p. 125) in the regularity of attacks and the distribution of joint damage.

It affects men and women with the same frequency, occurs at any age (peak 20-50 years). Clinical manifestations: Usually one or two joints are affected, most often knee (90%); V

In 65% of cases, only the knee joints are involved in the process, and in 60% of patients, a bilateral process or lesion is observed. knee joints seen in different periods illness; in other cases, only one knee joint is affected, sometimes the elbow joint (15%), very rarely the shoulder, ankle, temporomandibular joints, small joints of the hands and feet; during repeated attacks, the same joints are involved in the process; the attack is characterized by rapid (within 12-24 hours) the appearance of effusion in the joint, pain, limited mobility. On examination, a large effusion is found in the joint cavity, very rarely subfebrile fever; The effusion disappears within 2-6 days, and then reappears after a fixed period of time (3-30 days, especially often on days 10, 14 and 21). The frequency is strictly maintained for each patient. The process can recur over many years, but 60% of patients develop long-term remissions, lasting up to 10 years or more. Deformations usually do not develop.

X-ray examination: expansion of the joint space. sometimes when long term disease degenerative changes.

Laboratory examination: ESR is within normal limits, RF is not detected: synovial fluid non-inflammatory type: with a biopsy of the synovial membrane - nonspecific synovitis.

Treatment: analgesics, NSAIDs, fluid aspiration, intramuscular injection of GC, as a rule, does not have a significant effect; There is evidence of the effectiveness of gold salts, synovectomy, but this treatment should be reserved only for patients with the most severe course diseases.

ISCHEMIC BONE DISEASE

A syndrome in which the development of cartilage necrosis and bone tissue associated with circulatory disorders due to inflammation of the vessel (arteritis), thrombosis, embolism, changes external pressure on the vessel wall, injury.

Reasons: 1. Trauma (femoral neck fracture). 2. Arthropathy (RA, psoriatic arthritis, severe osteoarthritis, neuropathic joint). 3. Endocrine and metabolic diseases (treatment with GC, Cushing's disease, alcoholism, gout, osteomalacia). 4. Storage diseases (Gaucher disease (p. 68)). 5. Caisson disease. 6. Systemic rheumatic diseases (SLE), antiphospholipid syndrome(p. 52); giant cell arteritis. 7. Pancreatitis, pregnancy, burns, endocarditis, radiation, polycythemia, electric shock, local administration of GC, Perthes disease (p. 128), Thielman disease (p. 182). 8. Idiopathic avascular necrosis.

Ischemic necrosis often develops in the head hip bones in middle-aged men (age 30-60 years, male to female ratio 4:1), in 30% of cases the lesion is bilateral.

Clinical manifestations: pain varying degrees intensity, stiffness in the affected joint, limited mobility, effusion when the knee joint is affected.

X-ray examination: small areas of infarction against the background of sclerosis and osteoporosis, areas of collapse articular surface, necrotic fragments (the picture resembles osteochondritis dissecans,

Laboratory test: changes depend on the underlying disease.

Treatment: in the early stage, complete immobilization, analgesics; in the late stage, surgical treatment.

KAWASAKI DISEASE

Acute febrile illness childhood, first described in Japan in 1967. The etiology is unknown, however, the epidemiological features and the range of clinical manifestations indicate infectious nature diseases.

The disease is slightly more common in boys than in girls (ratio 1.4:1). The disease mainly affects children under 5 years of age (90%).

Clinical manifestations: 1. High, intermittent fever (1-2 weeks in the absence of treatment). 2. Conjunctivitis with a predominant lesion of the bulbar conjunctiva without pronounced exudation develops following an increase in temperature and persists for 1-2 weeks. 3. Erythema, dryness, peeling and bleeding of the lips, erythema of the tonsils, “crimson” tongue with diffuse erythema and hypertrophy of the papillae. 4. Erythema (or induration of the skin of the palms and soles, accompanied by severe pain, limited mobility, inability to make fine movements (10-20 days from the onset of fever); peeling of the fingers begins from the periungual zone, and then spreads to the palms

And soles. 5. Polymorphous rash (the first 5 days from the onset of fever); urticarial exanthema with large erythematous plaques, macropapular multiforme-like, scarlet-like erythroderma localized on the trunk and limbs, in the perineal area. 6. Single-sided or double-sided cervical lymphadenopathy; On palpation, the lymph nodes are dense and sometimes painful. 7. Unusually high excitability, more pronounced than in other febrile diseases in children. 8. Joint damage (30%): arthralgia or polyarthritis of the knees, ankle joints and small joints of the hands (develops during the first week, persists for about 3 weeks). 9. Damage to the cardiovascular system (45%): heart murmur, tachycardia, gallop rhythm, cardiomegaly, prolongation of the PQ interval and widening of the QT complex, decreased voltage, ST segment depression, arrhythmia; with coronary angiography

And echocardiographic study reveals aneurysms, narrowing, obstruction of blood vessels; described the development of myocardial infarction, usually during the first year of the disease, in 30% of asymptomatic patients.

The first 5 signs occur in more than 90% of patients, and 6 - in 50-75% (an increase in at least one lymph node more than 1.5 cm) are diagnostic criteria for the disease. 5 out of 6 signs are required to make a diagnosis.

Laboratory research: leukocytosis, neutrophilia, increased ESR, thrombocytosis, increased concentration of C-reactive protein, in urine tests - proteinuria and leukocyturia. Diagnostic criteria Kawasaki disease (p. 249). Treatment: aspirin at a dose of 80-120 mg/kg per day ( acute phase disease until normalization of C-reactive protein, then the dose is reduced to 30 mg / kg per day until normalization of ESR; maintenance dose during convalescence 3-5 mg/kg/day; intravenous immunoglobulin 400 mg/kg/day for 5 days (preferably in the first 10 days from the onset of illness).

LITERATURE.

Wortmann DW, Nelson AM. Kawasaki syndrome. Rheumatic Disease Clinic North. Amer. 1990; 16:363-375.

CALPROTECTIN

A non-glycosylated protein that makes up 60% of the soluble proteins of the cytosolic fraction of neutrophil granulocytes, which is released from cells during the period of their activation and destruction. Calprotectin has calcium-binding and antimicrobial activity. An increase in serum calprotectin concentration is observed in various infectious and chronic conditions. inflammatory diseases, including RA and SLE. In RA, the serum calprotectin level correlates with the concentration of CRP, ESR and clinical parameters activity, as well as RF detection. In SLE, calprotectin concentrations correlate with disease activity, anti-DNA antibody levels, and the development of arthritis. It is assumed that the level of calprotectin may be a new laboratory indicator of the activity of the pathological process in rheumatic diseases.

CARCINOID SYNDROME

Rare syndrome associated with the production of 5-hydroxytryptamine and other biologically active amines

carcinoid tumor, which originates from argentophilic cells small intestine. Occasionally, against the background of the disease, transient arthritis develops, characterized by symmetrical damage to the interphalangeal joints of the hands with severe swelling and pain, sometimes flexion contractures. A characteristic manifestation syndrome is a sharp reddening of the face, with subsequent development of persistent erythema and telangiectasia, weight loss, chronic diarrhea, asthmatic attacks, liver enlargement, tricuspid and valve damage pulmonary artery hearts. The diagnosis is confirmed by the detection of increased urinary excretion of 5-hydroxytryptamine.

KASHIN-BEK DISEASE (level disease)

An endemic disease based on disorders of enchondral ossification, leading to the development of multiple deforming osteoarthritis. The disease occurs in Eastern Siberia, Northern China, North Korea. The etiology is not clear; exogenous factors characteristic of the corresponding endemic zones are of undoubted importance.

It occurs with equal frequency in men and women and begins in childhood and adolescence. Clinical manifestations: Damage to small joints of the hands, wrists, ankles, knees, hip joints, then the spine. On examination, joint pain, swelling, stiffness, limited mobility, crepitus, and inflammatory changes are absent; later, severe deformation and shortening of the fingers, reminiscent of arthritis mutilans, may develop. The course is chronic, slowly progressive, leading to complete disability.

X-ray examination: degenerative changes in the form of narrowing of joint spaces, sclerosis, cystic clearings; in later stages - bone destruction, especially of the phalanges of the fingers.

Laboratory examination: no pathology is detected. Treatment: analgesics, NSAIDs.

KIKUCHI DISEASE (histiocytic necrotizing lymphadenitis)

Disease; manifested by painless, unilateral cervical lymphadenopathy, later generalized involvement of the lymph nodes (20%), fever, weakness, skin lesions like urticaria, occasionally splenomegaly, enlarged mesenteric lymph nodes simulating appendicitis; at laboratory research neutropenia, lymphocytosis, a sharp increase in ESR, an increase in the concentration of liver enzymes are detected; During immunological examination, antibodies to DNA (p. 70) and antilymphocyte antibodies (p. 103) are detected in the sera of patients. Usually the disease ends with spontaneous recovery within 3 months, less often it persists for up to a year. At histological examination lymph nodes reveal patchy paracortical (T zone) necrosis, consisting of eosinophilic fibrinoid material containing a large number of nuclear fragments, the necrosis zone is surrounded by histiocytes, macrophages, T cells in the absence of plasma cells and polymorphonuclear leukocytes.

Kikuchi disease is thought to be a benign lupus-like syndrome associated with infection with parvovirus B19; The development of characteristic clinical and pathomorphological signs of pathology in classical SLE and Still's disease is described. Treatment: prednisolone 1 mg/kg/day (relieves constitutional symptoms and fever).

LITERATURE.

Meyer OS. Kikuchi's disease revisited. Clin. Exp. Rheumatol. 1992; 10:1-2.

CLUTTON JOINTS

Bilateral hydrarthrosis of the knee joints, developing with secondary syphilis. This disease is sometimes misdiagnosed as Still's disease.

This form of articular pathology occurs with equal frequency in men and women, and develops at the age of 8-15 years in 10% of patients with congenital syphilis.

Clinical manifestations: 1. Asymmetrical involvement of the knee joints (damage to one joint often precedes damage to the other joint by several years; very rare pathological process develops in the ankle and elbow joints. The disease begins gradually with joint pain

Immune complex diseases (type III hypersensitivity) result from tissue deposition soluble complexes antigen-antibody. Which leads to inflammation.

The damage in this type of allergic reaction is caused by AG-AT immune complexes. Reactions constantly occur in the body with the formation of the AG-AT complex. These reactions are an expression protective function immunity and are not accompanied by damage. But under certain conditions, the AG-AT complex can cause damage and the development of the disease. Immune complexes are formed when there is an excess of antigen and antibodies. The concept that immune complexes (ICs) may play a role in pathology was proposed as early as 1905 by Pirquet and Schick. Since then, a group of diseases in the development of which IR plays a major role began to be called diseases of immune complexes.

Immune complex diseases can be:

* systemic - which are caused by circulating antibodies (for example, serum sickness);

* local - as a result of the formation of immune complexes at the site of penetration of antibodies (for example, the Arthus phenomenon).

There may also be delayed allergic reactions involving Ig G class antibodies, which are also fixed on mast cells with the participation of the C3 component of complement. They are also a manifestation of type 3 hypersensitivity reactions.

The conditions for the development of the immune complex mechanism of immunopathology are:

* presence of long-term (chronic) infectious process, which assumes a constant flow of antigens into the blood;

* predominance of antibody reactions, i.e. the advantage of type 2 T helper cells, which control the development of the humoral immune response;

* relative insufficiency of factors for the destruction and elimination of the CEC from the bloodstream, namely the complement system and the phagocytic reaction of neutrophils and macrophages;

* properties of the CEC. The pathogenic properties of CEC are determined by the totality of their physical and chemical properties, which include size, concentration, composition, solubility, and ability to fix complement. The molecular weight of CECs determines their size, which is the most important indicator pathogenicity. Also, the molecular weight determines the rate of elimination of CECs from the body: large CECs are quickly eliminated and are relatively low-pathogenic; small CECs are poorly eliminated, can be deposited subendothelially, and are not able to activate the complement system; Medium-sized CECs have a high complement-fixing ability and are the most pathogenic.

Immune complexes in type 3 allergic reactions are postponed until vascular wall or at basement membranes Oh. This deposition of immune complexes causes immune complex inflammation. Its essence comes down to the activation of the classical pathway of the complement system with the formation of C3a and C5a complement components. They attract macrophages, neutrophils, mast cells, which determine tissue damage. In addition, intravascular deposits of immune complexes lead to platelet aggregation with the formation of microthrombi, which enhance the accumulation of inflammatory mediators, resulting in the destruction of blood vessels and their replacement with connective tissue.

The following stages are distinguished in the pathogenesis of immune complex reactions:

I. Immunological stage. In response to the appearance of an allergen or antigen, the synthesis of antibodies begins, mainly of the IgM and IgG classes. These antibodies are also called precipitating antibodies for their ability to form a precipitate when combined with the corresponding antigens. When AT combines with AG, IR is formed. They can form locally, in tissues or in the bloodstream, which is determined by the routes of entry or the place of formation of antigens (allergens). The pathogenic significance of IR is determined by their functional properties and the localization of the reactions they cause.

II. Pathochemical stage. Under the influence of IR and in the process of its removal, a number of mediators are formed, the main role of which is to provide conditions conducive to phagocytosis of the complex and its digestion. However, under unfavorable conditions, the process of formation of mediators can be excessive, and then they begin to have a damaging effect.

The main mediators are:

1. Complement, under conditions of activation of which various components and subcomponents have a cytotoxic effect. The leading role is played by the formation of S3, C4, C5, which enhance certain components of inflammation (S3v enhances the immune adhesion of IC to phagocytes, S3 and C4a play the role of anaphylatoxins).

2. Lysosomal enzymes, the release of which during phagocytosis increases damage to basement membranes and connective tissue.

3. Kinins, in particular, bradykinin. With the damaging effect of IC, the Hageman factor is activated; As a result, bradykinin is formed from alpha globulins in the blood under the influence of kallikrein.

4. Histamine and serotonin play a large role in type III allergic reactions. Their source is mast cells, platelets and basophils. They are activated by the C3a and C5a complement components.

5. Superoxide anion radical is also involved in the development of type III allergic reactions.

All of these mediators enhance proteolysis.

III. pathophysiological stage. As a result of the action of mediators, inflammation develops with alteration, exudation and proliferation. Vasculitis develops, leading to the appearance, for example, of glomerulonephritis. Cytopenias, such as granulocytopenias, may occur. Due to activation of Hageman factor and/or platelets, intravascular coagulation may occur.

The third type of allergic reactions is leading in the development serum sickness, some cases of medicinal and food allergies, in some cases of autoimmune diseases, etc. With significant activation of complement, systemic anaphylaxis develops in the form of shock.

Description

Determination method

Solid phase linked immunosorbent assay(ELISA), CEC C1q-binding (IgG)

Material under study Blood serum

Determination of circulating immune complexes capable of activating complement via the classical pathway.

Increased intake of foreign antigens, decreased tolerance to autoangigens, disruption of the processes of elimination of immune complexes lead to advanced education immune complexes. Such complexes can form directly in tissues when provocative the antigen is associated with the corresponding cells and tissues. But if the antigens are soluble and circulate in the blood, there is an increase in the concentration of circulating immune complexes (CIC). Circulating complexes, under certain conditions (where the blood flow is slow or filtration occurs, as well as when their solubility decreases), can be deposited on membranes small vessels and accumulate in tissues. The accumulation of immune complexes, their binding to complement factors and activation of the complement system lead to the induction of local inflammation and damage to organ tissue. The potential pathogenicity of CECs may depend on the nature of the antigens and antibodies included in their composition, size, rate of formation and excretion, solubility, and ability to fix complement.

Increasing the CEC level is possible with autoimmune pathologies(for example, systemic lupus erythematosus - SLE, rheumatoid arthritis etc.), a number of chronic infectious diseases, in which the constant production of an antigen by an infectious agent is combined with an immune response to it, proliferative neoplastic diseases, allergic conditions. In itself, an increase in the level of CEC is not specific for any separate disease and is not absolute evidence of immune complex pathology and tissue damage, but if such an increase correlates with the observed clinical manifestations and other laboratory changes (for example, signs of increased activation of the complement system), one may suspect clinical role this factor. If a positive result is obtained, it is always recommended to repeat the study after a few weeks to assess the persistence of the presence of immune complexes in the circulation and thus their likelihood clinical significance. Dynamic studies of CEC can also be useful in monitoring clinical activity and the effectiveness of therapy for certain diseases (including SLE).

There are different methods for determining CEC, based on their physicochemical or biological properties. Results obtained different methods, do not always correlate with each other. Solid-phase ELISA methods using the property of CEC to bind to the C1q component of complement are currently among the preferred and most common, since they allow the detection of potentially pathogenic circulating immune complexes and are more sensitive than PEG precipitation methods. However, it should be taken into account that the study of CEC may still not be sensitive and specific enough in the diagnosis of diseases caused by immune complexes, and should be supplemented by the study of potential pathological manifestations the effect of the CEC on organ function, as well as assessing the activity of the complement system, including the determination of C3 and C4 complement components (), the number of which is reduced due to increased consumption in such conditions.

Limits of detection: 0.1 U/ml - 200 U/ml

Literature

1. Lapin S.V. Totolyan A.A. Immunological laboratory diagnostics autoimmune diseases/. Publishing house "Man", St. Petersburg, 2010.
2. Tietz's clinical manual on laboratory tests (ed. Wu A.), M. Labora, 2013, 1280 pp.
3. Nephrology. National leadership(Chief editor: Mukhin N.A.).. M., GEOTAR-Media, 2014, 608 p.
4. Podolska M.J. et al. Inflammatory etiopathogenesis of systemic lupus erythematosus: an update. Journal of Inflammation Research. 2015, Vol.:8, P. 161-171.
5. Materials from the company - the manufacturer of the reagents.

Preparation

On the eve of the study, it is necessary to exclude physical exercise and smoking. Biomaterial should be taken in the morning from 8 to 10 am on an empty stomach. At least 8 hours must pass between the last meal and blood collection. You can drink water.

Indications for use

1. Autoimmune diseases with an increase in the synthesis of immunoglobulins: SLE, Sjogren's syndrome, rheumatoid arthritis and other systemic diseases.
2. Immune complex vasculitis.
3. Glomerulonephritis of various origins.
4. Infectious processes.

Interpretation of results

Interpretation of research results contains information for the attending physician and is not a diagnosis. The information in this section should not be used for self-diagnosis or self-treatment. Accurate Diagnosis puts the doctor, using both the results of this examination¤, and the necessary information from other sources: anamnesis, results of other examinations, etc.

Units of measurement in the Independent Laboratory INVITRO: U/ml

Reference values:< 20 Ед/мл

Interpretation of results:

Promotion.

An increase in CEC concentration is possible with various systemic disorders, including autoimmune disorders, viral and bacterial infections, allergic diseases, oncological pathology. It should be noted that approximately 10% is practically healthy people may have moderate increased content Central Election Commission. Result laboratory test cannot serve as the sole basis for diagnosis and should always be considered in conjunction with clinical data and the results of other studies.