Autoimmune diseases affecting the joints. What are autoimmune diseases in simple words and a list of diseases Autoimmune disease related

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.

Name of the disease	Symptoms	Organs affected/ glands
Acute disseminated encephalomyelitis (ADEM)	Fever, drowsiness, headache, seizures and coma	Brain and spinal cord
Addison's disease	Fatigue, dizziness, vomiting, muscle weakness, anxiety, weight loss, increased sweating, mood swings, personality changes	Adrenal glands
Alopecia areata	Bald spots, tingling sensation, pain and hair loss	Body hair
Ankylosing spondylitis	Peripheral joint pain, fatigue and nausea	Joints
Antiphospholipid syndrome (APS)	Deep vein thrombosis (blood clots), stroke, miscarriage, pre-eclimpsia and stillbirth	Phospholipids (cell membrane substances)
Autoimmune hemolytic anemia	Fatigue, anemia, dizziness, shortness of breath, pale skin, and chest pain	Red blood cells
Autoimmune hepatitis	Enlarged liver, jaundice, skin rashes, vomiting, nausea and loss of appetite	Liver cells
Autoimmune inner ear disease	Progressive hearing loss	Cells of the inner ear
Bullous pemphigoid	Skin lesions, itching, rashes, mouth ulcers and bleeding gums	Leather
Celiac disease	Diarrhea, fatigue and lack of weight gain	Small intestine
Chagas disease	Romagna symptom, fever, fatigue, body pain, headache, rash, loss of appetite, diarrhea, vomiting, damage to the nervous system, digestive system and heart	Nervous system, digestive system and heart
Chronic obstructive pulmonary disease (COPD)	Shortness of breath, fatigue, persistent cough, chest tightness	Lungs
Crohn's disease	Abdominal pain, diarrhea, vomiting, weight loss, skin rashes, arthritis and eye inflammation	Gastrointestinal tract
Churg-Strauss syndrome	Asthma, severe neuralgia, purple patches on the skin	Blood vessels (lungs, heart, gastrointestinal system)
Dermatomyositis	Skin rashes and muscle pain	Connective tissues
Diabetes mellitus type 1	Frequent urination, nausea, vomiting, dehydration and weight loss	Pancreatic beta cells
Endometriosis	Infertility and pelvic pain	Female reproductive organs
Eczema	Redness, fluid accumulation, itching (also crusting and bleeding)	Leather
Goodpasture's syndrome	Fatigue, nausea, difficulty breathing, paleness, coughing up blood, and a burning sensation when urinating	Lungs
Graves' disease	Bloated eyes, dropsy, hyperthyroidism, rapid heart rate, difficulty falling asleep, hand tremors, irritability, fatigue and muscle weakness	Thyroid
Guillain-Barre syndrome	Progressive body weakness and respiratory failure	Peripheral nervous system
Hashimoto's thyroiditis	Hypothyroidism, muscle weakness, fatigue, depression, mania, cold sensitivity, constipation, memory loss, migraines and infertility	Thyroid cells
Hidradenitis suppurativa	Large and painful ulcers (boils)	Leather
Kawasaki disease	Fever, conjunctivitis, chapped lips, gunter's tongue, joint pain and irritability	Veins (skin, blood vessel walls, lymph nodes and heart)
Primary IgA nephropathy	Hematuria, skin rashes, arthritis, abdominal pain, nephrotic syndrome, acute and chronic renal failure	Kidneys
Idiopathic thrombocytopenic purpura	Low platelet count, bruising, nosebleeds, bleeding gums, and internal bleeding	Platelets
Interstitial cystitis	Pain during urination, abdominal pain, frequent urination, pain during intercourse and difficulty sitting	Bladder
Erythematous lupus	Joint pain, skin rashes, kidney, heart and lung damage	Connective tissue
Mixed connective tissue disease/Sharpe's syndrome	Joint pain and swelling, general malaise, Raynaud's phenomenon, muscle inflammation and sclerodactyly	Muscles
Ring-shaped scleroderma	Focal skin lesions, roughening of the skin	Leather
Multiple sclerosis (MS)	Muscle weakness, ataxia, speech difficulties, fatigue, pain, depression and unstable mood	Nervous system
Myasthenia gravis	Muscle weakness (in the face, eyelids, and swelling)	Muscles
Narcolepsy	Daytime somnolence, cataplexy, mechanical behavior, sleep paralysis, and hypnagogic hallucinations	Brain
Neuromyotonia	Muscle stiffness, muscle tremors and muscle cramps, spasms, increased sweating and delayed muscle relaxation	Neuromuscular activity
Opso-myoclonal syndrome (OMS)	Uncontrollable rapid eye movements and muscle cramps, speech disturbances, sleep disturbances and drooling	Nervous system
Pemphigus vulgaris	Skin blistering and skin separation	Leather
Pernicious anemia	Fatigue, hypotension, cognitive dysfunction, tachycardia, frequent diarrhea, pallor, jaundice and shortness of breath	Red blood cells
Psoriasis	Accumulation of skin cells in the elbows and knees	Leather
Psoriatic arthritis	Psoriasis	Joints
Polymyositis	Muscle weakness, dysphagia, fever, thickening of skin (on fingers and palms)	Muscles
Primary biliary cirrhosis of the liver	Fatigue, jaundice, itchy skin, cirrhosis and portal hypertension	Liver
Rheumatoid arthritis	Joint inflammation and stiffness	Joints
Raynaud's phenomenon	Changes in skin color (skin appears bluish or red depending on weather conditions), tingling sensation, pain and swelling	Fingers, toes
Schizophrenia	Auditory hallucinations, delusions, disorganized and unusual thinking and speech, and social withdrawal	Nervous system
Scleroderma	Rough and tight skin, skin inflammation, red spots, swollen fingers, heartburn, indigestion, shortness of breath and calcinosis	Connective tissues (skin, blood vessels, esophagus, lungs and heart)
Gougerot-Sjögren syndrome	Mouth and vaginal dryness and eye dryness	Exocrine glands (kidneys, pancreas, lungs and blood vessels)
Shackled person syndrome	Backache	Muscles
Temporal arteritis	Fever, headache, tongue lameness, vision loss, double vision, acute tinnitus and scalp tenderness	Blood vessels
Nonspecific ulcerative colitis	Diarrhea with blood and mucus, weight loss, and rectal bleeding	Intestines
Vasculitis	Fever, weight loss, skin lesions, stroke, tinnitus, acute vision loss, respiratory tract lesions and liver disease	Blood vessels
Vitiligo	Changes in skin color and skin lesions	Leather
Wegener's granulomatosis	Rhinitis, problems with the upper respiratory tract, eyes, ears, trachea and lungs, kidney damage, arthritis and skin lesions	Blood vessels

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. Deformations of the nail plates on fingers affected by arthritis are characteristic. 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

1. Ya.A.Sigidin, N.G. Guseva, M.M. Ivanova “Diffuse connective tissue diseases (systemic rheumatic diseases) Moscow “Medicine” 2004 ISBN 5-225-04281.3 638 pp.
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
5. Internal diseases in 2 volumes: textbook / Ed. ON THE. Mukhina, V.S. Moiseeva, A.I. Martynova - 2010. - 1264 p.
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
8. Carlos J Lozada, MD; Chief Editor: Herbert S Diamond, MD "Reactive Arthritis" Medscape Medical News Rheumatology Updated: Oct 31, 2015
9. Raj Sengupta, MD; Millicent A Stone, MD "The Assessment of Ankylosing Spondylitis in Clinical Practice" CME Released: 8/23/2007; Valid for credit through 8/23/2008
10. Sergio A Jimenez, MD; Chief Editor: Herbert S Diamond, MD "Scleroderma" Medscape Drugs and Diseases Updated: Oct 26, 2015

Autoimmune polyglandular syndrome (also polyendocrine, autoimmune polyendocrine syndrome - APS, polyglandular autoimmune syndrome - PGAS) is an endocrine disease of autoimmune origin. The syndrome is divided into 4 types, designated by Roman numerals I-IV. Diagnosis of the disease can be difficult because... it often lasts for a long time without symptoms. But in people being treated for some kind of endocrine disease (type 1, Addison's disease, etc.), it is possible to monitor antibody levels and diagnose the disease in accordance with them.

Characteristics of autoimmune syndromes

Autoimmune polyglandular syndrome is characterized by the presence of multiple autoimmune gland disorders. We are talking about painful conditions in which autoimmune inflammation affects several endocrine glands simultaneously, gradually disrupting their function, mainly in the form of hypofunction, less often in the form of hyperfunction of the affected organ. Often such damage affects various non-endocrine organs and tissues.

According to clinical symptoms and the presence of mutations in the AIRE gene, autoimmune polyglandular syndrome is divided into 2 different types (I and II). APS-I is characterized by the presence of 2 diseases from the triad:

• chronic mucocutal candidiasis;
• autoimmune hypoparathyroidism;
• Addison's disease.

To determine APS-II, at least 2 of the following diseases must be present:

• type 1 diabetes;
• Bazedow-Graves toxicosis;
• Addison's disease.

Already in the 19th century (1849), Thomas Addison, in the anamnesis of his patients, described the association of pernicious anemia, vitiligo and adrenal insufficiency. In 1926, Schmidt documented an obvious connection between Addison's disease and autoimmune thyropathy. In 1964, Carpenter identified insulin-dependent diabetes mellitus as an important component of Schmidt's syndrome. Autoimmune syndrome, as Addison's disease in association with other autoimmune diseases in the form of the generally accepted classification of APS type I, II, III, was defined by Neufeld in 1981.

Causes of APS

There are many factors associated with the development of APS. There is an increased tendency for autoimmune diseases in some families, suggesting a genetic component. But this does not mean that the illness necessarily originates in the sick child. For the development of autoimmune syndromes, the presence of risk factors acting simultaneously is necessary. These include:

• genetics;
• immunity (IgA or complement defect);
• hormones (estrogens);
• environmental factors.

In addition to genetic susceptibility to autoimmune syndromes, there is often a specific trigger. It can be:

• infections;
• certain foods (such as gluten);
• chemical exposure;
• medicines;
• extreme physical stress;
• physical injury.

Epidemiology

APS-I is a rare childhood disorder occurring in children, endemic in some families, especially in Iran and Finland, affecting boys and girls.

APS-II is more common than APS-I and affects more women than men (3-4:1). As a rule, the disease is detected in adults, the highest incidence is recorded after 50 years. Due to the increasing number of autoimmune diseases among the population, the incidence of APS-II is steadily increasing.

Manifestations of APS

It is a lifelong disease with multiple organ involvement, so the patient's clinical condition is often very complex. The disease makes it difficult for a person to work and social relationships (see photo above). The combination of various pathologies can lead to complete disability.

But the disease does not necessarily manifest itself clinically if the gland is affected less than 80-90%. APS most often occurs in children, but often occurs in adulthood. The first signs indicating the presence of the disease are fatigue, cardiovascular, metabolic symptoms, and impaired response to stress. Symptoms depend on the type of autoimmune polyglandular syndrome.

APS type I

Autoimmune polyglandular syndrome type 1 is an example of a monogenic autoimmune disease with autosomal recessive inheritance. It is also known as Johanson-Blizzard syndrome. The disease is characterized by a violation of central tolerance and negative selection in the thymus, which leads to the release of autoreactive T lymphocytes in the blood and destruction of endocrine target organs.

Autoimmune polyglandular syndrome type 1 is caused by a mutation in the AIRE gene, located on chromosome 21, encoding a protein of 545 amino acids. This gene appeared approximately 500 million years ago, before the formation of adaptive immunity. Its central role is the prevention of autoimmune diseases.

The AIRE gene mutation is the most important finding in the diagnosis of the disease. Today, more than 60 different mutations have been found.

Autoantigens are typical intracellular enzymes; the most typical of these is tryptophan hydroxylase (TPH), expressed by cells that produce serotonin in the intestinal mucosa. Autoantibodies to TPG are found in approximately 50% of patients and respond to intestinal malabsorption. Patients also have a high level of antibodies to interferons (these antibodies are a specific marker of the disease).

Autoimmune polyendocrine syndrome type 1 is a rare disease that affects women and men almost equally. The disease occurs in childhood, but there are cases where symptoms of hypoparathyroidism appear after 50 years, and Addison's disease follows 5-10 years later.

The first manifestation characterizing autoimmune polyendocrine syndrome type 1 is usually candidiasis, before 5 years of age. Hypoplatritism appears before the age of 10, and later, around 15 years of age, Addison's disease is diagnosed. Other diseases may occur during life.

APS type II

Autoimmune polyglandular syndrome type 2 is an autosomal dominant disease with incomplete penetration. The clinical picture necessarily includes Addison's disease with athemic thyroiditis (Schmidt's syndrome), type 1 diabetes (Carpenter's syndrome), or both.

Compared to type 1, autoimmune polyglandular syndrome type 2 occurs more frequently. The incidence of the disease predominates in women (1.83:1 compared to men). Manifestations increase during adolescence, reaching a peak around 30 years of age. Similar to APS-I, it may occur in early childhood. The following ailments may occur as secondary diseases induced by autoimmune polyglandular syndrome type 2:

• chronic lymphocytic gastritis;
• vitiligo;
• pernicious anemia;
• chronic active hepatitis;
• celiac disease;
• myasthenia gravis.

APS type III

Autoimmune polyglandular syndrome type 3, called thyrogastric syndrome, is characterized by autoimmune thyroiditis, type 1 diabetes, and autoimmune gastritis with pernicious anemia. This is the only subgroup without adrenal dysfunction. Alopecia and vitiligo can be observed as secondary ailments.

A familial origin of autoimmune polyglandular syndrome type 3 is assumed, with manifestations in middle and older age. The method of genetic transmission is not clear.

APS type IV

Polyglandular autoimmune syndrome type 4 involves a combination of at least 2 other autoimmune endocrinopathies not described in types I, II and III.

The following autoimmune diseases and their manifestations

This is a diverse group of diseases that are caused by an abnormal response of the immune system. The most well-known diseases associated with APS types I-III include the following ailments.

Sjögren's syndrome

Sjögren's syndrome is an immune system disorder identified by the 2 most pronounced manifestations - dry eyes and dry mouth.

The condition is often accompanied by other immune disorders such as rheumatoid arthritis, lupus. Sjögren's syndrome first affects both the moisture-producing glands and the mucous membranes, eventually leading to a decrease in the amount of tears and saliva.

Although the disease can occur at any age, most people are diagnosed with it after the age of 40. The disease is more common in women.

This syndrome also causes one or more of the following symptoms:

• joint pain, swelling, stiffness;
• swelling of the salivary glands;
• skin rash or dry skin;
• persistent dry cough;
• severe fatigue.

Dressler syndrome

Autoimmune Dressler syndrome is a secondary inflammation of the pericardium (pericarditis) or pleura (pleuritis) that occurs several weeks after myocardial infarction or cardiac surgery.

Symptoms of autoimmune Dressler syndrome:

• chest pain (stabbing in nature, worsens with a deep sigh, sometimes radiating to the left shoulder);
• fever;
• dyspnea;
• pericardial effusion;
• atrial murmur;
• typical ECG changes;
• increase in inflammatory markers (CRP, leukocytosis, etc.).

Werlhof's disease

Werlhof's disease is idiopathic thrombocytopenic purpura or autoimmune thrombocytopenia.

Bleeding in this disease is caused by a decrease in the number of platelets (the reasons for the decrease in their number are still little known). About 90% of patients (mostly women) are under 25 years of age.

The acute form is manifested by the following symptoms:

• temperature increase;
• pinpoint subcutaneous bleeding, merging into small spots;
• nosebleeds;
• bleeding from the mucous membranes, especially from the gums and nose;
• increased bleeding during menstruation.

In the chronic form, periods of bleeding alternate with periods of remission.

Crossover syndrome

Autoimmune crossover syndrome is an unpleasant liver disease, the basis of which is chronic inflammation of the liver. The disease affects the liver tissue and causes deterioration of liver function.

Autoantibodies attack liver cells, damaging them, causing chronic inflammation. The course of the disease varies. Sometimes the cross syndrome has the character of acute inflammation of the liver with expressive symptoms, including the following manifestations:

• jaundice;
• weakness;
• loss of appetite;
• liver enlargement.

Autoimmune crossover syndrome can lead to impaired liver function or chronic inflammation.

Lymphoproliferative syndrome

Autoimmune lymphoproliferative syndrome is a type of lymphoproliferative disease that occurs due to impairment of Fas-induced apoptosis of mature lymphocytes.

Autoimmune lymphoproliferative syndrome is accompanied by the following clinical manifestations:

• thrombocytopenia;
• hemolytic anemia;
• lymphatic infiltration of T-lymphocytes (splenomegaly, chronic non-malignant lymphadenopathy).

With this disease, there is an increased risk of developing lymphomas and severe attacks of immune cytopenia. The disease is rare.

Insulin syndrome

Autoimmune insulin syndrome is a rare disease that causes low blood sugar (hypoglycemia). The reason is the body’s production of a certain type of protein, an antibody, to “attack” insulin. People with autoimmune insulin syndrome have antibodies that attack the hormone, causing it to work too hard; At the same time, the blood sugar level drops too much. The syndrome can be diagnosed in a child, but is more common in adults.

Diagnostics

The diagnosis of APS is based on an analysis of the medical history, clinical symptoms, objective findings and laboratory tests.

Treatment of APS

Different types of drugs are used to treat specific diseases. The basis of therapy is the suppression of the human immune system through the use of immunosuppressants. The problem is that suppressing the immune system is dangerous due to the development of infections and cancer. Thus, immunodeficiency drugs are used under strict medical supervision!

The exception is type 1 diabetes and other autoimmune diseases that affect the hormonal glands. In these cases, the patient is given the missing hormones (for type 1 diabetes - insulin).

The most commonly used medications are corticosteroids, both in tablet form and in the form of skin ointments. However, immunosuppressants are more readily available; The use of a specific drug depends on the disease and its severity.

A relative novelty is biological therapy. The purpose of biological treatment is to weaken the immune system without impairing its general functions.

Prevention of APS

Autoimmune polyglandular syndromes cannot be prevented. It is recommended to eliminate risk factors that worsen existing (secondary) diseases. For example, it is advisable to avoid gluten (for celiac disease), infections, and stress.

APS forecast

Timely detection of the presence of an autoimmune disorder and the correct targeted therapeutic approach are the main factors in controlling the disease. But, it is important to keep in mind that the disease reduces a person’s productivity - patients with this disease are assigned disability groups II-III. People who have been diagnosed with an autoimmune disorder must be monitored (in most cases for life) by specialists from a number of medical fields. Laryngospasm, acute adrenal insufficiency, visceral candidiasis are conditions that can lead to the death of the patient, so monitoring the patient is the main action after acute treatment.

Related Posts

They still remain an incompletely solved mystery for modern science. Their essence is to counteract the body’s immune cells against its own cells and tissues, from which human organs are formed. The main reason for this failure is various systemic disorders in the body, as a result of which antigens are formed. A natural reaction to these processes is the increased production of leukocytes, which are responsible for devouring foreign bodies.

Classification of autoimmune diseases

Consider the list of the main types of autoimmune diseases:

Disorders caused by a violation of the histohematic barrier (for example, if sperm enters a cavity not intended for it, the body will respond by producing antibodies - diffuse infiltration, encephalomyelitis, pancreatitis, endophthalmitis etc.);

The second group occurs as a result of transformation of body tissues under physical, chemical or viral influence. The cells of the body undergo deep metamorphoses, as a result of which they are perceived as foreign. Sometimes in the tissues of the epidermis there is a concentration of antigens that entered the body from the outside, or exoantigens (drugs or bacteria, viruses). The body's reaction will be directed towards them, but this will cause damage to the cells that retain antigenic complexes on their membrane. In some cases, interaction with viruses leads to the formation of antigens with hybrid properties, which can cause damage to the central nervous system;

The third group of autoimmune diseases is associated with the coalescence of body tissues with exoantigens, which causes a natural reaction against the affected areas;

The fourth type is most likely generated by genetic abnormalities or the influence of unfavorable environmental factors, leading to rapid mutations of immune cells (lymphocytes), manifested in the form lupus erythematosus.

Main symptoms of autoimmune diseases

Symptoms of autoimmune diseases can be very different and, often, very similar to acute respiratory viral infections. At the initial stage, the disease practically does not manifest itself and progresses at a fairly slow pace. Further, headaches and muscle pain may occur as a result of the destruction of muscle tissue, and damage to the cardiovascular system, skin, kidneys, lungs, joints, connective tissue, nervous system, intestines, and liver may develop. Autoimmune diseases are often accompanied by other diseases in the body, which sometimes complicates the process of primary diagnosis.

Spasm of the smallest blood vessels of the fingers, accompanied by a change in their color as a result of exposure to low temperature or stress, clearly indicates symptoms of an autoimmune disease called Raynaud's syndrome – scleroderma. The lesion begins in the extremities and then spreads to other parts of the body and internal organs, mainly the lungs, stomach and thyroid gland.

Autoimmune diseases were first studied in Japan. In 1912, Scientist Hashimoto gave a comprehensive description of diffuse infiltration - a disease of the thyroid gland, which results in its intoxication with thyroxine. This disease is otherwise called Hashimoto's disease.

Violation of the integrity of blood vessels leads to the appearance vasculitis. This disease has already been discussed when describing the first group of autoimmune diseases. The main list of symptoms is weakness, fatigue, pallor, poor appetite.

Thyroiditis– inflammatory processes of the thyroid gland, causing the formation of lymphocytes and antibodies that attack the affected tissue. The body organizes a fight against the inflamed thyroid gland.

Observations of people with various spots on their skin were carried out even before our era. The Ebers Papyrus describes two types of discolored spots:
1) accompanied by tumors
2) typical spots without any other manifestations.
In Rus', vitiligo was called “dog,” thereby emphasizing the similarity of people suffering from this disease to dogs.
In 1842, vitiligo was identified as a separate disease. Until this point, it was confused with leprosy.

Vitiligo– a chronic disease of the epidermis, manifested by the appearance on the skin of many white areas devoid of melanin. These dispigments may coalesce over time.

Multiple sclerosis– a disease of the nervous system that is chronic in nature, in which foci of decay of the myelin sheath of the brain and spinal cord are formed. In this case, multiple scars form on the surface of the central nervous system (CNS) tissue - neurons are replaced by connective tissue cells. Around the world, about two million people suffer from this disease.

Alopecia– disappearance or thinning of body hair as a result of pathological hair loss.

Crohn's disease– chronic inflammatory damage to the gastrointestinal tract.

Autoimmune hepatitis– a chronic inflammatory liver disease, accompanied by the presence of autoantibodies and ᵧ-particles.

Allergy– the body’s immune reaction to allergens that it recognizes as potentially dangerous substances. It is characterized by increased production of antibodies, which cause various allergenic manifestations on the body.

Common diseases of autoimmune origin are rheumatoid arthritis, diffuse infiltration of the thyroid gland, multiple sclerosis, diabetes mellitus, pancreatitis, dermatomyositis, thyroiditis, vitiligo. Modern medical statistics record their growth rates in arithmetic order and without a downward trend.

Autoimmune disorders not only affect older people, but are also quite common in children. “Adult” diseases in children include:

- Rheumatoid arthritis;
- Ankylosing spondylitis;
- Nodular periarthritis;
- Systemic lupus.

The first two diseases affect joints in various parts of the body, often accompanied by pain and inflammation of the cartilage tissue. Periarthritis destroys arteries, systemic lupus erythematosus destroys internal organs and manifests itself on the skin.

Expectant mothers belong to a special category of patients. Women are five times more likely to naturally develop autoimmune lesions than men, and most often they appear during reproductive age, particularly during pregnancy. The most common among pregnant women are: multiple sclerosis, systemic lupus erythematosus, Hashimoto's disease, thyroiditis, thyroid diseases.

Some diseases experience remission during pregnancy and exacerbation during the postpartum period, while others, on the contrary, manifest themselves as a relapse. In any case, autoimmune diseases carry an increased risk for the development of a full-fledged fetus, completely dependent on the mother’s body. Timely diagnosis and treatment when planning pregnancy will help identify all risk factors and avoid many negative consequences.

The peculiarity of autoimmune diseases is that they occur not only in people, but also in domestic animals, in particular cats and dogs. The main diseases of pets include:

- Autoimmune hemolytic anemia;
- Immune thrombocytopenia;
- Systemic lupus erythematosus;
- Immune polyarthritis;
- Myasthenia gravis;
- Pemphigus foliaceus.

A sick animal may well die if it is not promptly injected with corticosteroids or other immunosuppressants to reduce the hyperreactivity of the immune system.

Autoimmune complications

Autoimmune diseases are quite rare in their pure form. Basically, they occur against the background of other diseases of the body - myocardial infarction, viral hepatitis, cytomegalovirus, tonsillitis, herpes infections - and significantly complicate the course of the disease. Most autoimmune diseases are chronic with manifestations of systematic exacerbations, mainly in the autumn-spring period. Basically, classic autoimmune diseases are accompanied by severe damage to internal organs and lead to disability.

Autoimmune diseases that accompany various diseases that caused their appearance usually go away along with the underlying disease.

The first person to study multiple sclerosis and characterize it in his notes was the French psychiatrist Jean-Martin Charcot. The peculiarity of the disease is indiscriminateness: it can occur in both older people and young people, and even children. Multiple sclerosis simultaneously affects several parts of the central nervous system, which entails the manifestation of various neurological symptoms in patients.

Causes of the disease

The exact causes of the development of autoimmune diseases are still not known. Exist external And internal factors causing disruption of the immune system. Internal ones include genetic predisposition and the inability of lymphocytes to distinguish between “self” and “foreign” cells. In adolescence, when the residual formation of the immune system occurs, one part of the lymphocytes and their clones are programmed to fight infections, and the other to destroy diseased and non-viable cells of the body. When control over the second group is lost, the process of destruction of healthy cells begins, which leads to the development of an autoimmune disease.

Possible external factors are stress and adverse environmental influences.

Diagnosis and treatment of autoimmune diseases

For most autoimmune diseases, an immune factor is identified that causes the destruction of cells and tissues of the body. Diagnosis of autoimmune diseases consists of identifying them. There are special markers for autoimmune diseases.
When diagnosing rheumatism, the doctor prescribes a test for rheumatic factor. Systemic lupus is determined using tests of Les cells that are aggressive against the nucleus and DNA molecules, scleroderma is detected by testing for antibodies Scl - 70 - these are the markers. There are a large number of them, the classification is differentiated into many branches, depending on the target affected by the antibodies (cells and their receptors, phospholipids, cytoplasmic antigens, etc.).

The second step should be a blood test for biochemistry and rheumatic tests. In 90% they give an affirmative answer to rheumatoid arthritis, in more than 50% they confirm Sjogren's syndrome and in a third of cases they indicate other autoimmune diseases. Many of them are characterized by the same type of development dynamics.

For residual confirmation of the diagnosis, immunological tests are required. In the presence of an autoimmune disease, there is an increased production of antibodies by the body against the background of the development of pathology.

Modern medicine does not have a single and perfect method for treating autoimmune diseases. Her methods are aimed at the final stage of the process and can only alleviate symptoms.

Treatment of an autoimmune disease should be strictly supervised by an appropriate specialist, since existing drugs cause suppression of the immune system, which, in turn, can lead to the development of cancer or infectious diseases.

The main methods of modern treatment:

Suppression of the immune system;
- Regulation of metabolic processes in body tissues;
- Plasmapheresis;
- Prescription of steroidal and non-steroidal anti-inflammatory drugs, immunosuppressants.

Treatment of autoimmune diseases is a long-term systematic process under the supervision of a physician.

Autoimmune polyendocrine (polyglandular) syndrome, abbr. APGS is a severe primary disease of several organs of the endocrine system simultaneously. The combination of affected glands, the involvement of other organs, and the clinical picture may be different. In general, there are two main types of AGPS. Whitaker syndrome, or candidopolyendocrine syndrome type 1, is a rare area-dependent disease that is most often diagnosed at the age of 10-13 years (one of the synonyms is juvenile, juvenile polyendocrinopathy) in relatively closed groups in Finland, Semitic communities of Iran, on the island of Sardinia ; the incidence in these regions is approximately 0.004% of the population. Type 2 ARPS (including Schmidt's syndrome and Carpenter's syndrome) occurs much more often, mainly in women of reproductive age, but its etiology remains unclear.

Causes:

Both types of ARPS are inherited diseases. In type 1, brothers and sisters in the same generation are affected; the gene responsible for the protein regulation of immunity at the cellular level and the creation of a mechanism of general immune resistance mutates.

Type 2 ARPS can occur in members of the same family for two or more generations. The disease develops against the background of pathological aggression of HLA antigens, which occurs as a result of external influence.

Symptoms:

A highly specific symptom of type 1 ARPS is a chronic fungal infection accompanied by hypoparathyroidism and/or renal failure. Candidomycosis affects nails, skin, respiratory organs, mucous membranes of the genital organs, oral cavity, and gastrointestinal tract. Inflammation of the eyelids, eyes, graying, and active hair loss are also noted. Signs of hypogonadism may appear, followed by the development of infertility in women and impotence in men. Adrenal insufficiency leads to hormonal imbalance; As a result, under the influence of stress, the disease worsens.

APGS type 2 is diagnosed in connection with chronic renal failure. Over the next 10 years, the development of diabetes mellitus and autoimmune thyroiditis is typical. The pathology may be accompanied by inflammation of the pleura, celiac disease, the formation of tumors in the pituitary gland, and damage to the optic nerves.

Diagnostics:

The preliminary diagnostic hypothesis about APGS, based on the results of examination, analysis of complaints and life/family history, is verified by a comprehensive examination, incl. laboratory tests (biochemical blood test for salt content, hormonal levels),

Ultrasound, CT or MRI, EchoCG, etc. Usually, additional consultation with highly specialized specialists is required - dermatologist, gynecologist-endocrinologist, etc.

Treatment:

Treatment of APGS essentially boils down to long-term symptomatic therapy, the main goal of which is to monitor the patient’s condition and the course of the disease. Treatment is complex and based on hormone replacement therapy. Glucocorticoid (mineralcorticoid) treatment of renal failure, antifungal therapy for candidiasis, immunosuppressive therapy for the combination of type 2 APGS with diabetes mellitus are prescribed.

Complications of APGS such as acute renal failure, laryngospasm, and visceral candidiasis can be fatal. However, early diagnosis of the disease, adherence to the prescribed hormone replacement therapy regimen, and constant monitoring by an endocrinologist provide a satisfactory quality of life, although usually APGS becomes the cause of partial loss of working capacity, i.e. disability group II or III.