What does the HLA b27 blood test show? HLA-B27 (molecular method)


A study to identify predisposition to diseases from the group of seronegative spondyloarthritis, during which the HLA-B27 antigen is determined using flow cytometry.

* The results of the study are issued with the conclusion of a doctor - allergist-immunologist, doctor of medical sciences.

Synonyms Russian

  • Human leukocyte antigen B27
  • Immunogenetic marker HLA-B27
  • Differential diagnosis of autoimmune diseases

SynonymsEnglish

  • HLA typing, flow cytometry (flow cytofluorometry)
  • Ankylosing spondylitis Histocompatibility Antigen
  • Ankylosing spondylitis Human Leukocyte Antigen

Research method

Flow cytometry.

What biomaterial can be used for research?

Venous blood.

How to properly prepare for research?

  • Eliminate alcohol from your diet for 24 hours before the test.
  • Do not eat for 12 hours before the test.
  • Avoid taking it completely medicines within 24 hours before the study (in consultation with the doctor).
  • Avoid physical and emotional stress for 24 hours before the test.
  • Do not smoke for 30 minutes before the test.

General information about the study

The HLA-B27 antigen is a specific protein found on the surface of immune cells. It belongs to the proteins of the human major histocompatibility complex, which mediates various immune responses. Carriage of the HLA-B27 antigen is associated with increased risk development of diseases from the group of seronegative spondyloarthritis. Thus, this antigen can be detected in 90-95% of patients with ankylosing spondylitis (Bechterew's disease), 75% of patients with reactive arthritis (Reiter's syndrome), 50-60% of patients with psoriatic arthropathy, 80-90% of patients with juvenile ankylosing spondylitis and 60-90% of patients with enteropathic arthritis. The presence of the HLA-B27 antigen in patients with other joint diseases (gout, rheumatoid arthritis, septic arthritis) does not exceed 7-8%. Considering this feature, detection of the HLA-B27 antigen is of great diagnostic importance in the clinic of rheumatological diseases.

Determination of the HLA-B27 antigen is of greatest importance in the diagnosis of early ankylosing spondylitis. In most cases, 5-10 years pass between the appearance of the first signs of the disease and the final diagnosis. This is due to the fact that the main diagnostic criterion The diseases are radiological signs of sacroiliitis, which develops only after several years of inflammatory process in the sacroiliac joints. Patients with complaints of back pain without radiological signs of sacroiliitis actually do not come to the attention of a rheumatologist. Detection of HLA-B27 in such a situation may be sufficient grounds for referring the patient to a specialized specialist.

Determination of the HLA-B27 antigen is indicated when examining a patient with complaints of inflammatory pain in the back in the absence of radiological signs of sacroiliitis or when examining a patient with asymmetric oligoarthritis.

The presence of HLA-B27 is associated with an increased risk of extra-articular manifestations of ankylosing spondylitis. Highest value have associations of the HLA-B27 antigen and acute anterior uveitis, aortic valve insufficiency, acute leukemia, IgA nephropathy and psoriasis. HLAB27 – positive patients are more at risk of tuberculosis and malaria. On the other hand, the presence of HLA-B27 also plays a certain “protective” role: some viral infections(flu, herpes viral infection type 2, infectious mononucleosis, hepatitis C and) occur in more mild form in HLA-B27 carriers.

Determination of the HLA-B27 antigen is carried out to predict complications of rheumatoid arthritis. The presence of HLA-B27 is associated with a threefold increase in the risk of atlantoaxial subluxation.

To determine the HLA-B27 antigen, various laboratory methods can be used: lymphocytotoxic test, molecular diagnostic methods (PCR), linked immunosorbent assay(ELISA) and flow cytometry method. Flow cytometry is a fast and reliable method for detecting the HLA-B27 antigen. However, it has some limitations that should be taken into account when interpreting the result. Thus, monoclonal antibodies to the HLA-B27 antigen used in the test are not absolutely specific, but can also react with other antigens of the HLA-B family (primarily HLA-B7, and to a lesser extent HLA-B40, 73 , 22, 42, 44). Given this feature, in order to avoid diagnostic errors, modern protocols for determining the HLA-B27 antigen use double antibodies that allow the HLA-B27 antigen to be differentiated from other antigens of the HLA-B family. This approach increases the specificity and sensitivity of the test to 97.6 and 98.8%, respectively.

Despite the presence of a strong association of the HLA-B27 antigen and the risk of developing spondyloarthritis, a positive test result does not always reflect the real risk of the disease in a particular patient. This is due to the fact that the HLA-B27 antigen is represented by 49 different variants, characterized by varying degrees of association with this group of diseases. Thus, the HLA-B2708 variant has the greatest association with the disease, while the HLA-B2706 and HLA-B2709 variants do not appear to be associated with disease risk at all. About 7-8% healthy people European population are carriers of the HLA-B27 antigen. Additional information about the patient's genetic background may help in interpreting a positive result.

It should be noted that there are other, both hereditary and acquired, risk factors for the development of seronegative spondyloarthritis. The absence of HLA-B27 does not contradict the diagnosis of ankylosing spondylitis. Ankylosing spondylitis is then classified as HLAB27 negative.

What is the research used for?

  1. For differential diagnosis articular syndrome (seronegative spondyloarthritis, rheumatoid and septic arthritis, gout and others);
  2. for screening, diagnosis and prognosis of ankylosing spondylitis;
  3. to assess the risk of developing atlantoaxial subluxation in rheumatoid arthritis.

When is the study scheduled?

  • For articular syndrome: asymmetric oligoarthritis, especially in combination with pain in the lumbar region of an inflammatory nature (morning stiffness for more than 1 hour, improvement with physical activity, worsening at night) and signs of enthesitis;
  • with a family history of ankylosing spondylitis;
  • for rheumatoid arthritis.

What do the results mean?

Presence of HLA-B27 antigen:

  • observed in 90-95% of patients with ankylosing spondylitis and juvenile ankylosing spondylitis, as well as in 60-90% with reactive arthritis and 50% with psoriatic arthropathy;
  • observed in 7-8% of healthy people in the European population.

Absence of HLA-B27 antigen:

  • Diagnosis of early rheumatoid arthritis
  • Who orders the study?

    Rheumatologist, surgeon, doctor general practice, chiropractor.

    Literature

    • Darke C, Coates E. One-tube HLA-B27/B2708 typing by flow cytometry using two "Anti-HLA-B27" monoclonal antibody reagents. Cytometry B Clin Cytom. 2010 Jan;78(1):21-30.
    • Seo BY, Won DI.Flow cytometric human leukocyte antigen-B27 typing with stored samples for batch testing. Ann Lab Med. 2013 May;33(3):174-83.
    • Seipp MT, Erali M, Wies RL, Wittwer C. HLA-B27 typing: evaluation of an allele-specific PCR melting assay and two flow cytometric antigen assays. Cytometry B Clin Cytom. 2005 Jan;63(1):10-5.
    • Levering WH, Sintnicolaas K, Wind H, Hooijkaas H, Gratama JW. Flow cytometric screening for the HLA-B27 antigen on peripheral blood lymphocytes. Curr Protoc Cytom. 2005 Aug;Chapter 6:Unit6.22. doi: 10.1002/0471142956.cy0622s33.

    About the approach to diagnosis and treatment adopted in Israel ankylosing spondylitis says Professor Ori Elkayam, rheumatologist, head of the therapeutic department at medical center Tel Aviv.

    The term "ankylosing spondylitis" is used to designate a whole group of diseases (Ankylosing Spondylitis, Strumpell-Bechterew-Marie disease, or Bechterew's disease), united by the concept of "spondyloarthropathy", affecting the joints of the pelvis and spine along its entire length, as well as peripheral joints.

    Genetic disease
    This disease has a genetic basis, as it is associated with changes in several genes. In 90% of cases, a simple genetic blood test detects the genetic marker HLA-B27 in patients. At the same time, it should be borne in mind that the mere presence of this factor is not enough for a person to feel sick.

    Ankylosing spondylitis affects mainly men. Its prevalence is 0.5% of the male population. The first manifestations of the disease occur between the ages of 20 and 40 years.

    Diagnostics - after 7 years

    Back pain

    The most common symptom. Prolonged back pain, lasting more than 3 months and having an inflammatory nature, is typical at night. The pain intensifies with rest and is accompanied by morning stiffness.

    It should be borne in mind that back pain is very common, and only 5% of all chronic pain is of an inflammatory nature, characteristic of ankylosing spondylitis. This explains the difficulties in diagnosing the disease. Usually, Diagnosis occurs on average after 7 years from the onset of symptoms.

    Pain in joints and tendons
    In about a third of patients, joints and tendons are involved in the pathological process. The most commonly affected joints are the shoulder, hip, knee joints and sometimes also the feet. There may also be pain in the Achilles tendons or ligaments in the soles of your feet.

    Damage to other organs
    Except musculoskeletal system, ankylosing spondylitis can also affect other organs of the body.

    Eyes
    Uveitis, characterized by redness and pain in the eye, is common. Unpleasant sensations can last up to several weeks and pass without causing significant harm to the eye.

    Lungs
    Complaints from the respiratory system are usually explained by skeletal damage, which causes a decrease in volume chest and reduces the possibility of its expansion, limiting respiratory movements.

    Digestive system
    More than half of patients with ankylosing spondylitis have hidden intestinal inflammation, which for a long time does not manifest itself clinically. However, as spondyloarthropathy progresses, the patient begins to develop symptoms of Crohn's disease or inflammation of the large intestine.

    Heart
    Cardiac involvement is rare, although pacemaker or aortic valve abnormalities have been noted

    Differences between men and women
    There is a difference in the manifestations of the disease in men and women. In men, the main symptom is back pain, while for most women, peripheral organ involvement is more typical, including inflammation of peripheral joints and soft tissue sensitivity.

    Signs identified during examination of the body
    In the early stages of the disease, you should look for symptoms of sacroiliitis (inflammation pelvic joints). As the disease continues, signs of limited mobility of the spine can be detected along its entire length, in all parts. The check also includes a detailed examination of the peripheral joints to determine their involvement in the pathological process.

    The inflammatory process is in a demonstrative stage
    In most cases, we are talking about inflammation in the joints of the pelvis, which spreads to the entire spine. Gradually the so-called syndesmophytes- bone bridges between the vertebrae that begin to lose mobility. This leads to increasingly severe limitation of mobility spinal column.

    Instrumental methods diagnostics
    Diagnosis, as a rule, requires X-ray and tomographic methods of examining the pelvic joints (sacroiliitis). Sometimes pathological changes are clearly visible even on a simple x-ray. However, in the first years of the disease there is often a need for additional studies, such as CT or MRI.

    At later stages of the disease, changes in syndesmophytes can be seen using x-rays. Laboratory tests show symptoms of inflammation - such as an increase in ESR (erythrocyte sedimentation rate), an increase in CRP (C-reactive protein), anemia (low hemoglobin), and an increase in the number of platelets. Detection of the HLA-B27 gene confirms the diagnosis.

    Physiotherapy and diet in addition to medication treatment

    Drug therapy

    - nonsteroidal anti-inflammatory drugs:
    naxin, voltaren, etopane, arcoxia, etc. These drugs can provide significant relief, but in most cases their effectiveness is limited. They also cannot affect other manifestations of the disease, such as eye damage.

    - salzopyrine.
    IN in rare cases When the main symptom is inflammation of the peripheral joints, some patients may receive relief by taking salzopyrine, which is an antirheumatic drug.

    - TNF blockers.
    This is the next stage of treatment, which includes the use of drugs such as Remicide, Humira and Enbrel. These three drugs are highly effective and have a similar side effect profile. The main difference lies in the way each medicine is administered. Remicide is administered intravenously every few weeks, Humira is administered once every two weeks as a subcutaneous injection, and Enbrel is also administered subcutaneously, but this time weekly.

    Before starting treatment, you should make sure that the patient does not suffer from latent tuberculosis, for which a Mantoux test and chest x-ray are performed. Treatment with TNF blockers has significantly changed the lives of many patients, providing them with a significant improvement in their quality of life.

    Non-drug treatment

    - physiotherapy It is extremely important for patients with ankylosing spondylitis, since it allows you to strengthen the muscles of the back and abdomen, ensure the correct position of the spine and thereby avoid its curvature and related problems.

    - proper nutrition
    increases life expectancy and avoids weight gain, which prevents the development of complications and concomitant diseases

    What to remember

    • back pain is the main manifestation of the disease, but for most people who complain of back pain, their cause is not an inflammatory process
    • inflammation is detected in only 5% of people experiencing chronic back pain
    • The disease is most often detected in people under 40 years of age
    • HLA-B27 is detected in most patients with ankylosing spondylitis, but most people who have HLA-B27 in their blood do not suffer from this disease and the presence of HLA-B27 in the body does not lead to the development of the disease.
    • treatment with TNF blockers changes the lives of patients with spondyloarthropathy for the better
    • You should carefully monitor the strengthening of the abdominal and back muscles, the correct position of the spine and normal body weight over the years.

    HLA-B27 (molecular method)

    Alternative names: Gene typing according to HLA-B27, English: Ankylosing spondylitis Histocompatibility Antigen.

    Determination of the immunogenetic marker HLA-B27 is a method of molecular genetic research that involves identifying the presence or absence of a specific 27 allele of the B locus in the genotype.

    The gene with this allele is responsible for the synthesis of one of the histocompatibility antigens, characteristic of some autoimmune diseases, namely spondyloarthropathies (pathologies of the axial skeleton).

    Special cases of such diseases are:

    1. Ankylosing spondylitis.
    2. Reiter's syndrome.
    3. Juvenile rheumatoid arthritis.
    4. Psoriatic arthritis.

    Most often, this allele is detected in so-called “seronegative” variants of these diseases, when it is impossible to confirm them by other methods, that is, typical tests for rheumatoid factor and autoantibodies give negative result.

    The HLA genes are located on the short arm of chromosome VI. They are characterized by high degree polymorphism - the presence of a large number of variant alleles. There are 136 alleles identified for HLA-B specifically, many of which are found only in people of a certain race or ethnicity.

    Material for research: venous blood in a volume of 5 ml.

    Research method: PCR – polymerase chain reaction.

    No special preparation is required for the analysis. It is not recommended to smoke immediately before donating blood.

    The analysis is used for differential diagnosis of the so-called articular syndrome, which includes the following symptoms:

    • asymmetric oligoarthritis (one or two joints on one side are affected);
    • pain in the lumbar region;
    • morning joint stiffness for more than 1 hour;
    • enthesitis - pain in the places where the ligaments are attached to the bones.

    It is advisable to prescribe analysis for rheumatoid arthritis.

    In widespread practice, the method is used for screening, primary diagnosis and assessment of the prognosis of ankylosing spondylitis.

    The analysis is qualitative in nature, that is, a given allele is either detected or not.

    A negative result is observed in most people and indicates a relatively low risk of developing spondyloarthropathies, although it does not completely exclude the possibility of their development.

    A positive result in people with articular syndrome indicates the presence of one of the autoimmune spondyloarthropathies. In the case of a positive screening result in a healthy person, the risk of developing the above-mentioned diseases is considered to be approximately 20 times higher. A positive result in healthy people occurs in 7-8% of the population. However, this does not mean that a person will definitely get sick.

    False-positive results occur when the lymphocytes in the blood sample are destroyed, so the test must be performed within 24 hours of blood collection.

    HLA-B27 typing is very important in the early diagnosis of ankylosing spondylitis. From the moment the first signs of the disease appear until the appearance of a detailed clinical picture, which allows one to make a diagnosis without a doubt, it takes from 5 to 10 years. This is due to the fact that the main criterion for diagnosis is radiological signs of sacroiliitis (long-term inflammation of the sacroiliac joints).

    The presence of only pain in the back forces such patients to undergo long-term treatment by neurologists without seeing a rheumatologist. Prescribing an HLA-B27 test in such a situation may be sufficient grounds for subsequently referring the patient to a rheumatologist. This will allow specific therapy to be started at an early stage of the disease and reduce the likelihood of disability. This is especially important in diagnosing such diseases in children.

    1. Lapin S.V., Mazina A.V., Bulgakova T.V. and others. Methodological guidelines for laboratory diagnosis of autoimmune diseases. St. Petersburg, ed. St. Petersburg State Medical University, 2011.
    2. McHugh K, Bowness P. The link between HLA-B27 and SpA-new ideas on an old problem. Rheumatology(Oxford). 2012 Sep;51(9):.

    HLA-B27 typing: research in the KDLmed laboratory

    Identification of genetic predisposition to spondyloarthritis, during which the HLA-B27 allele is determined using polymerase chain reaction.

    Detection of allele 27 of locus B of the human major histocompatibility complex, HLA-B 27 antigen.

    Ankylosing spondylitis Histocompatibility Antigen, Ankylosing spondylitis Human Leukocyte Antigen.

    Polymerase chain reaction (PCR).

    What biomaterial can be used for research?

    How to properly prepare for research?

    Do not smoke for 30 minutes before donating blood.

    General information about the study

    Spondyloarthritis is a group of inflammatory diseases of the axial skeleton that have a pronounced genetic orientation. These include ankylosing spondylitis (Bechterew's disease), reactive arthritis (Reiter's syndrome), psoriatic arthropathy and some other diseases. Most patients with spondyloarthritis are carriers of a specific allele of the human major histocompatibility complex locus B - HLA-B27. For screening, diagnosis, and prognosis of spondyloarthritis, genetic research(typing), which allows us to identify the presence or absence of the HLA-B27 allele.

    About 8% of people are carriers of the HLA-B27 allele (HLA-B27-positive, in the literature you can also find the expression “carriers of the HLA-B27 antigen”). The prevalence of ankylosing spondylitis in HLA-B27-positive people is 1.3%. It occurs in % of HLA-B27-positive patients who have a blood relative with ankylosing spondylitis, which corresponds to a 16-fold increase in the risk of this disease in the presence of a family history. A positive HLA-B27 typing result increases the risk of developing any disease from the group of spondyloarthritis by 20 times. That's why HLA typing-B27 can be used to assess the risk of developing spondyloarthritis.

    In the differential diagnosis of articular syndrome, the presence of HLA-B27 is a characteristic feature of spondyloarthritis: this allele is present in% of patients with ankylosing spondylitis, in% with reactive arthritis, in 50% with psoriatic arthropathy and in% with juvenile ankylosing spondylitis. The presence of HLA-B27 in patients with other diseases affecting the joints (gout, rheumatoid arthritis, septic arthritis) does not exceed 7-8%. HLA-B27 typing is particularly useful when the diagnosis of a disease cannot be formulated based on basic diagnostic criteria.

    HLA-B27 typing is of greatest importance in the diagnosis of early ankylosing spondylitis. In most cases, 5-10 years pass between the appearance of the first signs of the disease and the final diagnosis. This is due to the fact that the main diagnostic criterion is the radiological signs of sacroiliitis, which develops only after several years of inflammation in the sacroiliac joints. Patients with complaints of back pain without radiological signs of sacroiliitis actually do not come to the attention of a rheumatologist. Detection of HLA-B27 in such a situation may be sufficient grounds for referral to a specialist. Typing is indicated when examining a patient with complaints of inflammatory pain in the back in the absence of radiological signs of sacroiliitis or when examining a patient with asymmetric oligoarthritis.

    The presence of HLA-B27 is associated with an increased risk of extra-articular manifestations of ankylosing spondylitis. The most significant associations are the HLA-B27 allele and acute anterior uveitis, aortic valve insufficiency, acute leukemia, IgA nephropathy and psoriasis. HLA-B27-positive patients are at higher risk of tuberculosis and malaria. On the other hand, the presence of HLA-B27 also plays a certain “protective” role: some viral infections (influenza, herpes virus infection type 2, infectious mononucleosis, hepatitis C and HIV) occur in a milder form in HLA-B27 carriers.

    It should be noted that there are other, both hereditary and acquired, risk factors for the development of spondyloarthritis. The absence of HLA-B27 does not contradict the diagnosis of ankylosing spondylitis, in which case it is classified as HLA-B27-negative and develops at a later age than HLA-B27-positive spondylitis.

    In addition, HLA-B27 typing is used to predict complications of rheumatoid arthritis. The presence of HLA-B27 is associated with a threefold increase in the risk of atlantoaxial subluxation.

    What is the research used for?

    • For differential diagnosis of articular syndrome (seronegative spondyloarthritis, rheumatoid and septic arthritis, gout and others).
    • For screening, diagnosis and prognosis of ankylosing spondylitis.
    • To assess the risk of developing atlantoaxial subluxation in rheumatoid arthritis.

    When is the study scheduled?

    • For articular syndrome: asymmetric oligoarthritis, especially in combination with pain in the lumbar region of the back of an inflammatory nature (morning stiffness for more than 1 hour, improvement with physical activity, worsening at night) and signs of enthesitis.
    • With a family history of ankylosing spondylitis.
    • For rheumatoid arthritis.

    What do the results mean?

    Reference values: negative.

    • occurs in% of patients with ankylosing spondylitis and juvenile ankylosing spondylitis,
    • in% of patients with reactive arthritis,
    • in 50% with psoriatic arthropathy,
    • in 7-8% of people in the European population.
    • observed in% of people in the European population,
    • in 10% of patients with ankylosing spondylitis (HLA-B27-negative spondylitis).

    What can influence the result?

    • Hemolysis of lymphocytes in a blood sample results in a false negative result.
    • The presence of HLA-B27 increases the risk of developing any disease from the group of spondyloarthritis by 20 times.
    • The absence of HLA-B27 does not contradict the diagnosis of ankylosing spondylitis.

    Who orders the study?

    Rheumatologist, surgeon, general practitioner, chiropractor.

    1. Sieper J. How to screen for axial spondyloarthritis in primary care? Curr Opin Rheumatol. 2012 Jul;24(4):359-62. Review.
    2. McHugh K, Bowness P. The link between HLA-B27 and SpA-new ideas on an old problem. Rheumatology (Oxford). 2012 Sep;51(9):.
    3. Sheehan NJ. HLA-B27: what's new? Rheumatology (Oxford). 2010 Apr;49(4):621-31. Epub 2010 Jan 18.
    4. Sheehan NJ. The ramifications of HLA-B27. J R Soc Med. 2004 Jan;97(1):10-4.
    5. Chernecky C. C. Laboratory Tests and Diagnostic Procedures / S.S. Chernecky, V.J. Berger; 5th ed. - Saunder Elsevier, 2008.

    Reactive arthritis (Reiter's syndrome). Causes, symptoms, signs, diagnosis and treatment of pathology

    Reactive arthritis belongs to rheumatological diseases and is treated in departments of this profile. They occur in approximately 2.5% of cases after intestinal infections and in 0.8% of cases after genitourinary infections. The disease mainly affects people aged 20 to 40 years. According to various studies, men get sick approximately 10–15 times more often than women (especially a big difference in prevalence in Reiter's syndrome). An uneven distribution of incidence depending on geographical location has also been noted. This is explained by the different prevalence of infections that can cause reactive arthritis.

    Representatives of some nations have a certain predisposition to the development of reactive arthritis and Reiter's syndrome. This is explained by genetic factors. Almost 20% of the population of Scandinavian countries, approximately 4% of the population of northern African countries, and only 0.5–2% of Japanese have antigens that increase the likelihood of this pathology. In Europe, on average, the prevalence of these antigens is 5–8%. Reactive arthritis is an inflammatory process that is caused by the activity of the body's own immune system. Joint damage is explained by the effects of antibodies that attack connective tissue cells. These antibodies are absent in a healthy body, but appear as a result of infectious diseases. There are a number of infections in which the risk of developing reactive arthritis is especially high.

    The connection between infection and cells is explained by the fact that in the structure of bacteria and body cells there are proteins similar in structure (this phenomenon is also called molecular mimicry). The immune system uses these proteins to recognize the pathogen and attack it. Joint cells are attacked by mistake due to similarities in structural proteins. The genetic factor also plays a certain role. It has now been clearly established that the presence of specific genes increases the risk of developing arthritis after infection.

    With Reiter's syndrome, not only the joints are affected, but also the mucous membrane of the eyes. In the classic course, there are also signs of chronic genitourinary infection. The mechanism of inflammation in Reiter's syndrome is the same as in other reactive arthritis. Since the immune system needs time to recognize the disease and form specific antibodies, joint damage occurs some time after the onset of the infectious disease. Typically this period ranges from 2 weeks to 2 months.

    Most often, reactive arthritis develops after the following infectious diseases:

    • chlamydia;
    • other genitourinary infections;
    • intestinal infections;
    • respiratory infections;
    • other infectious diseases.

    The most common types of chlamydia are:

    • C. psittaci;
    • C. pneumoniae;
    • C. trachomatis.

    The latter type is most important in the development of Reiter's syndrome. It is the causative agent of urogenital chlamydia in more than 90% of cases. The reason for the launch of the autoimmune process is antigens - special proteins present in the structure of chlamydia.

    The most important chlamydia antigens are:

    • heat-stable antigen;
    • heat labile antigen.

    These antigens are business card bacteria. Thanks to them, it is possible to determine the type and subtype of the pathogen. Antigens stimulate the production of antibodies, which serological studies are aimed at searching for.

    Urogenital chlamydia is one of the most common genitourinary infections in both men and women. This partly explains the frequency of cases of reactive arthritis in medical practice (namely Reiter's syndrome).

    In addition to chlamydia, in rare cases the disease can be triggered by ureaplasma or mycoplasma infection. These microorganisms are also carriers of antigens that can trigger a pathological chain leading to the development of reactive arthritis. Unlike chlamydia, in the case of mycoplasmosis, the mucous membrane of the eyes is rarely affected. Thus, we are talking about damage to only the joints.

    The group of mycoplasmas that can cause reactive arthritis includes:

    The following intestinal infections can lead to the development of reactive arthritis:

    Eye damage typical of Reiter's syndrome is usually not observed after these infections. These microorganisms can persist in the body for a long time, supporting the inflammatory process in the joints. In this regard, careful diagnosis and comprehensive treatment of the infection are necessary to achieve recovery. In medical practice, there are cases of the development of reactive arthritis after respiratory (breathing) infections. Most often, these are certain types of influenza or other viral diseases. In the general structure of reactive arthritis, respiratory infections account for no more than 5–10% of cases. Proteins in viruses rarely bear much resemblance to body cells. As a rule, for the development of arthritis, there must be a congenital genetic predisposition. In rare cases, reactive arthritis can develop after viral hepatitis, HIV or other viral or bacterial infections. The mechanism of inflammation development remains the same as with the above infections. The most important feature is that the microorganisms themselves in reactive arthritis are never found in the joints. Damage to connective tissue occurs exclusively by antibodies. Many doctors rush to make a diagnosis, which is why they define reactive arthritis without ruling out the usual septic lesion (when the microbe itself enters the joint through the bloodstream and causes inflammation).

    Reactive arthritis that developed after vaccination in children is considered separately. They are a rare complication that is observed in no more than 0.2 - 0.5% of cases. Joint damage in these cases is caused by the introduction of microbial agents into the body, which trigger autoimmune reaction. The first symptoms of the disease appear within a month after vaccination. Along with damage to the joints, a moderate increase in temperature, general anxiety, poor appetite. Typically, reactive arthritis in children after vaccination is mild; spontaneous recovery is often observed within 10–15 days. However, to avoid the development of the disease, it is necessary to consult a rheumatologist for advice.

    Reactive arthritis rarely develops after the use of vaccines against the following infections:

    Vaccination of adults for special indications can also trigger an autoimmune process. In adults, arthritis will be somewhat more severe and will require a separate course of treatment. In addition to infectious agents, genetic factors play a role in the development of reactive arthritis and Reiter's syndrome. First of all, this is a special antigen HLA-B27. It is a protein located on the surface of cells that predisposes to the development of autoimmune joint damage. If this antigen is present, there is a chance that infectious process complicated by reactive arthritis, increases 5-10 times. In addition, the disease in these cases will be more severe and respond worse to treatment. It is believed that there are other congenital genetic factors that may predispose to the development of reactive arthritis. The first symptoms of reactive arthritis usually appear 2 to 10 weeks after the onset of the infectious disease. During this time, the immune system recognizes foreign antigens and produces a sufficient amount of antibodies to them. Antibodies begin to attack not only the infection, but also the body’s own cells, which leads to the appearance of the first symptoms. In some cases, reactive arthritis can develop in parallel with an infectious disease. This happens if the patient’s body has already come into contact with this infection before. For example, if a patient has had chlamydia in the past, his body has retained cellular memory. Then, when chlamydia enters the body again, antibodies will be produced faster, and arthritis will develop in parallel with a genitourinary infection.

    Symptoms of reactive arthritis can be divided into the following groups:

    • general symptoms;
    • symptoms of concomitant infections;
    • articular manifestations;
    • symptoms of Reiter's syndrome;
    • skin symptoms;
    • specific lesions of other organs.

    General symptoms are manifestations of reactive arthritis that do not relate specifically to any system, but affect the entire body as a whole. First of all, these include an increase in body temperature. The temperature is constantly elevated, without significant changes during the day. At the same time, indicators rarely exceed 38 degrees. In addition to the increase in temperature, significant weight loss, muscle weakness, and sleep disturbances may be observed. As explained above, reactive arthritis develops after infectious diseases. Some of them already pass at the time of damage to the joints, but some become chronic. In such cases, in addition to the symptoms of arthritis itself, the patient will experience moderate symptoms infectious diseases. They are determined by location primary focus infections in the body.

    In parallel with joint damage, signs of the following types of infection may be observed:

    • Urogenital infections. Signs of a genitourinary infection include redness of the opening urethra(in men), burning sensation when urinating, frequent urge to urinate. Women with chronic infection may experience dysmenorrhea (failures menstrual cycle) and increased pain during menstruation. In addition, genitourinary infections during exacerbation lead to discharge from the urethra ( this symptom more noticeable in men).
    • Intestinal infections. With chronic intestinal infections, symptoms are usually scant. However, patients may recall episodes of diarrhea (lasting from several days to several weeks) and vomiting. Also typical signs are nausea, moderate abdominal pain, loss of appetite, increased gas formation.
    • Respiratory infections. The main symptoms of respiratory diseases will be a prolonged dry cough, sneezing, hoarseness, nasal discharge, moderate redness of the mucous membrane of the throat. These are all symptoms typical of the common cold. However, as mentioned above, such infections can also trigger an autoimmune process affecting the joints.

    Signs of joint damage are leading in any type of reactive arthritis. As a rule, they appear already 2–3 weeks after the onset of the disease. The intensity of manifestations can increase slowly, over several days, or develop quickly, over 12 to 24 hours. In most cases, it is the symptoms associated with joint inflammation that lead the patient to consult a doctor.

    Joints are affected mainly in the lower extremities. Signs of inflammation are asymmetrical (that is, if the knee joint is affected on the right leg, then similar symptoms are usually not observed on the left). At the same time, signs of inflammation appear on 3–4 joints (oligoarthritis). The lesion occurs in an ascending manner - from the underlying joints upward. The joints of the toes are often the first to be affected.

    Typical joint manifestations of reactive arthritis are:

    • Moderate joint pain. They are usually more pronounced in the morning and may worsen with movement.
    • Swelling of the joints. The swelling is sometimes noticeable even to the naked eye. On palpation (palpation), the tissues around the joint are not dense, slightly swollen.
    • Redness of the skin over the joint. Redness of the skin is explained by the inflammatory process, in which blood rushes to the tissues.
    • Damage to periarticular structures. The inflammatory process in reactive arthritis is not limited to the articular surfaces of the bones. As the disease progresses, inflammation of the joint capsule (bursitis), tendons (tendonitis) and tendon sheaths (tenosynovitis) is observed. If these inflammatory processes develop in the foot area (plantar fasciitis), the patient may experience severe pain when walking. Outwardly, this is manifested by noticeable lameness.
    • Enlarged lymph nodes. In case of severe inflammation The lymph nodes increase due to increased outflow of fluid from tissues. If the joints of the upper extremities are affected, the lymph nodes in the armpits are palpated, and if the joints of the lower extremities are affected, the inguinal lymph nodes are palpated. During palpation, they are usually painless and mobile (easily move under the skin).

    Depending on other predisposing factors (presence of the HLA-B27 antigen, previous injuries in the joint area, etc.), the symptoms of reactive arthritis may progress. Sometimes the disease occurs in the form of polyarthritis (multiple joint damage). The peak usually occurs 5–7 weeks after acute infectious manifestations have subsided.

    In reactive arthritis, the following joints can be affected (from more commonly affected joints to rarer variants):

    • knee;
    • ankle;
    • interphalangeal joints of the toes and hands;
    • elbows;
    • wrist (hand);
    • others (intervertebral, sacroiliac, sternoclavicular, mandibular).

    Reiter's syndrome is characterized by a special set of symptoms that distinguishes it even from many other reactive arthritis. Another name for Reiter's syndrome is urethro-oculosynovial syndrome. This indicates the main areas of damage. First of all, symptoms of a genitourinary infection (usually chlamydia) appear, then signs of inflammation of the mucous membrane of the eyes, and then joint symptoms. This is what a typical triad looks like in Reiter's syndrome. However, other symptoms characteristic of reactive arthritis are often observed.

    The distinctive symptoms of Reiter's syndrome are:

    • Symptoms of eye damage. They can be observed as early as 1 – 2 weeks after an exacerbation of chlamydia. Symptoms can be either unilateral or bilateral. First of all, patients complain of redness of the eyes, their dryness or, conversely, tearing, moderate cutting pain. With severe inflammation, a sensation of a foreign body in the eye or photophobia may appear. However, conjunctivitis (inflammation of the mucous membrane of the eye) in some cases can be asymptomatic. If the manifestations of the disease lasted 1–2 days and did not cause serious discomfort, patients may not notice the pathology.
    • Sausage-shaped thickening of the toes is a consequence of inflammatory edema and swelling in the area of ​​the interphalangeal joints.
    • Signs of damage to the genitourinary tract (described above in the corresponding section). In addition, due to chronic chlamydial infection, prostatitis (in men) and cervicitis or vaginitis (in women) can develop in parallel.

    Reiter's syndrome is characterized by a chronic relapsing course. In other words, the above symptoms appear and disappear for a while. This is mainly due to exacerbations of chlamydial infection. If chlamydia is completely cured, arthritis will disappear. However, after unprotected sexual intercourse and repeated contact with chlamydia, the disease will develop again. Skin symptoms in patients with reactive arthritis are relatively rare. They usually occur simultaneously with the articular manifestations of the disease, but can also occur during other periods of the disease. Skin symptoms can vary - from redness of individual areas of the skin to the appearance of small erosions. The latter resemble skin lesions due to psoriasis. To the touch, the affected areas of the skin are firm, but painless. Sometimes keratoderma is observed - roughening of the skin and its increased peeling. This symptom primarily affects the skin of the palms and soles. Along with skin damage, signs of damage to the mucous membranes often appear. Erosion on the mucous membrane of the mouth and genitals can complement the main triad of symptoms in Reiter's syndrome. Lesions of the skin and mucous membranes in reactive arthritis are never purulent, because pus suggests the presence of microbes. In rare cases, an autoimmune process can affect the functioning of other organs and systems, leading to tissue inflammation. This will lead to the appearance of symptoms unusual for reactive arthritis. Then the doctor may have problems with diagnosis, especially if the signs of joint damage are minor.

    In rare cases, with reactive arthritis, symptoms of damage to the following organs and tissues may appear:

    • Kidney damage. May manifest as urinary retention and changes in its biochemical and cellular composition.
    • Damage to the heart muscle. Myocardial damage is manifested by periodic disturbances in heart rhythm. Specific signs can be seen on an ECG (electrocardiogram).
    • Damage to the pericardium (heart sac). Pericarditis after an infection can cause moderate chest pain and pericardial friction rub during auscultation (listening).
    • Polyneuritis (inflammation of peripheral nerves). Polyneuritis develops extremely rarely in advanced forms of the disease. The patient may complain of moderate migrating pain, sensory disturbances, and rapid numbness of the limbs.

    Thus, the symptoms of reactive arthritis can be very diverse. Signs of joint damage are almost always present. Inflammation of the mucous membrane of the eyes and accompanying symptoms are characteristic of Reiter's syndrome after chlamydial infection. Other manifestations of the disease may vary from case to case.

    Depending on the duration of the above symptoms, there are following forms course of reactive arthritis:

    • acute course of reactive arthritis – up to six months;
    • protracted course - from six months to a year;
    • chronic course - more than 1 year.

    This classification plays a certain role in the selection of treatment. If the disease becomes protracted or chronic, it is necessary to reverse Special attention to eradicate an infection that appears to be difficult to treat. At the moment, no unified diagnostic criteria have been developed that would be the standard for detecting reactive arthritis. This is largely due to the diversity of manifestations of this disease and its similarities with other rheumatological pathologies. Each of the stages in the diagnosis of reactive arthritis is very important, as it can provide information about the course of the disease and exclude other pathologies. The first stage is a general examination of the patient and collection of anamnesis. Then, to clarify the diagnosis, laboratory and instrumental methods. A general examination is carried out at a doctor's appointment. The initial examination can be carried out by a general practitioner or family doctor, but a rheumatologist can collect the most information about joint damage. At accompanying signs damage to the eyes or other organs seek the help of appropriate specialists.

    During a general examination, the doctor pays attention to the following features:

    • Nature of joint damage. In reactive arthritis, including Reiter's syndrome, the joints are usually affected asymmetrically. In addition, unlike many other diseases, the inflammatory process affects the joint capsule and muscle tendons. The doctor discovers the corresponding symptoms precisely during an objective examination of the patient.
    • Erosion on the oral mucosa. Erosion on the mucous membranes of the mouth (less often the genitals or on the skin) also increases the likelihood that the patient has reactive arthritis. Often, patients notice small ulcerations, but do not attach much importance to them, since they cannot associate them with joint damage. Because of this, the doctor must carefully examine the mucous membranes himself.
    • Symptoms of eye damage. Damage to the eyes and joints is characteristic of Reiter's syndrome. In other types of reactive arthritis, it is most often absent. Thus, signs of eye inflammation indicate that further tests need to be done, aimed at looking for a genitourinary infection.
    • Signs of chronic genitourinary infection. If reactive arthritis is suspected, the doctor should examine the external genitalia. Redness of the mucous membrane may indicate a chronic inflammatory process. This will guide diagnostic tests and help rule out other joint diseases.

    In addition, the doctor clarifies whether the patient has been ill in recent months various infectious diseases. Pay attention to such characteristic manifestations such as itching in the genital area, burning during urination, vomiting or diarrhea, as well as cough and cold symptoms. The absence of these symptoms when interviewing the patient does not exclude the diagnosis of reactive arthritis. The fact is that such infections often occur latently, without symptoms and end in spontaneous recovery (without specific treatment). However, the absence of signs of acute infection upon interview reduces the likelihood of diagnosis. Laboratory research methods are the most informative in diagnosing reactive arthritis and Reiter's syndrome. With their help, you can determine changes in the blood test characteristic of a given disease, as well as detect signs of the infectious process that started the pathological chain. Based on the results of laboratory tests, a final diagnosis can be made.

    To diagnose reactive arthritis, the following laboratory research methods are used:

    A blood test for reactive arthritis is of great importance, since many characteristic changes can be detected in it. Depending on the purpose of the study, either blood from a vein or blood from a finger can be taken. If necessary, blood will be taken several more times during treatment to confirm a positive trend. Changes in reactive arthritis and Reiter's syndrome will be observed both in general and in biochemical blood tests. First of all, they indicate the presence of an inflammatory process.

    With reactive arthritis, the following changes may be observed in the blood test:

    • Leukocytosis. An increase in the level of leukocytes over 9 million/ml is a sign of an inflammatory process. With reactive arthritis, leukocytosis will be moderate, usually up to 11 - 12 thousand.
    • Increased erythrocyte sedimentation rate (ESR). This indicator is also a sign of the inflammatory process. The norm is up to 10 mm/h for men, and up to 15 mm/h for women. False increase in ESR may occur during pregnancy or in older people (after 60 years).
    • Moderate anemia. Decreased levels of red blood cells and hemoglobin (less than 110 g/l).
    • Detection in blood C-reactive protein. This protein indicates the presence of an acute inflammatory process in the body. Its concentration is usually directly proportional to the intensity of inflammation. In addition to C-reactive protein, other signs of the inflammatory process can be detected - sialic acids, seromucoid.

    Other specific tests are performed to rule out certain diseases. First of all, these are rheumatoid factor and LE cells. These tests are not available in all laboratories and require a separate referral from your doctor. Urinalysis in certain cases can also indicate the presence of an inflammatory process. In addition, many rheumatic diseases that affect the joints also affect kidney function. Thus, a urine test is performed, among other things, to detect kidney damage.

    Characteristic changes in urine analysis for reactive arthritis are:

    • Proteinuria is the excretion of increased amounts of blood proteins in the urine.
    • Microhematuria is the presence of a small amount of blood in the urine. Usually this amount is so small that it does not change the color of the urine and cannot be seen by the naked eye. Blood is detected using a special biochemical analysis.
    • Leukocyturia – increased secretion leukocytes in urine. May be observed due to leukocytosis, infectious or inflammatory process in the kidneys.

    A stool test is performed to detect an intestinal infection that could cause the development of reactive arthritis. With its help it is sometimes possible to detect increased amount bacteria from the families Salmonella, Shigella, Yersinia. The patient is asked to bring the feces themselves in a special sterile container. A repeat test may be needed at the end of treatment to confirm its success. As noted above, this antigen greatly increases the risk of developing a number of joint diseases, including reactive arthritis. The analysis is prescribed to patients with signs of joint damage at an early stage, when symptoms that allow an accurate diagnosis have not yet appeared. If a patient has the HLA-B27 antigen, the likelihood that reactive arthritis caused joint damage is very high. Therefore, the doctor will be able to start treatment earlier and prevent possible complications.

    Analysis is carried out PCR method(polymerase chain reaction). It allows you to accurately determine the presence of genes in DNA responsible for the formation of a given antigen. The analysis requires the patient's venous blood. It is not recommended to smoke before donating blood (at least an hour before the test), as this may affect the final results.

    If the test comes back positive, it increases the likelihood that the patient has reactive arthritis by about 20 times. In other words, the doctor can be almost sure of the correct diagnosis already at an early stage of the disease. The chance that if the test result is positive, the inflammation of the joints is still not of an autoimmune nature is approximately 10 - 15%. A negative HLA-B27 test result does not exclude the diagnosis of reactive arthritis, but it greatly reduces its likelihood. Microbiological examination is done to detect various infections that could lead to the development of reactive arthritis or damage to joints of another nature. First of all, they look for genitourinary and intestinal infections, since they are usually complicated by inflammation of the joints. In the diagnosis of respiratory infections, microbiological research methods are almost never used.

    To detect infections that led to reactive arthritis, the following materials from the patient can be examined:

    • blood;
    • urine;
    • synovial fluid (fluid obtained from the joint cavity during puncture);
    • smear from the mucous membrane of the genital organs.

    The essence microbiological research consists in accurately determining the type of bacteria. When examining blood, a microbiological test will be positive only in case of bacteremia (when the pathogen circulates in the blood). This is not typical for reactive arthritis, but analysis may be ordered to exclude other forms of joint damage. In the urine, pathogenic microorganisms can appear with simultaneous kidney damage or with the development of infection in the lower urinary tract. It is safer, however, in this case to take a smear or scraping from the mucous membrane.

    To detect infection in patients with reactive arthritis, the following microbiological methods are used:

    • Microscopy. Microscopic examination involves the usual analysis of a sample under a microscope. The doctor pays attention to the shape of the bacteria and their susceptibility to certain dyes. Microscopy can be done by taking a smear from the genital mucosa or by examining stool.
    • Sowing on nutrient media. Another way to detect microbes is to inoculate them on special nutrient media. Under favorable conditions, microorganisms will multiply, forming entire colonies. By observing the growth of colonies and their characteristics, the doctor can determine the type of pathogen. Cultures can be done from stool, urine, blood, synovial fluid, smear from the mucous membrane.
    • Antibioticogram. An antibioticogram is a microbiological analysis that is carried out after obtaining a colony of the pathogen. In laboratory conditions, doctors check which antibiotics a given pathogen is most sensitive to. This helps prescribe the most effective treatment. An antibioticogram is prescribed to patients with chronic intestinal or genitourinary infections who have already undergone treatment in the past.
    • PCR. The polymerase chain reaction, which was already mentioned above, can also be successfully used to detect various infections. In this case, the DNA of the pathogen is searched. The study is expensive but produces very reliable results. PCR detects signs of infection even when acute period the disease ended, and other microbiological tests were inconclusive. With reactive arthritis, this is very important, because joint damage usually occurs a few weeks after the illness.

    Serological studies are a group of tests that are based on searching in the blood for specific antibodies against a specific infection. These tests do not give a 100% result, since the infectious process at the time of damage to the joints has already ended. However, antibodies continue to circulate in the blood for some time (usually 2 weeks to 2 months, depending on the disease). During this period, using serological tests, it is possible to confirm that the patient has suffered a particular infection. For serological testing, the patient's blood is taken. The result is usually obtained within 24 hours. In Reiter's syndrome, for example, tests for antibodies against chlamydia are detected in 50–65% of patients. Enough high performance and for other pathogens. The detection of antibodies indicates a high probability of reactive joint damage in response to infection, making it possible to exclude other rheumatological diseases. Synovial fluid is obtained by puncture of the inflamed joint. Normally, this fluid promotes better gliding of the articular surfaces and improves movement in the joint. The puncture is performed under local anesthesia. The doctor inserts a special needle and collects a certain amount of synovial fluid. It is subsequently used for microbiological and cytological studies. In reactive arthritis, no pathogens are found in the synovial fluid, since inflammation is caused not by infection, but by the influence of the body’s own immunity. At the same time, you can find antibodies to the corresponding infection (most often to chlamydia). There will also be high level leukocytes, which indicates an intense inflammatory process.

    Instrumental diagnostics are necessary, first of all, to clarify the nature of joint damage. Many rheumatological diseases are associated with deformation of the articular surfaces, which are easily determined during special studies. With reactive arthritis, characteristic changes are usually not observed. Therefore, in the first stages of the disease, in acute cases, prescribe instrumental studies pointless. However, if the arthritis is protracted or chronic (which is not very typical for reactive autoimmune processes), there is a need for additional diagnostic procedures. Prolonged inflammation at this point already leads to some structural changes.

    The following instrumental examination methods are used in the diagnosis of reactive arthritis:

    • radiography;
    • ultrasound examination (ultrasound);
    • arthroscopy.

    Radiography is a diagnostic method based on obtaining images using x-rays. The rays pass through the thickness of the tissue and fall on a special sensitive film. Subsequently, based on the resulting image, doctors make conclusions about changes in the joint.

    In chronic arthritis, the following changes may be observed on the radiograph:

    • Periarticular osteoporosis. In the picture it appears as an area of ​​softening of the bone tissue near the joint, under the cartilage.
    • Narrowing of the joint space. Normally, there is a certain distance between the bones in the image. With intense inflammation due to edema and swelling of the cartilage, it decreases.
    • Erosion of the articular surface. This defect in the image looks like unevenness or roughness of the surface of the cartilage in the joint cavity.
    • Bone spurs. Bone spurs are small growths that are usually located on the heel bones, but can sometimes appear on the wrist bones or vertebrae.
    • Signs of damage to the intervertebral joints.

    Despite the fact that radiography is a quick, cheap and painless method of examination, it is not prescribed very often. Only in 8–10% of patients with reactive arthritis or Reiter's syndrome will it be possible to notice characteristic changes in the picture. However, it is with the help of radiography that a number of other rheumatological pathologies can be excluded. The fact is that many of them lead to severe joint deformation, which is not typical for reactive arthritis. X-rays of joints can be carried out, including for pregnant women, if there is an urgent need for this. Modern devices make it possible to minimize the radiation dose and focus the rays within the joint. In addition, special screens will be used to protect the most sensitive parts of the body. Ultrasonography consists of examining the joint using sound waves. It allows you to identify a number of pathologies that are invisible on an x-ray. In particular, we are talking about inflammatory processes in the periarticular tissues.

    Ultrasound can detect following signs reactive arthritis:

    • bursitis;
    • tendinitis;
    • Tenosynovitis.

    In addition, ultrasound can provide information about damage to the kidneys or pericardium if the inflammatory process is very intense. Ultrasound is also a painless, quick and cheap test that has virtually no contraindications. The examination lasts 3–5 minutes for each of the affected large joints. The use of this research method in cases of damage to small joints is pointless, because the devices do not have sufficient high resolution. In other words, minimal foci of inflammation and changes in the joints simply cannot be distinguished. Arthroscopy is a relatively rare method of examination for reactive arthritis. The essence of the method is to introduce a special camera into the joint cavity. With its help, the doctor has the opportunity to assess with his own eyes the condition of the tissues within the joint. In the vast majority of cases, arthroscopy refers to the examination of the knee joint. It is large enough for this procedure. Other joints, due to their anatomical structure, are less suitable for this study.

    During arthroscopy, the doctor can evaluate the condition of the following structures of the knee joint:

    • articular cartilage;
    • synovial membrane;
    • cruciate ligaments;
    • surface of the menisci.

    In reactive arthritis, foci of inflammation are noted during arthroscopy. Often a small amount of fluid and fibrin deposits are found in the joint. The synovium may be hyperemic (reddened due to increased blood flow). This procedure It is painful and is therefore performed under anesthesia. In addition, it requires special equipment, which increases the cost of the study. Of the possible complications, the most dangerous is the introduction of infection into the joint cavity with the development of septic arthritis. All this limits the use of arthroscopy in medical practice. It is prescribed only in cases where it is impossible to clarify the diagnosis or the effectiveness of treatment by other means. In addition to the above signs of reactive arthritis, there are a number of indications for excluding this diagnosis. Finding any of these criteria in a patient will force the physician to continue searching for the correct diagnosis, despite the presence of HLA-B27 antigen, recent infection, and other typical features.

    The criteria for excluding reactive arthritis are the following diagnostic data:

    • detection of rheumatoid factor in the blood (typical of other rheumatic joint diseases);
    • detection of tophi - specific nodes with uric acid salts (typical of gout);
    • rheumatic and rheumatoid nodules on the skin;
    • psoriasis of the scalp;
    • increased titer of antistreptolysin-O.

    Treatment of reactive arthritis should be carried out by rheumatologists. If it develops in parallel with an acute infectious disease, an infectious disease specialist may become the treating specialist. The main role will be played by which symptoms predominate in a particular patient. In case of Reiter's syndrome with severe eye damage, consultation with an ophthalmologist may be necessary.

    Treatment of reactive arthritis and Reiter's syndrome can be carried out as follows: inpatient conditions(in the hospital) and at home. As a rule, at first the patient is admitted to the hospital for a proper examination and an accurate diagnosis. With moderate intensity of symptoms, hospitalization is not necessary. Then the responsibility for carrying out all diagnostic procedures falls on the patient himself.

    For unconditional hospitalization of a patient in the first stages, there are the following indications:

    • the need for individual selection of anti-inflammatory drugs;
    • exacerbation of the disease during treatment with basic anti-inflammatory drugs;
    • appearance atypical forms diseases (pericarditis, nephritis, vasculitis - inflammatory lesion vessels);
    • suspicion of septic (bacterial) arthritis;
    • the need for arthroscopy or other invasive studies;
    • high temperature and severe general condition of the patient.

    Regardless of whether the patient is being treated in hospital or at home, the main role is played by drug treatment. Only properly selected drugs can quickly improve the patient’s condition and prevent the development of the disease. Self-medication or treatment folk remedies with reactive arthritis it is dangerous, as it can cause a deterioration in the patient’s condition.

    Drug treatment of reactive arthritis can be divided into several main areas:

    • elimination of the inflammatory process;
    • treatment of intestinal or respiratory infection;
    • treatment of chlamydia;
    • treatment of conjunctivitis in Reiter's syndrome.

    The main problem with reactive arthritis and Reiter's syndrome is inflammation of the joints. Antibiotic therapy helps eradicate the infection that started pathological mechanism, but it does not in any way affect the inflammatory process itself. Even after the death of microorganisms, antibodies may still circulate in the blood for some time, continuing to attack connective tissue. To quickly improve the patient's condition, various anti-inflammatory drugs are prescribed. Their selection and dosage is made by the attending physician depending on the severity of the disease.

    The main anti-inflammatory drugs used for reactive arthritis

    Antigen HLA-B27 can be found in healthy people (6-8% of the population), as well as in patients with nonspecific ulcerative colitis, with Crohn's disease. Immunoglobulins of various classes (G, A, M, E, D) are studied to diagnose primary or secondary immunodeficiency. In rheumatic diseases, IgA immunodeficiency is noted, you just need to take into account the fact that it may be due to the influence of such drugs, How penicillamine, sulfasalazine, captopril An increase in IgA content is often observed in seroregative spondyloarthropathies. Important diagnostic criteria for rheumatic diseases are the detection of cryoglobulins in the blood and circulating immune complexes(CEC), Type III cryoglobulinemia occurs in SLE, RA, systemic scleroderma, Sjögren's syndrome. The presence of this protein in the blood should alert the doctor to the possibility of complications in such patients in the form of vasculitis, purpura, glomerulonephritis, neuropathy, and Raynaud's syndrome. Detection of cryoglobulins in the blood (more than 0.016 units of optical mass) for SLE associated with the activity of the process and kidney damage, and in Sjögren's syndrome - with the development of systemic manifestations of the disease. The study of the content of circulating immune complexes in the blood of rheumatological patients has a certain value. An increase in their concentration reflects the inflammatory and immunological activity of the pathological process in SLE, RA, and seronegative spondyloarthropathies. Certain diagnostic value presents a study of some blood enzymes (especially in muscle pathology), such as creatine phosphokinase (CPK), alkaline phosphatase, transaminases, lactate dehydrogenase, etc. However, an increase in their levels in the blood is also possible in some non-rheumatic diseases.
    Source:

    A study to identify predisposition to diseases from the group of seronegative spondyloarthritis, during which, using the method flow cytometry determined HLA-B27 antigen.

    Synonyms Russian

    Human leukocyte antigen B27

    Immunogenetic marker HLA-B27

    Differential diagnosis of autoimmune diseases

    English synonyms

    HLA typing, flow cytometry (flow cytofluorometry)

    Ankylosing spondylitis Histocompatibility Antigen

    Ankylosing spondylitis Human Leukocyte Antigen

    Research method

    Flow cytometry.

    What biomaterial can be used for research?

    Venous blood.

    How to properly prepare for research?

    Eliminate alcohol from your diet for 24 hours before the test.

    Do not eat for 12 hours before the test.

    Completely avoid taking medications for 24 hours before the test (in consultation with your doctor).

    Avoid physical and emotional stress for 24 hours before the test.

    Do not smoke for 30 minutes before the test.

    General information about the study

    Antigen HLA-B27 – this is specific protein, detectable on the surface of immune cells. It belongs to the proteins of the human major histocompatibility complex, which provides various immune responses. Carriage of the HLA-B27 antigen is associated with an increased risk of developing diseases from the group of seronegative spondyloarthritis. Thus, this antigen can be detected in 90-95% of patients with ankylosing spondylitis (Bechterew's disease), 75% of patients with reactive arthritis (Reiter's syndrome), 50-60% of patients with psoriatic arthropathy, 80-90% of patients with juvenile ankylosing spondylitis and 60-90% of patients with enteropathic arthritis. The presence of the HLA-B27 antigen in patients with other joint diseases (gout, rheumatoid arthritis, septic arthritis) does not exceed 7-8%. Taking into account this feature, in The detection of the HLA-B27 antigen is of great diagnostic importance in the clinic of rheumatological diseases.

    Determination of the HLA-B27 antigen is of greatest importance in the diagnosis of early ankylosing spondylitis. In most cases, between the appearance of the first signs of the disease and the final diagnosis 5-10 years pass. This is due to the fact that the main diagnostic criterion for the disease is radiological signs of sacroiliitis, which develops only after several years of inflammation in the sacroiliac joints. Patients with complaints of back pain without radiological signs of sacroiliitis actually do not come to the attention of a rheumatologist. Detection of HLA-B27 in such a situation may be sufficient grounds for referring the patient to a specialized specialist.

    Determination of the HLA-B27 antigen is indicated when examining a patient with complaints of inflammatory pain in the back in the absence of radiological signs of sacroiliitis or when examining a patient with asymmetric oligoarthritis.

    The presence of HLA-B27 is associated with an increased risk of extra-articular manifestations of ankylosing spondylitis. The most significant associations are the HLA-B27 antigen and acute anterior uveitis, aortic valve insufficiency, acute leukemia, IgA nephropathy and psoriasis. HLAB27 – positive patients are more at risk of tuberculosis and malaria. On the other hand, the presence of HLA-B27 also plays a certain “protective” role: Some viral infections (influenza, herpes virus infection type 2, infectious mononucleosis, hepatitis C and HIV) occur in a milder form in HLA-B27 carriers.

    Determination of the HLA-B27 antigen is carried out to predict complications of rheumatoid arthritis. The presence of HLA-B27 is associated with a threefold increase in the risk of atlantoaxial subluxation.

    To determine the HLA-B27 antigen Various laboratory methods can be used: lymphocytotoxicity test, molecular diagnostic methods (PCR), enzyme-linked immunosorbent assay (ELISA) and flow cytometry method. Flow cytometry is a fast and reliable method for detecting the HLA-B27 antigen. However, it has some limitations that should be taken into account when interpreting the result. Thus, monoclonal antibodies to the HLA-B27 antigen used in the test are not absolutely specific, but can also react with other antigens of the HLA-B family (primarily HLA-B7, and to a lesser extent HLA-B40, 73 , 22, 42, 44). Given this feature, in order to avoid diagnostic errors, modern protocols for determining the HLA-B27 antigen use double antibodies that allow the HLA-B27 antigen to be differentiated from other antigens of the HLA-B family. This approach increases the specificity and sensitivity of the test to 97.6 and 98.8%, respectively.

    Despite the presence of a strong association of the HLA-B27 antigen and the risk of developing spondyloarthritis, a positive test result does not always reflect the real risk of the disease in a particular patient. This is due to the fact that the HLA-B27 antigen is represented by 49 different variants, characterized by varying degrees of association with this group of diseases. Thus, the HLA-B2708 variant has the greatest association with the disease, while the HLA-B2706 and HLA-B2709 variants do not appear to be associated with disease risk at all. About 7-8% of healthy people in the European population are carriers of the HLA-B27 antigen. Additional information about the patient's genetic background may help in interpreting a positive result.

    It should be noted that there are other, both hereditary and acquired, risk factors for the development of seronegative spondyloarthritis. The absence of HLA-B27 does not contradict the diagnosis of ankylosing spondylitis. Ankylosing spondylitis is then classified as HLAB27 negative.

    What is the research used for?

    For differential diagnosis of articular syndrome (seronegative spondyloarthritis, rheumatoid and septic arthritis, gout and others);

    for screening, diagnosis and prognosis of ankylosing spondylitis;

    to assess the risk of developing atlantoaxial subluxation in rheumatoid arthritis.

    When is the study scheduled?

    For articular syndrome: asymmetric oligoarthritis, especially in combination with pain in the lumbar region of an inflammatory nature (morning stiffness for more than 1 hour, improvement with physical activity, worsening at night) and signs of enthesitis;

    with a family history of ankylosing spondylitis;

    for rheumatoid arthritis.

    What do the results mean?

    Presence of HLA-B27 antigen:

    observed in 90-95% of patients with ankylosing spondylitis and juvenile ankylosing spondylitis, as well as in 60-90% with reactive arthritis and 50% with psoriatic arthropathy;

    observed in 7-8% of healthy people in the European population.

    Absence of HLA-B27 antigen:

    observed in 10% of patients with ankylosing spondylitis (HLAB27-negative spondylitis);

    observed in 92-93% of people in the European population.

    Important Notes

    Detection of the HLA-B27 antigen increases the risk of developing any disease from the group of spondyloarthritis by 20 times;

    the absence of the HLA-B27 antigen does not contradict the diagnosis of ankylosing spondylitis.

    Rheumatological manifestations of gastrointestinal diseases
    1. What intestinal diseases are combined with inflammatory arthritis?

    Idiopathic inflammatory bowel diseases (ulcerative colitis, Crohn's disease).

    Microscopic colitis and collagenous colitis.

    Infectious gastroenteritis.

    Whipple's disease.

    Gluten-sensitive enteropathy (celiac disease, or celiac disease, non-tropical sprue).

    Arthritis when applying intestinal bypass anastomoses.
    2. What is the incidence of development of peripheral arthritis and arthritis of the spine (spondylitis) in patients with idiopathic inflammatory bowel diseases?

    3. Which joints are most often affected during the development of inflammatory peripheral arthritis in patients with ulcerative colitis and Crohn's disease?
    The upper extremities and small joints are more often affected in ulcerative colitis than in Crohn's disease. Crohn's disease primarily affects the knee and ankle joints.
    4. List the characteristic clinical manifestations of peripheral inflammatory arthritis caused by idiopathic inflammatory bowel diseases.
    Arthritis occurs with equal frequency in men and women; children are affected as often as adults. Typical arthritis is characterized by an acute onset, a migrating asymmetrical nature of the lesion, and involvement in the process, usually less than 5 joints (the so-called oligoarthritis). Analysis of synovial fluid allows us to determine the presence of inflammatory exudate, in which the content of leukocytes reaches 50,000 cells/mm3 (mainly neutrophils). There is no crystalline sediment in the synovial fluid; bacterial studies give negative results. In most cases, episodes of arthritis resolve within 1-2 months and do not lead to the development of radiographic changes or joint deformities.
    5. What other extraintestinal manifestations are common in patients with idiopathic inflammatory bowel disease and inflammatory peripheral arthritis?
    Pyoderma gangrenosum (< 5 %).

    Aphthous stomatitis (< 10 %).

    Inflammatory eye diseases (acute anterior uveitis) (5-10%).

    Erythema nodosum (< 10 %).
    6. Is there a relationship between the prevalence and activity of inflammatory bowel diseases and the activity of peripheral inflammatory arthritis?
    In patients with ulcerative colitis and Crohn's disease, peripheral arthritis develops more often in the presence of widespread lesions colon. Most arthritis attacks occur within the first year after the onset of the disease. These episodes coincide with outbreaks of bowel disease activity in 60-70% of patients. Sometimes arthritis precedes the onset of symptoms of inflammatory bowel disease, especially in children with Crohn's disease. Therefore, the absence of symptoms of inflammatory bowel disease and a negative stool test result occult blood with guaiacol does not at all exclude the possibility of the existence of Crohn's disease in patients with characteristic arthritis.
    7. List the characteristic clinical manifestations of inflammatory arthritis of the spine (spondylitis) in patients suffering from idiopathic inflammatory bowel diseases.
    The clinical manifestations and nature of the course of arthritis affecting the joints of the spine in inflammatory bowel diseases are similar to those in ankylosing spondylitis. Inflammatory arthritis of the spine is more common in men than in women (3:1 ratio). Patients complain of back pain and spinal immobility, especially at night and in the morning (after sleep). Pain and immobility of the spine decrease with exercise and movement. An objective examination of patients reveals pain in the area of ​​the iliosacral joints, general decline mobility of the spine and, sometimes, a decrease in chest excursion.
    8. What features revealed when collecting anamnesis and conducting an objective examination allow us to distinguish between inflammatory arthritis of the spine and mechanical pain in the lower back in patients suffering from inflammatory bowel diseases?
    Based on medical history and objective examination of patients, in 95% of cases it is possible to distinguish patients with inflammatory arthritis of the spine from patients with mechanical pain in the lower back.
    9. Is there a relationship between the activity of spinal arthritis and the activity of inflammatory bowel diseases?
    No. Sacroiliitis or spondylitis may begin several years earlier, later, or simultaneously with inflammatory bowel diseases. Moreover, arthritis of the spine occurs completely independently of the course of inflammatory bowel diseases.
    10. What type of human leukocyte antigen (HLA) is found in patients with inflammatory arthritis who suffer from inflammatory bowel disease more often than others?


    11. List the typical radiological signs of inflammatory sacroiliitis and spondylitis in patients suffering from inflammatory bowel diseases.
    Radiographic changes in patients with inflammatory bowel disease and inflammatory arthritis of the spine are similar to those observed in ankylosing spondylitis. In patients with inflammatory sacroiliitis at the onset of the disease, plain radiographs often do not reveal any changes. When performing magnetic resonance imaging (MRI) of the sacroiliac joints in these patients, signs of inflammation and tissue swelling are determined. After several months or years, patients develop sclerosis and ulceration of the lower 2/3 of the sacroiliac joints. In some patients, these joints are completely destroyed.

    Patients with spondylitis in the early stages of the disease may also have no changes on radiographs. Later, so-called “shiny angles” may appear on radiographs in the area of ​​the fibrous rings, in the anterior parts of the vertebrae and in the area of ​​​​formed syndesmophytes. Syndesmophytes are generally thick, marginal and bilateral. Some patients also exhibit joint surface destruction and calcification of the supraspinous ligaments.
    12. What other rheumatological lesions are common in patients with inflammatory bowel disease?
    Inflammation of the Achilles tendon (tenosynovitis)/inflammation of the fascia of the foot (fasciitis).

    Deformation of the nail phalanges like “drumsticks”.

    Hypertrophic osteoarthropathy.

    Abscesses of the lumbar muscles or septic lesions of the thigh due to the formation of fistulas (in patients with Crohn's disease).

    Secondary osteoporosis due to intake medications(for example, prednisone).

    Vasculitis.

    Amyloidosis.
    13. What is a “bamboo” spine?
    With the so-called bamboo-shaped spine, radiographs reveal bilateral syndesmophytes throughout the entire spinal column (lumbar, thoracic and cervical regions). Such changes occur in only 10% of patients suffering from sacroiliitis or spondylitis. For patients who develop inflammatory lesions of the hip joints, the risk of subsequently developing bamboo spine is higher.
    16. Why do patients with inflammatory bowel disease develop inflammatory arthritis more often?
    Antigens environment, penetrating the body through the mucous membrane respiratory tract, skin or mucous membrane of the gastrointestinal tract, can cause the development of various rheumatological diseases. The human gastrointestinal tract has a surface area of ​​1000 m2, and its functions are not limited to absorption nutrients. One of the functions of the gastrointestinal tract is also the removal from the body of potentially dangerous antigens. Organs of the lymphatic system localized in the intestine include Peyer's patches, lamina propria, and intraepithelial T cells. All these formations make up 25% of the mucous membrane of the gastrointestinal tract, and it is they that block penetration into internal environment the body of bacteria and other foreign antigens. Although the upper gastrointestinal tract is not normally exposed to germs, lower sections the gastrointestinal tract are constantly in contact with millions of bacteria (up to 1012/g feces).

    Inflammation, which occurs in both idiopathic inflammatory bowel diseases and infections caused by pathogenic microorganisms, can disrupt the normal integration and functioning of the intestine, leading to increased permeability of the intestinal wall. With an increase in the permeability of the intestinal wall, bacterial antigens incapable of independent existence penetrate more easily from the intestinal lumen into the internal environment of the body. These microbial antigens can either be directly deposited in the synovium of the joints, resulting in a local inflammatory response, or they can trigger a systemic immune response, during which immune complexes are formed, which are then deposited in the joints and other tissues of the body.
    17. What are reactive arthritis?
    Reactive arthritis is a sterile inflammatory arthritis that develops within 1-3 weeks after the appearance of precursors of extra-articular inflammatory diseases (usually the gastrointestinal or genitourinary tract).
    18. What pathogenic agents causing diseases gastrointestinal tract, can cause the development of reactive arthritis?
    Yersinia enterocolitica or Y. pseudotuberculosis. Salmonella enteridias or S. typhimurium. Shigella dysenteria or S. flexneri. Campilobacter jejuni.
    19. What is the frequency of development of reactive arthritis after epidemic outbreaks of infectious gastroenteritis?
    Approximately 1-3% of patients who have had infectious gastroenteritis during the epidemic subsequently develop reactive arthritis. The frequency of their occurrence reaches 20% in Yersinia-infected patients.
    21. Describe the clinical manifestations of postenteritic reactive arthritis.
    Demographic characteristics - men are affected somewhat more often than women; the average age of patients is 30 years.

    The onset of arthritis is sudden.

    Joint involvement is asymmetrical, characterized by oligoarthritis; the lower extremities are affected in 80-90% of cases. Sacroiliitis is observed in 30% of cases.

    Examination of synovial fluid - inflammatory exudate (usually 10,000-50,000 leukocytes/mm3), no crystals, bacterial studies are negative.

    Course and prognosis - in 80% of patients, symptoms resolve within 1-6 months; In 20%, the course becomes chronic, and X-ray changes in the peripheral and/or sacroiliac joints develop.
    22. List the extra-articular manifestations of postenteritic reactive arthritis.
    Sterile urethritis (15-70%).

    Conjunctivitis.

    Acute anterior uveitis.

    Mouth ulcers (painful or painless).

    Erythema nodosum (5% in Yersinia infections).

    Circular balanoposthitis (25% in infections caused by Shigella).

    Blennorrhagic keratoderma.
    23. Which of the radiological signs of inflammatory sacroiliitis and spondylitis in patients with postenteritic reactive arthritis differ from those in patients with inflammatory bowel diseases?
    Comparative characteristics of radiological signs of spinal arthritis in postenteritis reactive arthritis and inflammatory bowel diseases

    24. How often do patients with postenteritis reactive arthritis have Clinical signs Reiter's syndrome?
    Clinical signs of Reiter's syndrome, including inflammatory arthritis, urethritis, conjunctivitis, uveitis and lesions of the skin and mucous membranes, can develop 2-4 weeks after acute urethritis or diseases accompanied by diarrhea. The frequency of development of these signs varies depending on the pathogen that caused the underlying disease: for diseases caused by Shigella, it is 85%; Salmonella - 10-15%; Yersinia - 10%; Campylobacter - 10%.
    25. What is the HLA-B27 abundance in patients with postenteritic reactive arthritis compared to the normal healthy population?
    70-80% of patients with reactive martritis have HLA-B27; in a normal control population, the frequency of HLA-B27 carriage does not exceed 4-8%.

    In patients of Caucasian race and with radiological signs of sacroiliitis, the frequency of HLA-B27 carriage is significantly higher.

    People who are HLA-B27 carriers are 30 to 50 times more likely to develop reactive arthritis after gastroenteritis than people who are not HLA-B27 carriers.

    Only 20-25% of all HLA-B27-positive people who have had infectious gastroenteritis caused by Shigella, Salmonella or Yersinia subsequently develop post-enteritis reactive arthritis.
    27. What is modern theory pathogenesis of postenteritic reactive arthritis?
    Bacterial lipopolysaccharide antigens of exogenous pathogenic pathogens (Yersinia, Salmonella), which cause the development of infectious gastroenteritis, are deposited in the patient’s joints, as a result of which post-enteritis reactive arthritis subsequently develops. These wall components bacterial cells can cause inflammation in the joints. The role played by HLA-B7 in the pathogenesis of postenteritic reactive arthritis has not yet been fully elucidated. One of the possible pathogenesis is that HLA-B27 molecules present these bacterial antigens to the body's immune system in a certain way, which leads to the development of an inflammatory response. In addition, it is hypothesized that there is molecular mimicry between HLA-B27 molecules and bacterial antigens, which is the cause of the abnormal immune response. It is important to remember that intact viable organisms do not produce bacterial growth when synovial fluid is cultured from the joints of patients with reactive arthritis.
    28. Who is Whipple?
    George Hoyt Whipple, M.D., published a case report in 1907 in which he described a 36-year-old medical missionary suffering from diarrhea, malabsorption syndrome with weight loss, mesenteric lymphadenopathy, and migratory polyarthritis. He called this disease "intestinal lipodystrophy", but it became known as Whipple's disease. Dr. Whipple also won the Nobel Prize in Physiology in 1934 and founded Medical school(Faculty) at the University of Rochester.
    29. List the multisystem manifestations of Whipple's disease.
    Hypotrophy/weight loss.

    Hyperpigmentation (skin).

    Interstitial nephritis.

    Abdominal pain.

    Skin rash.

    Pleurisy.

    * Inflammation of the eyes.

    Pneumonitis.

    Lymphadenopathy.

    Subcutaneous nodules.

    Encephalopathy.

    Endocarditis.

    Steatorrhea.
    30. Describe the clinical manifestations of arthritis developing in Whipple's disease.
    Whipple disease most often affects middle-aged white men. In 60% of patients, seronegative oligoarthritis or polyarthritis manifests itself clinically; over the years, symptoms of intestinal damage may appear. In more than 90% of patients, arthritis develops at some stage in the course of the disease. Arthritis in this case is inflammatory, often migrating in nature and is not associated with symptoms of intestinal damage. Sacroiliitis or spondylitis occurs in 5-10% of patients, especially in HLA-B27 carriers (33% of patients). Analysis of synovial fluid shows the presence of inflammatory exudate with a leukocyte content of 5000-100,000 cells/mm3. X-ray changes are usually insignificant.
    31. What is the etiology of Whipple's disease?
    In patients with Whipple's disease, many tissues have characteristic deposits that stain with periodic acid (Schiff reaction). These deposits contain rod-shaped free bacilli that can be seen under electron microscopy. Recently, these bacilli were identified as a new microorganism, a Gram-positive actinomycete, called Tropheryma whippelii.
    32. What is the treatment strategy for patients with Whipple's disease?
    Tetracycline, penicillin, erythromycin, or trimethoprim-sulfamethoxazole (TMP/SMZ) must be taken for at least 1 year. After treatment, relapses may develop (in 30% of cases). If the central nervous system is affected, it is recommended to prescribe chloramphenicol or TMP/SMZ.
    33. What rheumatological manifestations are described in patients with celiac disease (gluten-sensitive enteropathy)?
    Arthritis. Symmetrical polyarthritis, involving predominantly large joints (knees and ankles more often than hips and shoulders); may precede the onset of enteropathy symptoms in 50% of patients.

    Osteomalacia. Associated with steatorrhea that occurs with severe enteropathy.

    Herpes-like dermatitis.
    34. Which HLA type is more common in patients with celiac disease than in healthy controls?
    HLA-DR3, often together with HLA-B8, is found in 95% of patients with celiac disease (compared to 12% in healthy controls).
    35. What is the treatment strategy for secondary arthritis in patients with celiac disease?
    When switching to a gluten-free diet, polyarthritis in patients with celiac disease goes away quickly.
    36. Describe the arthritis/dermatitis syndrome in patients who have undergone intestinal bypass anastomoses.
    This syndrome occurs in 20-80% of patients who have undergone intestinal bypass surgery for the treatment of obesity. A characteristic feature This syndrome is an inflammatory symmetrical polyarthritis, often migrating, affecting the joints of both the upper and lower extremities. The X-ray picture is usually normal, despite the fact that 25% of patients have a chronic relapsing course of arthritis. Approximately 80% of patients develop skin lesions, the most common of which are maculopapular and vesiculopustular rashes. The pathogenesis of this syndrome includes overgrowth bacterial microflora in the blind (disconnected) loops of the intestine, which leads to antigenic stimulation, which, in turn, causes the formation of immune complexes (often containing cryoprecipitable components of bacterial antigens) and the formation of deposits in the joints and skin. Treatment includes non-steroidal anti-inflammatory drugs and antibiotics for oral administration, which is usually accompanied by a decrease in the severity of clinical symptoms. Surgical recovery passage of the contents through the blind loops of the intestine leads to the complete disappearance of the symptoms of the disease.

    7. What diseases of the pancreas are accompanied by the development of rheumatological syndromes?
    Pancreatitis, pancreatic carcinoma and pancreatic insufficiency.

    38. List the clinical manifestations of pancreatic panniculitis (cellulite) syndrome.
    Pancreatic panniculitis (cellulitis) is systemic syndrome, which occurs in some patients with pancreatitis and pancreatic acinar cell carcinoma. Clinical manifestations of this syndrome include:

    Soft, red nodules, usually found on the extremities, often mistaken for erythema nodosum and which are actually areas of pan-niculitis with necrosis of subcutaneous fatty tissue.

    Arthritis (60%) and arthralgia, usually of the ankle and knee joints. In this case, as a rule, there are no signs of inflammation in the synovial fluid; it is cream-colored and contains droplets of fat, which turn black when stained with Sudan.

    Eosinophilia.

    Osteolytic bone lesions due to necrotic changes bone marrow, pleuropericarditis, fever.

    For memorization, it is good to use the mnemone PANCREAS: P - pancreatitis; A - arthritis;

    N - nodules, which are necrosis of adipose tissue (nodules); C - pancreatic cancer (cancer); R - radiographic changes (osteolytic bone lesions) (radiographic);

    E - eosinophilia;

    A - increased concentrations of amylase, lipase and trypsin (amilase); S - serositis, including pleuropericarditis (serositis).

    39. What is the cause of the development of pancreatic panniculitis syndrome?
    When examining biopsies of the skin and synovium of the joints, necrosis of adipose tissue is detected, caused by the release of trypsin, amylase and lipase due to diseases of the pancreas.

    40. What bone lesions occur in pancreatic insufficiency?
    Osteomalacia associated with malabsorption fat-soluble vitamin D.

    HLA-B27 typing genetic blood test using PCR method is laboratory test blood tests, carried out for the purpose of diagnosing certain autoimmune diseases and assessing the risk of developing diseases of the joints and spine.
    Deadlines up to 15 days
    Synonyms (rus) method for detecting gene material
    Methods Polymerase chain reaction (PCR)
    Units Not provided.
    Preparing for the study no special preparation is required for the test
    Type of biomaterial and methods of taking it venous blood sampling

    HLA antigens

    On the surface of any cell in the body there are protein molecules called histocompatibility antigens. HLA antigens got their name from their location on the white blood cells. Each person is characterized by an individual set of such molecules that are synthesized through 6th chromosome. Antigens perform a protective function of the body, responding with an immune reaction to foreign cells (cancer, viruses, bacteria, etc.). However, they are also the cause of some autoimmune diseases in the presence of certain gene alleles.

    Diseases provoked by HLA-B27

    Antigen HLA-B27 in most cases it is a contributing factor seronegative spondyloarthropathies. The clinical picture of such diseases is accompanied by arthritis of the joints of the periphery and axial skeleton. It is worth noting the absence of rheumatoid factor and other autoantibodies. The group of diseases caused by the HLA-B27 antigen includes: recurrent uveitis, reactive and psoriatic arthritis, ankylosing spondylitis. The most common are Reiter's syndrome, ankylosing spondylitis, and juvenile arthritis.

    Reiter's syndrome is a disease accompanied by inflammatory processes in the joints. It occurs against the background of infections of the genitourinary system and intestines and is accompanied by autoimmune processes. Most often, the cause of the syndrome is infection with chlamydia, less often with Shigella, Yersenia and other microorganisms.

    Signs ankylosing spondylitis- ossification of the spinal ligaments, leading to loss of its flexibility, limitation of joint mobility due to bone fusion. The cause is considered to be a dysfunction of the body's immune system. Juvenile rheumatoid arthritis has an unknown etiology and occurs in children under 16 years of age.

    Indications for HLA B27 typing study

    HLA-B27 typing is carried out in the following cases:
    • risk assessment autoimmune diseases origin;
    • diagnosis of diseases associated with the presence of this antigen;
    • examinations of children with juvenile arthritis;
    • differential diagnosis of arthritis in adults and children.

    Research methodology: HLA B27 typing

    The polymerase chain reaction (PCR) method is in a modern way detection of certain sections of DNA molecules of biological objects. It is performed in three stages: isolation, reproduction and recognition of DNA fragments. The doubling of DNA molecules is carried out repeatedly to produce the required amount of biomaterial. Identification of certain DNA fragments, in particular the HLA-B27 antigen, is carried out using reference genetic detectors.

    Interpretation of HLA-B27 typing results

    This study does not make it possible to make an accurate diagnosis, however, given the infrequent occurrence of the gene in the European race, the presence of clinical manifestations of spondyloarthropathy increases the likelihood of developing the disease. In the presence of the HLA-B27 antigen, it increases 90 times. In healthy people, the antigen may also be present (in 5% of cases). The final conclusion is made by a specialist.
    Analysis period: up to 10 days

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