Autoimmune disease related. Autoimmune diseases

Autoimmune diseases are a large group of diseases that can be combined on the basis that their development involves an immune system aggressive against its own body.

The causes of almost all autoimmune diseases are still unknown.

Given the huge variety autoimmune diseases, as well as their manifestations and the nature of their course, these diseases are studied and treated by a variety of specialists. Which ones exactly depend on the symptoms of the disease. So, for example, if only the skin suffers (pemphigoid, psoriasis), a dermatologist is needed, if the lungs (fibrosing alveolitis, sarcoidosis) - a pulmonologist, joints (rheumatoid arthritis, ankylosing spondylitis) - a rheumatologist, etc.

However, there are systemic autoimmune diseases when different organs and tissues are affected, for example, systemic vasculitis, scleroderma, systemic lupus erythematosus, or the disease “goes beyond” one organ: for example, with rheumatoid arthritis, not only joints, but also skin can be affected, kidneys, lungs. In such situations, most often the disease is treated by a doctor whose specialization is related to the most striking manifestations of the disease, or by several different specialists.

The prognosis of the disease depends on many reasons and varies greatly depending on the type of disease, its course and the adequacy of the therapy.

Treatment of autoimmune diseases is aimed at suppressing the aggressiveness of the immune system, which no longer distinguishes between “our own and someone else’s.” Medicines aimed at reducing the activity of immune inflammation are called immunosuppressants. The main immunosuppressants are Prednisolone (or its analogues), cytostatics (Cyclophosphamide, Methotrexate, Azathioprine, etc.) and monoclonal antibodies, which act most specifically on individual parts of inflammation.

Many patients often ask questions: how can one suppress their own immune system? How can I live with “bad” immunity? It is not possible to suppress the immune system in autoimmune diseases, but it is necessary. The doctor always weighs what is more dangerous: the disease or the treatment, and only then makes a decision. So, for example, with autoimmune thyroiditis there is no need to suppress the immune system, but with systemic vasculitis (for example, microscopic polyangitis) it is simply vital.

People live with suppressed immunity for many years. At the same time, the frequency of infectious diseases increases, but this is a kind of “payment” for treating the disease.

Patients are often interested in whether they can take immunomodulators. There are different types of immunomodulators, most of them are contraindicated for people suffering from autoimmune diseases, however, some drugs may be useful in certain situations, for example, intravenous immunoglobulins.

Systemic autoimmune diseases

Autoimmune diseases often present diagnostic difficulties, require special attention from doctors and patients, are very different in their manifestations and prognosis, and, nevertheless, most of them are successfully treated.

This group includes diseases of autoimmune origin that affect two or more organ systems and tissues, for example, muscles and joints, skin, kidneys, lungs, etc. Some forms of the disease become systemic only as the disease progresses, for example, rheumatoid arthritis, while others immediately affect many organs and tissues. As a rule, systemic autoimmune diseases are treated by rheumatologists, but such patients can often be found in the departments of nephrology and pulmonology.

Major systemic autoimmune diseases:

• Systemic lupus erythematosus;
• systemic sclerosis (scleroderma);
• polymyositis and dermapolymyositis;
• antiphospholipid syndrome;
• rheumatoid arthritis (does not always have systemic manifestations);
• Sjögren's syndrome;
• Behçet's disease;
• systemic vasculitis (this is a group of different individual diseases, united on the basis of a symptom such as vascular inflammation).

Autoimmune diseases primarily affecting the joints

These diseases are treated by rheumatologists. Sometimes these diseases can affect several different organs and tissues at once:

• Rheumatoid arthritis;
• spondyloarthropathy (a group of different diseases united on the basis of a number of common symptoms).

Autoimmune diseases of the endocrine system

This group of diseases includes autoimmune thyroiditis (Hashimoto's thyroiditis), Graves' disease (diffuse toxic goiter), type 1 diabetes mellitus, etc.

Unlike many autoimmune diseases, this particular group of diseases does not require immunosuppressive therapy. Most patients are observed by endocrinologists or family doctors (therapists).

Autoimmune blood diseases

Hematologists specialize in this group of diseases. The most well-known diseases are:

• Autoimmune hemolytic anemia;
• thrombocytopenic purpura;
• autoimmune neutropenia.

Autoimmune diseases of the nervous system

A very broad group. Treatment of these diseases is the prerogative of neurologists. The most well-known autoimmune diseases of the nervous system are:

• Multiple (multiple) sclerosis;
• Guillain-Bart syndrome;
• Myasthenia Gravis.

Autoimmune diseases of the liver and gastrointestinal tract

These diseases are treated, as a rule, by gastroenterologists, less often by general practitioners.

• Autoimmune hepatitis;
• primary biliary cirrhosis;
• primary sclerosing cholangitis;
• Crohn's disease;
• ulcerative colitis;
• celiac disease;
• Autoimmune pancreatitis.

Treatment autoimmune diseases skin is the prerogative of dermatologists. The most well-known diseases are:

• Pemphingoid;
• psoriasis;
• discoid lupus erythematosus;
• isolated cutaneous vasculitis;
• chronic urticaria (urticarial vasculitis);
• some forms of alopecia;
• vitiligo.

Autoimmune kidney diseases

This group of diverse and often serious diseases is studied and treated by both nephrologists and rheumatologists.

• Primary glomerulonephritis and glomerulopathies (a large group of diseases);
• Goodpasture's syndrome;
• systemic vasculitis with kidney damage, as well as other systemic autoimmune diseases with kidney damage.

Autoimmune heart diseases

These diseases are within the scope of activity of both cardiologists and rheumatologists. Some diseases are treated primarily by cardiologists, for example, myocarditis; other diseases - almost always rheumatology (vasculitis with heart damage).

• Rheumatic fever;
• systemic vasculitis with heart damage;
• myocarditis (some forms).

Autoimmune lung diseases

This group of diseases is very extensive. Diseases that affect only the lungs and upper respiratory tract are treated in most cases by pulmonologists; diseases of a systemic nature that affect the lungs are treated by rheumatologists.

• Idiopathic interstitial lung diseases (fibrosing alveolitis);
• pulmonary sarcoidosis;
• systemic vasculitis with lung damage and other systemic autoimmune diseases with lung damage (derma- and polymyositis, scleroderma).

Autoimmune diseases are diseases that develop when the body's immune system becomes overly sensitive for any reason. Normally, the work of the immune system is to protect and protect the human body from various kinds of antigens and external factors that harm it. However, under certain conditions, this system begins to function incorrectly and becomes hypersensitive. It begins to overreact to external conditions that are otherwise normal, and over time causes the development of various diseases.

One of the symptoms of an autoimmune disease is sudden hair loss

Autoimmune diseases- These are diseases that the human body develops on its own. They can be either genetic or acquired, and are not only a problem for adults - their symptoms are also found in children. People with such diseases need to be very careful about their lifestyle. The following list includes many autoimmune diseases, but there are others that are still being researched to understand their causes and therefore remain on the list of suspected autoimmune diseases.

The symptoms of autoimmune diseases are numerous. They include a wide variety of manifestations (ranging from headaches to skin rashes) that affect almost all body systems. There are many of them, since the number of autoimmune diseases themselves is large. Below is a list of these symptoms, covering almost all autoimmune diseases along with their common signs.

After reviewing this list, it becomes clear that even a simple health problem can be a sign of an autoimmune disease. A number of autoimmune diseases have already been studied, and the symptoms associated with them have been described. However, there are many other diseases that are still waiting to be included in the above list. Thus, the list of autoimmune diseases continues to grow daily, and the number of their symptoms increases exponentially. As can be seen from the table, one symptom can be common to various diseases, so diagnosis based only on symptoms is difficult. In this regard, instead of assuming that you have any of the listed diseases, it is recommended to consult a doctor and begin treatment aimed at eliminating/controlling the existing symptoms.

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Autoimmune diseases often affect vital organs such as the heart, lungs and others

General characteristics of autoimmune diseases affecting the joints

Most autoimmune diseases affecting the joints are diffuse connective tissue diseases (systemic rheumatic diseases). This is a large group of diseases, each of which has a complex classification, complex diagnostic algorithms and rules for formulating a diagnosis, as well as multicomponent treatment regimens.

Since the connective tissue that is affected in these diseases is present in many organs, these diseases are characterized by a variety of clinical manifestations. Often vital organs (heart, lungs, kidneys, liver) are involved in the pathological process - this determines the life prognosis for the patient.

In systemic rheumatic diseases, the joints are affected along with other organs and systems. Depending on the nosology, this may determine the clinical picture of the disease and its prognosis (for example, with rheumatoid arthritis) or perhaps less significant against the background of damage to other organs, as with systemic scleroderma.

In other autoimmune diseases and diseases that are not fully understood, joint damage is an additional symptom and is not observed in all patients. For example, arthritis in autoimmune inflammatory bowel diseases.

In other cases, joint lesions may be involved in the process only in severe cases of the disease (for example, with psoriasis). The degree of joint damage can be pronounced and determine the severity of the disease, the prognosis of the patient’s ability to work and his quality of life. Or, conversely, the degree of damage may cause only completely reversible inflammatory changes. In this case, the prognosis of the disease may be associated with damage to other organs and systems (for example, with acute rheumatic fever).

The cause of most diseases in this group is not fully understood. Many of them are characterized by a hereditary predisposition, which can be determined by certain genes encoding antigens of the so-called major histocompatibility complex (referred to as HLA or MHC antigens). These genes are contained on the surface of all nucleated cells of the body (HLA C class I antigens) or on the surface of the so-called antigen-presenting cells:

An acute infection can provoke the onset of many autoimmune diseases

• B-lymphocytes,
• tissue macrophages,
• dendritic cells (HLA class II antigens).

The name of these genes is associated with the phenomenon of organ transplant rejection, but in the physiology of the immune system they are responsible for the presentation of antigen to T lymphocytes and for the initiation of the development of an immune response to the pathogen. Their connection with a predisposition to the development of systemic autoimmune diseases is currently not fully understood.

As one of the mechanisms, the phenomenon of so-called “antigenic mimicry” has been proposed, in which the antigens of common pathogens of infectious diseases (viruses that cause acute respiratory viral infections, Escherichia coli, streptococcus, etc.) have a similar structure to the proteins of a person who is a carrier of certain genes of the major histocompatibility complex and causes .

The infection suffered by such a patient leads to an ongoing immune response to antigens of the body’s own tissues and the development of an autoimmune disease. Therefore, for many autoimmune diseases, the factor that provokes the onset of the disease is an acute infection.

As the name of this group of diseases suggests, the leading mechanism of their development is the aggression of the immune system towards its own connective tissue antigens.

Of the main types of pathological reactions of the immune system (see) in systemic autoimmune connective tissue diseases, type III is most often realized (immune complex type - in rheumatoid arthritis and systemic lupus erythematosus). Less commonly occurs type II (cytotoxic type - in acute rheumatic fever) or IV (delayed hypersensitivity - in rheumatoid arthritis).

Often different mechanisms of immunopathological reactions play a role in the pathogenesis of one disease. The main pathological process in these diseases is inflammation, which leads to the appearance of the main clinical signs of the disease - local and general symptoms (fever, malaise, weight loss, etc.), its result often being irreversible changes in the affected organs. The clinical picture of the disease has its own characteristics for each nosology, some of which will be described below.

Since the incidence of systemic autoimmune diseases is low and many of them do not have specific symptoms that are not observed in other diseases, only a doctor can suspect the presence of a disease from this group in a patient based on a combination of characteristic clinical signs, the so-called diagnostic criteria for the disease, approved in international guidelines for its diagnosis and treatment.

Reasons for examination to exclude systemic rheumatic diseases

• the patient develops joint symptoms at a relatively young age,
• lack of connection between symptoms and increased load on the affected joints,
• suffered joint injuries,
• signs of metabolic disorders (obesity and metabolic syndrome, which may be accompanied by gout),
• burdened hereditary history.

The diagnosis of systemic connective tissue disease is established by a rheumatologist.

It is confirmed by specific tests for a specific nosology or laboratory tests identifying markers that may be common to the entire group of systemic rheumatic diseases. For example, C-reactive protein, rheumatoid factor.

Laboratory diagnostics is based on the identification of specific antibodies to one’s own organs and tissues, immune complexes formed during the development of the disease, antigens of the major histocompatibility complex, characteristic of certain diseases of this group and identified using monoclonal antibodies, genes encoding these antigens, identified by determining specific DNA sequences.

Instrumental diagnostic methods make it possible to determine the degree of damage to the affected organs and their functionality. To assess changes in the joints, radiography and magnetic resonance imaging of the joint are used. In addition, joint puncture is used to take samples for synovial fluid analysis and arthroscopy.

All of the above examinations are necessary to identify the disease and clarify the degree of its severity.

To avoid disability and death, constant medical supervision and therapy that meets the standards is necessary

Certain key changes in the necessary laboratory and instrumental examinations are included in the diagnosis. For example, for rheumatoid arthritis - the presence or absence of rheumatoid factor in the blood, the stage of radiological changes. This is important in determining the scope of therapy.

Making a diagnosis for a rheumatologist when identifying signs of autoimmune damage to organs and systems is often difficult: the symptoms identified in a patient and examination data can combine signs of several diseases of this group.

Treatment of systemic connective tissue diseases includes the prescription of immunosuppressive and cytostatic drugs, drugs that slow down the pathological formation of connective tissue, and other special chemotherapy agents.

Non-steroidal anti-inflammatory drugs are used as symptomatic therapy, and even glucocorticosteroids for these diseases cannot always be used as a means of basic treatment. Medical observation and prescription of therapy in accordance with standards is a prerequisite for preventing the development of serious complications, including disability and death.

A new direction of treatment is the use of biological therapy drugs - monoclonal antibodies to key molecules involved in immunological and inflammatory reactions in these diseases. This group of drugs is highly effective and has no side effects of chemotherapy. In complex treatment for joint damage, surgical interventions are used, physical therapy and physiotherapy are prescribed.

Rheumatoid arthritis

Rheumatoid arthritis is the most common human systemic autoimmune disease.

The disease is based on the production of autoantibodies to immunoglobulin G with the development of an inflammatory process in the lining of the joint and gradual destruction of the joints.

Clinical picture

• gradual onset
• presence of constant pain in the joints,
• morning stiffness in the joints: stiffness and stiffness in the muscles surrounding the joint after waking up or a long rest with the gradual development of arthritis of the small peripheral joints of the hands and feet.

Less commonly, large joints are involved in the process - knees, elbows, ankles. It is necessary to involve five or more joints in the process; symmetry of joint damage is characteristic.

A typical sign of the disease is deviation of the first and fourth fingers to the ulnar (inner) side (the so-called ulnar deviation) and other deformities associated with the involvement of not only the joint itself, but also the adjacent tendons, as well as the presence of subcutaneous “rheumatoid nodules.”

Damage to joints in rheumatoid arthritis is irreversible and limits their function.

Extra-articular lesions in rheumatoid arthritis include the above-mentioned “rheumatoid nodules”, muscle damage in the form of atrophy and muscle weakness, rheumatoid pleurisy (damage to the pleura of the lung) and rheumatoid pneumonitis (damage to the alveoli of the lung with the development of pulmonary fibrosis and respiratory failure).

A specific laboratory marker of rheumatoid arthritis is rheumatoid factor (RF) - IgM class antibodies to one's own immunoglobulin G. Depending on their presence, RF-positive and RF-negative rheumatoid arthritis are distinguished. In the latter case, the development of the disease is associated with antibodies to IgG of other classes, the laboratory determination of which is unreliable, and the diagnosis is established on the basis of other criteria.

It should be noted that rheumatoid factor is not specific for rheumatoid arthritis. It can occur in other autoimmune connective tissue diseases and should be assessed by a doctor in conjunction with the clinical picture of the disease.

Specific laboratory markers of rheumatoid arthritis

• antibodies to cyclic citrulline-containing peptide (anti-CCP)
• antibodies to citrullinated vimentin (anti-MCV), which are specific markers of this disease,
• antinuclear antibodies, which can occur in other systemic rheumatoid diseases.

Treatment of rheumatoid arthritis

Treatment of the disease includes the use of both to relieve pain and relieve inflammation in the initial stages and the use of basic drugs aimed at suppressing the immunological mechanisms of disease development and joint destruction. The slow onset of a lasting effect of these drugs necessitates their use in combination with anti-inflammatory drugs.

Modern approaches to drug therapy are the use of monoclonal antibodies to tumor necrosis factor and other molecules that play a key role in the pathogenesis of the disease - biological therapy. These drugs are free of the side effects of cytostatics, but due to their high cost and the presence of their own side effects (the appearance of antinuclear antibodies in the blood, the risk of lupus-like syndrome, exacerbation of chronic infections, including tuberculosis), they limit their use. They are recommended for use in the absence of sufficient effect from cytostatics.

Acute rheumatic fever

Acute rheumatic fever ( a disease that in the past was called “rheumatism”) is a post-infectious complication of tonsillitis (tonsillitis) or pharyngitis caused by group A hemolytic streptococcus.

This disease manifests itself as a systemic inflammatory disease of connective tissue with primary damage to the following organs:

• cardiovascular system (carditis),
• joints (migratory polyarthritis),
• brain (chorea is a syndrome characterized by erratic, jerky, irregular movements, similar to normal facial movements and gestures, but more elaborate, often reminiscent of dance),
• skin (ring-shaped erythema, rheumatic nodules).

Acute rheumatic fever develops in predisposed individuals - more often in children and young people (7-15 years). Fever is associated with the body's autoimmune response due to cross-reactivity between streptococcal antigens and the affected human tissues (the phenomenon of molecular mimicry).

A characteristic complication of the disease that determines its severity is chronic rheumatic heart disease - marginal fibrosis of the heart valves or heart defects.

Arthritis (or arthralgia) of several large joints is one of the leading symptoms of the disease in 60-100% of patients with the first attack of acute rheumatic fever. The knee, ankle, wrist and elbow joints are most often affected. In addition, there is pain in the joints, which are often so severe that they lead to a significant limitation of their mobility, swelling of the joints, and sometimes redness of the skin over the joints.

The characteristic features of rheumatoid arthritis are its migratory nature (signs of damage to some joints almost completely disappear within 1-5 days and are replaced by equally pronounced damage to other joints) and rapid complete reverse development under the influence of modern anti-inflammatory therapy.

Laboratory confirmation of the diagnosis is the detection of antistreptolysin O and antibodies to DNAase, identification of hemolytic streptococcus A during bacteriological examination of a throat smear.

Antibiotics of the penicillin group, glucocorticosteroids and NSAIDs are used for treatment.

Ankylosing spondylitis (Bechterew's disease)

Ankylosing spondylitis (Bechterew's disease)- a chronic inflammatory disease of the joints, predominantly affecting the joints of the axial skeleton (intervertebral joints, sacroiliac joint) in adults, and causing chronic back pain and limited mobility (rigidity) of the spine. The disease can also affect peripheral joints and tendons, eyes and intestines.

Difficulties in differential diagnosis of pain in the spine in ankylosing spondylitis with osteochondrosis, in which these symptoms are caused by purely mechanical reasons, can lead to a delay in diagnosis and prescription of the necessary treatment up to 8 years from the moment the first symptoms appear. The latter, in turn, worsens the prognosis of the disease and increases the likelihood of disability.

Signs of difference from osteochondrosis:

• features of the daily rhythm of pain - they are stronger in the second half of the night and in the morning, and not in the evening, as with osteochondrosis,
• young age of onset of the disease,
• presence of signs of general malaise,
• involvement of other joints, eyes and intestines in the process,
• the presence of an increased erythrocyte sedimentation rate (ESR) in repeated general blood tests,
• the patient has a burdened hereditary history.

There are no specific laboratory markers of the disease: predisposition to its development can be established by identifying the major histocompatibility complex antigen HLA - B27.

For treatment, NSAIDs, glucocorticosteroids and cytostatic drugs, and biological therapy are used. To slow down the progression of the disease, therapeutic exercises and physiotherapy play an important role as part of complex treatment.

Joint damage in systemic lupus erythematosus

The causes of systemic lupus erythematosus are still not understood

In a number of autoimmune diseases, joint damage may occur, but is not a characteristic sign of the disease that determines its prognosis. An example of such diseases is systemic lupus erythematosus - a chronic systemic autoimmune disease of unknown etiology, in which an immunoinflammatory process develops in various organs and tissues (serous membranes: peritoneum, pleura, pericardium; kidneys, lungs, heart, skin, nervous system, etc.), leading as the disease progresses to the formation of multiple organ failure.

The causes of systemic lupus erythematosus remain unknown: the influence of hereditary factors and viral infection is assumed to be the trigger for the development of the disease; the unfavorable influence of certain hormones (primarily estrogens) on the course of the disease has been established, which explains the high prevalence of the disease among women.

Clinical signs of the disease are: erythematous rashes on the skin of the face in the form of a “butterfly” and discoid rash, the presence of ulcers in the oral cavity, inflammation of the serous membranes, kidney damage with the appearance of protein and leukocytes in the urine, changes in the general blood test - anemia, decreased number leukocytes and lymphocytes, platelets.

Joint involvement is the most common manifestation of systemic lupus erythematosus. Joint pain may precede the onset of multisystem involvement and immunological manifestations of the disease by many months and years.

Arthralgia occurs in almost 100% of patients at various stages of the disease. The pain may occur in one or more joints and may be short-lived.

With high activity of the disease, the pain may be more persistent, and a picture of arthritis later develops with pain during movement, pain in the joints, swelling, inflammation of the membranes of the joint, redness, increased skin temperature over the joint and disruption of its function.

Arthritis can be migratory in nature without residual effects, as in acute rheumatic fever, but more often they occur in the small joints of the hands. Arthritis is usually symmetrical. Articular syndrome in systemic lupus erythematosus may be accompanied by inflammation of the skeletal muscles.

Serious complications of the disease from the musculoskeletal system are aseptic necrosis of bones - the head of the femur, humerus, and less commonly the bones of the wrist, knee joint, elbow joint, and foot.

Markers identified during laboratory diagnosis of the disease are antibodies to DNA, anti-Sm antibodies, detection of antinuclear antibodies not associated with taking medications that can cause their formation, identification of so-called LE - cells - neutrophil leukocytes containing phagocytosed fragments of the nuclei of other cells.

For treatment, glucocorticosteroids, cytostatic drugs, as well as group 4 chemotherapy drugs - aminoquinoline derivatives, which are also used in the treatment of malaria, are used. Hemosorption and plasmapheresis are also used.

Joint damage due to systemic sclerosis

The severity of the disease and life expectancy in systemic scleroderma depend on the deposition of connective tissue macromolecules in vital organs

Systemic scleroderma- an autoimmune disease of unknown origin, characterized by progressive deposition of collagen and other connective tissue macromolecules in the skin and other organs and systems, damage to the capillary bed and multiple immunological disorders. The most pronounced clinical signs of the disease are skin lesions - thinning and coarsening of the skin of the fingers with the appearance of paroxysmal spasms of the blood vessels of the fingers, the so-called Raynaud's syndrome, areas of thinning and coarsening, dense swelling and atrophy of the facial skin, and the appearance of foci of hyperpigmentation on the face. In severe cases of the disease, similar skin changes are diffuse.

The deposition of connective tissue macromolecules in vital organs (lungs, heart and great vessels, esophagus, intestines, etc.) in systemic scleroderma determines the severity of the disease and the patient’s life expectancy.

Clinical manifestations of joint damage in this disease are pain in the joints, limited mobility, the appearance of the so-called “tendon friction noise”, detected during a medical examination and associated with the involvement of tendons and fascia in the process, pain in the muscles surrounding the joint and muscle weakness.

Complications are possible in the form of necrosis of the distal and middle phalanges of the fingers due to disruption of their blood supply.

Markers for laboratory diagnosis of the disease are anticentromere antibodies, antibodies to topoisomerase I (Scl-70), antinuclear antibodies, antiRNA antibodies, antibodies to ribonucleoproteins.

In the treatment of the disease, in addition to immunosuppressive glucocorticosteroid and cytostatic drugs, a key role is also played by drugs that slow down fibrosis.

Psoriatic arthritis

Psoriatic arthritis is a joint damage syndrome that develops in a small number (less than 5%) of patients suffering from psoriasis (for a description of the disease, see the corresponding one).

In most patients with psoriatic arthritis, clinical signs of psoriasis precede the development of the disease. However, in 15-20% of patients, signs of arthritis develop before the appearance of typical skin manifestations.

The joints of the fingers are predominantly affected, with the development of joint pain and swelling of the fingers. Characteristic deformities of the nail plates on fingers affected by arthritis. Other joints may also be involved: intervertebral and sacroiliac.

If arthritis appears before the development of skin manifestations of psoriasis or if there are foci of skin lesions only in places inaccessible for examination (perineum, scalp, etc.), the doctor may have difficulties in differential diagnosis with other autoimmune diseases of the joints.

Cytostatic drugs are used for treatment; the modern direction of therapy is drugs of antibodies to tumor necrosis factor alpha.

Arthritis in ulcerative colitis and Crohn's disease

Joint lesions can also be observed in some patients with chronic inflammatory bowel diseases: Crohn's disease and ulcerative colitis, in which joint lesions can also precede the intestinal symptoms characteristic of these diseases.

Crohn's disease is an inflammatory disease involving all layers of the intestinal wall. It is characterized by diarrhea mixed with mucus and blood, abdominal pain (often in the right iliac region), weight loss, and fever.

Nonspecific ulcerative colitis is an ulcerative-destructive lesion of the mucous membrane of the colon, which is localized mainly in its distal parts.

Clinical picture

• bleeding from the rectum,
• frequent bowel movements,
• tenesmus - false painful urge to defecate;
• abdominal pain is less intense than with Crohn's disease and is most often localized in the left iliac region.

Joint lesions in these diseases occur in 20-40% of cases and occur in the form of arthritis (peripheral arthropathy), sacroiliitis (inflammation in the sacroiliac joint) and/or ankylosing spondylitis (as in ankylosing spondylitis).

Characterized by asymmetric, migrating damage to the joints, most often the lower extremities: knee and ankle joints, less often the elbow, hip, interphalangeal and metatarsophalangeal joints. The number of affected joints usually does not exceed five.

Articular syndrome occurs with alternating periods of exacerbations, the duration of which does not exceed 3-4 months, and remissions. However, patients often complain only of pain in the joints and, upon objective examination, no changes are detected. Over time, exacerbations of arthritis become less frequent. In most patients, arthritis does not lead to joint deformation or destruction.

The severity of symptoms and the frequency of relapses decrease as the underlying disease is treated.

Reactive arthritis

Reactive arthritis, described in the corresponding section of the article, can develop in individuals with a hereditary tendency to autoimmune pathology.

This pathology is possible after an infection (not only Yersinia, but also other intestinal infections). For example, Shigella - the causative agent of dysentery, salmonella, campollobacter.

Also, reactive arthritis can appear due to pathogens of urogenital infections, primarily Chlamydia trachomatis.

Clinical picture

1. acute onset with signs of general malaise and fever,
2. non-infectious urethritis, conjunctivitis and arthritis affecting the toes, ankles or sacroiliac joints.

As a rule, one joint on one limb is affected (asymmetric monoarthritis).

The diagnosis of the disease is confirmed by the detection of antibodies to suspected infectious pathogens and the detection of the HLA-B27 antigen.

Treatment includes antibacterial therapy and drugs aimed at treating arthritis: NSAIDs, glucocorticosteroids, cytostatics.

The effectiveness and safety of biological therapy drugs are currently being studied.

Symptoms of allergic diseases in autoimmune joint diseases

A number of autoimmune diseases that affect the joints may have symptoms characteristic of. They can often precede a detailed clinical picture of the disease. For example, recurrent may be the first manifestation of a disease such as urticarial vasculitis, in which there may also be damage to joints of various locations in the form of transient joint pain or severe arthritis.

Often, urticarial vasculitis can be associated with systemic lupus erythematosus, for which joint damage is characteristic.

Also, with systemic lupus erythematosus, the development in some patients of severe acquired angioedema associated with a C1 esterase inhibitor against the background of the disease has been described.

Thus, autoimmune diseases of the joints by their nature are more severe diseases compared to the pathology that develops against the background of their mechanical overload (osteoarthrosis, osteochondrosis). These diseases are a manifestation of systemic diseases that affect internal organs and have a poor prognosis. They require systematic medical supervision and adherence to drug treatment regimens.

Literature

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2. P.V. Kolhir Urticaria and angioedema. "Practical Medicine" Moscow 2012 UDC 616-514+616-009.863 BBK 55.8 K61 pp. 11-115, 215, 286-294
3. R.M. Khaitov, G.A. Ignatieva, I.G. Sidorovich "Immunology" Moscow "Medicine" 2002 UDC 616-092:612.017 (075.8) BBK 52.5 X19 pp. 162-176, 372-378
4. A. V. Meleshkina, S. N. Chebysheva, E. S. Zholobova, M. N. Nikolaeva “Articular syndrome in chronic inflammatory bowel diseases: the view of a rheumatologist” Medical scientific and practical journal #01/14
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6. Anwar Al Hammadi, MD, FRCPC; Chief Editor: Herbert S Diamond, MD "Psoriatic Arthritis" Medscape Diseases/Conditions Updated: Jan 21, 2016
7. Howard R Smith, MD; Chief Editor: Herbert S Diamond, MD "Rheumatoid Arthritis" Medscape Diseases/Conditions Updated: Jul 19, 2016
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Autoimmune polyendocrine syndrome (or simply: autoimmune syndrome) is (even judging by the name) an autoimmune disease, as a result of which endocrine organs are susceptible to damage (and several at once).
Autoimmune syndrome is classified into 3 types:
-1st type: MEDAS syndrome. It is characterized by moniliasis of the skin and mucous membranes, adrenal insufficiency and hypoparathyroidism. Sometimes this type of syndrome leads to diabetes mellitus.
-2nd type: Schmidt syndrome. This type of autoimmune syndrome most often affects women (up to 75% of all cases). This is primarily lymphocytic thyroiditis, the same insufficiency of the adrenal glands, as well as gonads, hypoparathyroidism, and possible type 1 diabetes (rare).
-3rd type. This is the most common type of autoimmune syndrome and it is a combination of pathology of the thyroid gland (diffuse goiter, autoimmune thyroiditis) and pancreas (type 1 diabetes mellitus).

Autoimmune thrombocytopenia is common. This is nothing more than a blood disease and is characterized by the formation of autoimmune antibodies to its own platelets. In this case, the autoimmune system fails for various reasons: due to a lack of vitamins, excessive use of medications, various types of infections, and exposure to various toxins.

Autoimmune thrombocytopenia by its nature is divided into:
-idiopathic thrombocytopenic purpurra (actually autoimmune thrombocytopenia);
- thrombocytopenia in other autoimmune disorders.
The main and most dangerous syndrome of this disease is bleeding (tendency to it) and subsequent anemia. The greatest danger is caused by bleeding into the central nervous system.

To understand how the autoimmune system “works” it is necessary to understand what autoimmune antibodies are. After all, diseases of this type appear only after autoimmune antibodies or, simply put, clones of T cells that are able to come into contact with their own antigens begin to appear in the body. This is where autoimmune damage begins. And this is what leads to damage to one’s own tissues. So, autoimmune antibodies are elements that appear as an autoimmune reaction to the tissues of one’s own body. So everything is simple and clear. This is exactly how the autoimmune system works. Well, strictly speaking, it is clear that an autoimmune lesion is a disease caused by autoimmune antibodies that are directed against the tissues of their native body.

To identify all such diseases, so-called autoimmune tests are done. This is the same as immune tests, only the main difference is that autoimmune tests are carried out to identify autoimmune antibodies and, on the basis of this, a mechanism for treating this type of disease is developed. This is also easy to understand. Autoimmune tests are also based on a “scan” of the patient’s blood.

The treatment mechanisms are very complex and ambiguous, because there is no drug, except one, that would not give dangerous side effects. And this only drug is Transfer Factor. This is a unique drug. And its uniqueness is not only that it does not give any side effects. Its uniqueness also lies in its mechanism of action on our protective functions. But you can find out more about this on other pages of our website. This is a different story.

Autoimmune diseases are pathologies that occur when the body's defenses malfunction. Women are more likely to experience such diseases than men.

What is it and the reasons for its development

Autoimmune pathologies occur due to disorders in the body, which can be triggered by a number of factors. Most often, it is based on a hereditary predisposition. Immune cells, instead of foreign agents, begin to attack the tissues of various organs. Often this pathological process occurs in the thyroid gland and joints.

The necessary substances do not have time to replenish the losses received from the destructive effects of one’s own immune system. Such disorders in the body can be provoked by:

• harmful working conditions;
• viral and bacterial infections;
• genetic mutations during fetal development.

Main symptoms

Autoimmune processes in the body manifest themselves in the form of:

• hair loss;
• inflammatory process in joints, gastrointestinal tract and thyroid gland;
• arterial thrombosis;
• numerous miscarriages;
• joint pain;
• weaknesses;
• skin itching;
• enlargement of the affected organ;
• menstrual irregularities;
• abdominal pain;
• digestive disorders;
• deterioration of general condition;
• weight changes;
• urinary disorders;
• trophic ulcers;
• increased appetite;
• mood changes;
• mental disorders;
• convulsions and trembling of limbs.

Autoimmune disorders provoke pallor, allergic reactions to cold, as well as cardiovascular pathologies.

List of diseases

The most common autoimmune diseases, the causes of which are similar:

1. Alopecia areata - baldness occurs as the immune system attacks the hair follicles.
2. Autoimmune hepatitis - inflammation of the liver occurs, as its cells come under the aggressive influence of T-lymphocytes. The skin color changes to yellow, and the causative organ increases in size.
3. Celiac disease is gluten intolerance. At the same time, the body responds to the consumption of cereals with a violent reaction in the form of nausea, vomiting, diarrhea, flatulence and stomach pain.
4. Type 1 diabetes - the immune system attacks the cells that produce insulin. With the development of this disease, a person is constantly accompanied by thirst, increased fatigue, blurred vision, etc.
5. Graves' disease is accompanied by increased production of thyroid hormones by the thyroid gland. In this case, symptoms such as emotional instability, hand tremors, insomnia, and disruptions in the menstrual cycle occur. An increase in body temperature and a decrease in body weight may occur.
6. Hashimoto's disease develops as a result of decreased production of thyroid hormones. In this case, the person is accompanied by constant fatigue, constipation, sensitivity to low temperatures, etc.
7. Julian-Barre syndrome - manifests itself in the form of damage to the nerve bundle connecting the spinal cord and brain. As the disease progresses, paralysis may develop.
8. Hemolytic anemia - the immune system destroys red blood cells, causing tissues to suffer from hypoxia.
9. Idiopathic purpura - platelets are destroyed, resulting in impaired blood clotting ability. There is an increased risk of bleeding, prolonged and heavy menstruation and bruises.
10. Inflammatory bowel disease is Crohn's disease or ulcerative colitis. Immune cells attack the mucous membrane, causing an ulcer, which occurs with bleeding, pain, weight loss and other disorders.
11. Inflammatory myopathy - damage to the muscular system occurs. The person experiences weakness and feels unsatisfactory.
12. Multiple sclerosis - your own immune cells attack the nerve sheath. In this case, coordination of movements is impaired, and problems with speech may arise.
13. Biliary cirrhosis - the liver and bile ducts are destroyed. A yellow tint to the skin, itching, nausea and other digestive disorders appear.
14. Myasthenia gravis - the affected area includes nerves and muscles. A person constantly feels weak, any movement is difficult.
15. Psoriasis - destruction of skin cells occurs, as a result, the layers of the epidermis are distributed incorrectly.
16. Rheumatoid arthritis is a systemic autoimmune disease. The body's defenses attack the lining of the joints. The disease is accompanied by discomfort during movement and inflammatory processes.
17. Scleroderma is a pathological growth of connective tissue.
18. Vitiligo - cells that produce melanin are destroyed. In this case, the skin is colored unevenly.
19. Systemic lupus erythematosus - the affected area includes the joints, heart, lungs, skin and kidneys. The disease is extremely difficult.
20. Sjögren's syndrome - the salivary and lacrimal glands are affected by the immune system.
21. Antiphospholipid syndrome - the lining of blood vessels, veins and arteries is damaged.