Autoimmune diseases- These are diseases that develop when the body's immune system, for any reason, becomes overly sensitive. 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 malfunction and becomes more sensitive. She begins to overreact to external conditions that are otherwise normal, and over time causes the development of various diseases.

One of the symptoms of autoimmune disease is sudden hair loss

Autoimmune diseases are diseases that the human body develops in itself. They can be both genetic and acquired, and are not only a problem for adults - their symptoms are found in children as well. People with such diseases need to be very careful about their lifestyle. The list below includes many autoimmune diseases, but there are others that are still being investigated to understand their causes and therefore remain on the list of suspected autoimmune diseases.

The symptoms of autoimmune diseases are numerous. They include a 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 nearly all autoimmune diseases along with their common symptoms.

Name of the disease	Symptoms	Affected organs/ glands
Acute disseminated encephalomyelitis (AREM)	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 sensations, 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, preeclipsia, and stillbirth	Phospholipids (substance of cell membranes)
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 disease of the inner ear	Progressive hearing loss	Inner ear cells
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, rashes, 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 lesions on the skin	Blood vessels (lungs, heart, gastrointestinal system)
Dermatomyositis	Skin rashes and muscle pain	Connective tissue
Type 1 diabetes mellitus	Frequent urination, nausea, vomiting, dehydration, and weight loss	Pancreatic beta cells
Endometriosis	Infertility and pelvic pain	Female reproductive organs
Eczema	Redness, fluid buildup, itching (also crusting and bleeding)	Leather
Goodpasture Syndrome	Fatigue, nausea, shortness of breath, pallor, coughing up blood, and burning sensation while urinating	Lungs
Basedow's disease	Bulging eyes, dropsy, hyperthyroidism, heart palpitations, difficulty falling asleep, hand tremors, irritability, fatigue, and muscle weakness	Thyroid
Guillain-Barré Syndrome	Progressive weakness in the body and respiratory failure	Peripheral nervous system
Hashimoto's thyroiditis	Hypothyroidism, muscle weakness, fatigue, depression, mania, sensitivity to cold, constipation, memory loss, migraines, and infertility	Thyroid cells
Purulent hydradenitis	Large and painful abscesses (boils)	Leather
Kawasaki disease	Fever, conjunctivitis, chapped lips, Hunter'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	Kidney
Idiopathic thrombocytopenic purpura	Low platelet count, bruising, nosebleeds, bleeding gums, and internal bleeding	Platelets
Interstitial cystitis	Pain while urinating, 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 / Sharp syndrome	Joint pain and swelling, general malaise, Raynaud's phenomenon, muscle inflammation and sclerodactyly	Muscle
Annular scleroderma	Focal skin lesions, rough skin	Leather
Multiple sclerosis (MS)	Muscle weakness, ataxia, difficulty speaking, fatigue, pain, depression, and unstable mood	Nervous system
Myasthenia gravis	Muscle weakness (in the face, eyelids, and swelling)	Muscle
Narcolepsy	Daytime sleepiness, 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)	Uncontrolled rapid eye movements and muscle cramps, speech disturbances, sleep disturbances, and drooling	Nervous system
Pemphigus vulgaris	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 around the elbows and knees	Leather
Psoriatic arthritis	Psoriasis	Joints
Polymyositis	Muscle weakness, dysphagia, fever, skin thickening (on fingers and palms)	Muscle
Primary biliary cirrhosis	Fatigue, jaundice, itchy skin, cirrhosis, and portal hypertension	Liver
Rheumatoid arthritis	Inflammation and stiffness of the joints	Joints
Raynaud's phenomenon	Discoloration of the skin (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 isolation	Nervous system
Scleroderma	Rough and tight skin, skin inflammation, red lesions, swelling of the fingers, heartburn, indigestion, shortness of breath and calcification	Connective tissues (skin, blood vessels, esophagus, lungs and heart)
Guzhero-Sjogren Syndrome	Dry mouth and vagina and dry eyes	Exocrine glands (kidneys, pancreas, lungs and blood vessels)
Constrained person syndrome	Backache	Muscle
Temporal arteritis	Fever, headache, tongue lameness, loss of vision, 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, ringing in the ears, severe vision loss, respiratory tract damage, and liver disease	Blood vessels
Vitiligo	Skin discoloration 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 reading 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 associated symptoms have been described. However, there are many other diseases that are still awaiting inclusion 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 for various diseases, therefore, a diagnosis based only on taking into account the 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.

Video

Autoimmune polyendocrine syndrome (or simply: autoimmune syndrome) is (even judging by the name) an autoimmune disease, as a result of which endocrine organs are affected (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's 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 the gonads, hypoparathyroidism, possible type 1 diabetes mellitus (rarely).
-3rd type. It is the most common type of autoimmune syndrome and is a combination of thyroid (diffuse goiter, autoimmune thyroiditis) and pancreas (type 1 diabetes) disorders.

Autoimmune thrombocytopenia is common. This is nothing more than a blood disease and it is characterized by the formation of autoimmune antibodies to their own platelets. The autoimmune system in this case fails for various reasons: with a lack of vitamins, with excessive use of drugs, with various kinds of infections, when exposed to various toxins.

Autoimmune thrombocytopenia, by its nature, is subdivided into:
-idiopathic thrombocytopenic purpura (actually autoimmune thrombocytopenia);
-thrombocytopenia in other autoimmune disorders.
The main and most dangerous syndrome of this disease is bleeding (tendency to them) 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, in other words, 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 its own tissues. So, autoimmune antibodies are elements that appear as an autoimmune reaction on the tissues of their own organism. That's how everything is simple and clear. This is exactly how the autoimmune system works. Well, in fact, it is clear that autoimmune damage is a disease caused by autoimmune antibodies that are directed against the tissues of their own 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 in order to detect 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 "scanning" the patient's blood.

Mechanisms of treatment 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 in the fact that it does not give any side effects. Its uniqueness also lies in its mechanism of action on our protective functions. But you can learn more about this on other pages of our site. This is another story.

Autoimmune diseases are a large group of diseases that can be combined on the basis that the immune system aggressively opposed to its own body takes part in their development.

The reasons for the development of almost all autoimmune diseases are still unknown.

Given the huge variety autoimmune diseases, as well as their manifestations and the nature of the course, study and treat these diseases by a variety of specialists. Which one depends 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, in rheumatoid arthritis, not only joints, but also the skin can be affected. kidneys, lungs. In such situations, most often the disease is treated by a doctor whose specialization is associated with the most striking manifestations of the disease, or 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 "ours and others". Medicines that reduce the activity of immune inflammation are called immunosuppressants. The main immunosuppressants are "Prednisolone" (or its analogs), cytostatics ("Cyclophosphamide", "Methotrexate", "Azathioprine", etc.) and monoclonal antibodies, which act as targeted as possible on individual links of inflammation.

Many patients often ask questions, how can you suppress your own immune system, how will I live with "bad" immunity? Suppressing the immune system in autoimmune diseases is not possible, but necessary. The doctor always weighs what is more dangerous: illness or treatment, and only then makes a decision. So, for example, with autoimmune thyroiditis, it is not necessary to suppress the immune system, but with systemic vasculitis (for example, microscopic polyanginitis) it is simply vital.

People have been living with suppressed immune systems for many years. At the same time, the frequency of infectious diseases increases, but this is a kind of "payment" for the treatment of the disease.

Often patients are interested in whether it is possible to take immunomodulators. Immunomodulators are different, most of them are contraindicated for people suffering from autoimmune diseases, however, some drugs in certain situations can be useful, for example, intravenous immunoglobulins.

Systemic autoimmune diseases

Autoimmune diseases often pose a diagnostic difficulty, require special attention from doctors and patients, 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 systems of organs and tissues, for example, muscles and joints, skin, kidneys, lungs, etc. Some forms of the disease become systemic only with the progression of the disease, for example, rheumatoid arthritis, others immediately affect many organs and tissues. As a rule, systemic autoimmune diseases are treated by rheumatologists, but often such patients can 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);
• Sjogren's syndrome;
• Behcet's disease;
• systemic vasculitis (a group of different separate diseases combined on the basis of a symptom such as vascular inflammation).

Autoimmune diseases with predominant joint damage

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

• Rheumatoid arthritis;
• spondyloarthropathies (a group of different diseases combined 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 group of diseases does not require immunosuppressive therapy. Most patients are seen by endocrinologists or family doctors (therapists).

Autoimmune blood diseases

Hematologists are specialized in this group of diseases. The most famous diseases are:

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

Autoimmune diseases of the nervous system

A very large group. Treatment of these diseases is the prerogative of neurologists. The most famous autoimmune diseases of the nervous system are:

• Multiple (multiple) sclerosis;
• Guien-Bare syndrome;
• myasthenia gravis.

Autoimmune diseases of the liver and gastrointestinal tract

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

• 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 famous diseases are:

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

Autoimmune kidney disease

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

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

Autoimmune heart disease

These diseases are in the field of activity of both cardiologists and rheumatologists. Some diseases are treated primarily by cardiologists, for example, myocarditis; other diseases - almost always rheumatologists (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 affecting only the lungs and upper respiratory tract are treated in most cases by pulmonologists, diseases of a systemic nature with lung damage - by rheumatologists.

• Idiopathic interstitial lung disease (fibrosing alveolitis);
• sarcoidosis of the lungs;
• systemic vasculitis with lung damage and other systemic autoimmune diseases with lung damage (dermis and polymyositis, scleroderma).

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

General characteristics of autoimmune diseases affecting joints

Most of the autoimmune diseases affecting the joints are diffuse connective tissue diseases (systemic rheumatic diseases). This is a wide 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, which 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 prognosis of life for the patient.

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

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

In other cases, joint lesions can be involved in the process only in case of a severe course 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 the quality of his life. Or, on the contrary, the degree of damage can only cause completely reversible inflammatory changes. In this case, the prognosis of the disease may be associated with damage to other organs and systems (for example, in 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 the antigens of the so-called major histocompatibility complex (referred to as HLA or MHC antigens). These genes are found 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:

A postponed 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 the antigen to T-lymphocytes and for the onset of the development of an immune response to the pathogen. Their relationship 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 antigens of common pathogens of infectious diseases (viruses that cause ARVI, E. coli, streptococcus, etc.) have a similar structure to human proteins - the carrier of certain genes of the main histocompatibility complex and cause ...

An infection transferred 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 to its own antigens of the connective tissue.

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

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, loss of body weight, etc.), its result is often irreversible changes in the affected organs. The clinical picture of the disease has its own characteristics for each of the nosologies, some of which will be described below.

Since the incidence of systemic autoimmune diseases is low and for many of them there are no specific symptoms that are not observed in other diseases, only a doctor can suspect a patient from this group on the basis of a combination of characteristic clinical signs, the so-called diagnostic criteria of the disease, approved in international guidelines. for its diagnosis and treatment.

Reasons for screening to rule out systemic rheumatic diseases

• the onset of joint symptoms in a patient at a relatively young age,
• lack of connection between symptoms and increased stress 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 a systemic connective tissue disease is established by a rheumatologist.

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

The basis of laboratory diagnostics is the identification of specific antibodies to their own organs and tissues, immune complexes formed during the development of the disease, antigens of the main histocompatibility complex characteristic of certain diseases of this group and detected using monoclonal antibodies, genes encoding these antigens, detected by determining specific DNA sequences.

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

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

To avoid disability and death, you need constant medical supervision and therapy that meets the standards

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

Making a diagnosis for a rheumatologist when detecting 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 appointment of immunosuppressive and cytostatic drugs, drugs that slow down the pathological formation of connective tissue, and other special chemotherapy drugs.

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

A new area 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 drugs. In the complex treatment for joint damage, surgical interventions are used, physiotherapy exercises and physiotherapy are prescribed.

Rheumatoid arthritis

Rheumatoid arthritis is the most common systemic autoimmune disease in humans.

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

Clinical picture

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

Less often, large joints are involved in the process - knee, elbow, ankle. Involvement of five or more joints in the process is obligatory; the symmetry of the joint lesions is characteristic.

A typical sign of the disease is the deviation of fingers I and IV 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 in the process, as well as the presence of subcutaneous "rheumatoid nodules".

The damage to the joints in rheumatoid arthritis is irreversible with limited 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 antibodies to its own immunoglobulin G. Depending on their presence, RF-positive and RF-negative rheumatoid arthritis are distinguished. With the latter, 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 made 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 lesions and should be assessed by a physician in conjunction with the clinical picture of the disease.

Specific laboratory markers for 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 be found in other systemic rheumatoid diseases.

Treatment for rheumatoid arthritis

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

Modern approaches to drug therapy are the use of a preparation 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 devoid of the side effects of cytostatics, however, 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 appointment in the absence of a sufficient effect from cytostatics.

Acute rheumatic fever

Acute rheumatic fever ( the disease, which in the past was called "rheumatism") is a post-infectious complication of tonsillitis (sore throat) or pharyngitis caused by group A hemolytic streptococcus.

This disease manifests itself in the form of a systemic inflammatory disease of the connective tissue with a predominant lesion of the following organs:

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

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

A characteristic complication of the disease, which 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. Knee, ankle, wrist and elbow joints are more often affected. In addition, joint pains are noted, which are often so pronounced 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 migratory in 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 a 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 DNA - ase, the detection of hemolytic streptococcus A during bacteriological examination of a smear from the throat.

For treatment, antibiotics of the penicillin group, glucocorticosteroids and NSAIDs are used.

Ankylosing spondylitis (ankylosing spondylitis)

Ankylosing spondylitis (ankylosing spondylitis)- chronic inflammatory joint disease, 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. Also, with the disease, peripheral joints and tendons, eyes and intestines can be affected.

Difficulties in the differential diagnosis of pain in the spine in ankylosing spondyloarthritis with osteochondrosis, in which these symptoms are caused by purely mechanical reasons, can lead to a delay in the diagnosis and the appointment 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, 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,
• the presence of signs of general malaise,
• involvement in the process of other joints, eyes and intestines,
• 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: a predisposition to its development can be established by detecting the antigen of the main histocompatibility complex HLA - B27.

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

Joint damage with systemic lupus erythematosus

The causes of systemic lupus erythematosus are still not understood.

In a number of autoimmune diseases, joint damage can occur, but it 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 immune-inflammatory 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: they suggest the influence of hereditary factors and viral infection as a triggering mechanism for the development of the disease, an unfavorable effect 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 rash 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, a decrease in the number leukocytes and lymphocytes, platelets.

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

Arthralgias occur in almost 100% of patients at various stages of the disease. Pain can occur in one or more joints and be short-lived.

With a high activity of the disease, the pain can be more persistent, in the future a picture of arthritis develops with pain during movement, soreness in the joints, swelling, inflammation of the membranes of the joint, redness, increased skin temperature over the joint and dysfunction.

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 the bones - the femoral head, humerus, less often the bones of the wrist, knee, elbow, foot.

The markers detected in the laboratory diagnosis of the disease are antibodies to DNA, anti-Sm antibodies, the detection of antinuclear antibodies that are not associated with the intake of drugs that can cause their formation, the identification of the so-called LE - cells - neutrophilic leukocytes containing phagocytosed fragments of the nuclei of others cells.

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

Joint damage in systemic sclerosis

The severity of the course of the disease and life expectancy in systemic scleroderma depends 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 vessels of the fingers, the so-called Raynaud's syndrome, foci of thinning and coarsening, dense edema and atrophy of the facial skin, manifestation 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, limitation of mobility, the appearance of the so-called "friction noise of the tendon" detected during a medical examination and associated with the involvement of tendons and fasciae 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 a violation of their blood supply.

Markers of laboratory diagnosis of the disease are anticentromeric 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, drugs that slow down fibrosis also play a key role.

Psoriatic arthritis

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

In most patients with psoriatic arthritis, the 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 cutaneous manifestations.

Mostly the joints of the fingers are affected, with the development of joint pain and swelling of the fingers. Characterized by deformities of the nail plates on the fingers affected by arthritis. Involvement of other joints is also possible: 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.

For treatment, cytostatic drugs are used, the modern direction of therapy is antibodies to tumor necrosis factor alpha.

Arthritis in ulcerative colitis and Crohn's disease

Joint lesions can also occur in some patients with chronic inflammatory bowel diseases: Crohn's disease and ulcerative colitis, in which articular 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.

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 in Crohn's disease and is localized most often in the left iliac region.

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

Characteristically asymmetric, migratory joint lesion is more often of the lower extremities: knee and ankle joints, less often elbow, hip, interphalangeal and metatarsophalangeal joints. The number of affected joints usually does not exceed five.

The articular syndrome proceeds 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, with an objective examination, changes are not detected. Over time, exacerbations of arthritis become less frequent. In most patients, arthritis does not lead to deformation or destruction of the joints.

The severity of symptoms and the frequency of relapses decrease with treatment of the underlying disease.

Reactive arthritis

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

Such a pathology is possible after an infection (not only Yersinia, but also other intestinal infections). For example, shigella - causative agents of dysentery, salmonella, campollobacter.

Also, reactive arthritis can appear due to the causative agents 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 joints of the toes, ankle, or sacroiliac joint.

Typically, one joint on one limb is affected (asymmetric monoarthritis).

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

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

Currently, the efficacy and safety of biological therapy drugs is being studied.

Symptoms of allergic diseases in autoimmune joint diseases

For a number of autoimmune diseases affecting the joints, symptoms characteristic of. They can often precede a detailed clinical picture of the disease. So, 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 localization 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, in systemic lupus erythematosus, the development in some patients of severe acquired angioedema associated with an inhibitor of C1 esterase in the background of the disease has been described.

Thus, autoimmune diseases of the joints are by their nature more serious diseases in comparison with the pathology that develops against the background of their mechanical overload (osteoarthritis, 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. Kolkhir Urticaria and angioedema. "Practical Medicine" Moscow 2012 UDC 616-514 + 616-009.863 BBK 55.8 K61 str. 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) LBC 52.5 X19 p. 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. 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 polyendocrine 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. Diagnosing the disease can be challenging. it often goes on for a long time without symptoms. But in people being treated for some kind of endocrine disease (type 1, Addison's disease, etc.), you can control the levels of antibodies, and in accordance with them, diagnose the disease.

Characterization of autoimmune syndromes

Autoimmune polyglandular syndrome is characterized by the presence of multiple autoimmune glandular disorders. We are talking about painful conditions in which autoimmune inflammation affects several endocrine glands at the same time, gradually disrupting their function, mainly in the form of hypofunction, less often in the form of hyperfunction of the affected organ. Often, such a lesion 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 mucoctal candidiasis;
• autoimmune hypoparathyroidism;
• Addison's disease.

To determine APS-II, the presence of at least 2 of the following diseases is required:

• type 1 diabetes;
• Basedow-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 link 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, like Addison's disease in association with other autoimmune diseases in the form of the generally accepted classification of APS types I, II, III, was defined by Neufeld in 1981.

Causes of APS

There are many factors associated with the development of APS. In some families, there is an increased tendency for autoimmune disease, indicating a genetic component. But this does not mean the obligatory origin of the disease in the patient's child. The development of autoimmune syndromes requires the presence of risk factors acting simultaneously. These include:

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

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

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

Epidemiology

APS-I is a rare childhood disorder that occurs 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 found in adults, the highest incidence is recorded after 50 years. Due to the increase in the number of autoimmune diseases among the population, the frequency of APS-II is steadily increasing.

Manifestations of APS

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

But the disease does not necessarily manifest itself clinically if the lesion of the gland is less than 80-90%. APS is more common in children, but often occurs in adulthood. The first signs that indicate the presence of illness 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 impaired central tolerance and negative selection in the thymus, which leads to the release of autoreactive T-lymphocytes in the blood, destruction of endocrine target organs.

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

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

Autoantigens are typical intracellular enzymes; the most typical of these is tryptophan hydroxylase (TPH), which is expressed by cells that produce serotonin in the intestinal mucosa. Autoantibodies to TPH are found in about 50% of patients and respond to intestinal malabsorption. Also, patients 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 when symptoms of hypoparathyroidism occur after 50 years, and Addison's disease follows after 5-10 years.

The first manifestation characterizing type 1 autoimmune polyendocrine syndrome is usually candidiasis, up to 5 years of age. Until the age of 10, hypoplatritism appears, and later, at about 15 years of age, Addison's disease is diagnosed. Other illnesses may occur during life.

APS type II

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

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

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

APS type III

Type 3 autoimmune polyglandular syndrome, 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 seen as secondary ailments.

A familial origin of type 3 autoimmune polyglandular syndrome with manifestations in middle and older age is suggested. The method of genetic transmission has not been clarified.

APS type IV

Type 4 polyglandular autoimmune syndrome 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, the nature of which is an abnormal response of the immune system. The most famous diseases associated with APS types I-III include the following ailments.

Sjogren's Syndrome

Sjogren's syndrome is a disorder of the immune system, identified by the 2 most pronounced manifestations - dry eyes and mouth.

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

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

This syndrome also has 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 tiredness.

Dressler syndrome

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

Symptoms of Autoimmune Dressler Syndrome:

• chest pain (stabbing in nature, increases with a deep breath, sometimes radiates to the left shoulder);
• fever;
• dyspnea;
• pericardial effusion;
• atrial murmur;
• typical ECG changes;
• growth of 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 younger than 25 years old.

The acute form is manifested by the following symptoms:

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

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

Cross syndrome

Autoimmune crossing syndrome is an unpleasant liver disease that is based on chronic inflammation of the liver. The disease affects the liver tissue, causing deterioration in liver function.

Autoantibodies attack liver cells, damage them, and cause 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;
• enlargement of the liver.

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

Lymphoproliferative Syndrome

Autoimmune lymphoproliferative syndrome is a type of lymphoproliferative disease resulting from a disturbance in 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, severe attacks of immune cytopenia. The disease is rare.

Insulin syndrome

Autoimmune insulin syndrome is a rare condition that causes low blood sugar levels (hypoglycemia). The reason is the production of a certain type of protein in the body, an antibody for the "attack" of insulin. People with autoimmune insulin syndrome have antibodies that attack the hormone, causing it to work too hard; the blood sugar drops too low. The syndrome can be diagnosed in a child, but is more common in the adult population.

Diagnostics

Establishing the diagnosis of APS is based on the analysis of anamnesis, clinical symptoms, objective finding and laboratory tests.

APS treatment

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

Exceptions are type 1 diabetes and other autoimmune diseases that affect hormonal glands. In these cases, the patient is injected with the missing hormones (in type 1 diabetes - insulin).

The most commonly used drugs are corticosteroids, both in the form of tablets and in the form of skin ointments. However, immunosuppressants are more readily available; the use of a particular 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 disrupting its general functions.

Prevention of APS

Prevention of autoimmune polyglandular syndromes is not possible. It is recommended to eliminate the risk factors that worsen the present (secondary) diseases. For example, it is advisable to avoid gluten (for celiac disease), infections, stress.

APS forecast

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

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