The most common cause of reactive arthritis is urogenital or intestinal infection. However, the manifestation of reactive arthritis is not entirely related to infection in the swelling, and secondary inflammation of the swelling does not develop in all patients who have suffered from infection and illness.
Such vibrancy, from the point of view of the immunogenetic theory, is explained by the tendency to reactive arthritis due to the hyperreaction of the immune system to microbial agents that circulate in the blood and persist in the tissues And the country and the fabrics. As a result of microbial mimicry - the similarity of antigens of the infectious organism and lymph tissues - the immune hyperresponse of animals not only to microorganisms, but also to autologous tissues. As a result of complex immunochemical processes, aseptic (non-purulent) reactive inflammation develops in the areas.
According to the etiological understanding, the following groups of reactive arthritis are seen:
The classic triad of signs of reactive arthritis includes the development of conjunctivitis, urethritis and arthritis.
Symptoms of reactive arthritis usually appear 2-4 days after a sexually transmitted or intestinal infection. The kidney develops urethritis, which is characterized by rapid discharge of urine and pain in the liver. Following are the signs of conjunctivitis – lacrimation, redness and rashes in the eyes. In typical cases, signs of urethritis and conjunctivitis are weakly expressed.
The remaining manifestation is arthritis, which is manifested by arthralgia, swelling, local hyperthermia, and reddened skin. The onset of arthritis is acute with low-grade fever, self-esteem pain, pain in 1-2 joints of the lower ends (interphalangeal, metatarsophalangeal, ankle, heel, knee), and sometimes – joints of the hands. Due to severe swelling and pain, the functions of the joints suffer, and vertebralgia is often present.
Symptoms of reactive arthritis persist for 3-12 months, then a reversal of the clinical course occurs. The danger of reactive arthritis lies in the high rate of recurrence and chronic inflammation with progressive attacks of an increasingly large number of joints.
Before typical forms of reactive arthritis, Reiter's disease is necessary, which means igniting changes in the joints, eyes and sechostates.
In connection with reactive arthritis, some patients (about 12%) develop foot deformity. Important forms of inflammation can result in destruction and loss of tissue (ankylosis). Recurrent or unsatisfying symptoms are associated with rapid development of cataracts.
Changes in the peripheral blood in reactive arthritis are manifested by increased erythrocyte sedimentation fluidity; In venous blood, an increase in C-reactive protein is detected in the presence of negative tests for rheumatoid factor (RF) and antinuclear factor (ANF). A specific marker to indicate the presence of reactive arthritis is the detection of the HLA 27 antigen.
For differential diagnosis of reactive arthritis from rheumatic gait arthritis, consultation with a rheumatologist is necessary. If there is an infection that causes reactive arthritis, the patient is referred to a urologist or venereologist for treatment.
PLR testing of biological material (blood, smears, stool) makes it possible to identify the probable cause of the infection and the cause of reactive arthritis. In this case, in the sowing of the nodules, there are daily alarms, which makes it possible to differentiate the diagnosis of bacterial arthritis.
In reactive arthritis, radiography of the joints does not have much diagnostic value, but often reveals the presence of heel spurs, paravertebral ossification, and periosteum of the feet. Subglobal puncture or arthroscopy is absolutely not necessary.
The main principle of therapy for reactive arthritis is the reduction of the primary infectious lesion in the urogenital or intestinal tract. Etiologically primed antimicrobial therapy is recommended in optimal dosages in lines of at least 4 days. For reactive arthritis caused by chlamydial infection, drugs from the macrolide, tetracycline, and fluoroquinolone groups are used. In case of negative tests for chlamydia, immediate treatment is recommended for partners. Whenever there are changes after the antibacterial course, drugs from a different group are re-prescribed.
To eliminate the ignition reaction in the corners, the NPZZ is cleaned; in case of severe arthritis - corticosteroids (prednisolone), both systemically and with the help of intraarticular and periarticular injections. The injection of corticosteroids into the area of the glomerular tendons is carried out under CT control.
Prolonged recovery from reactive arthritis may preclude the use of anti-inflammatory therapy with basic drugs - sulfasalazine, methotrexate.
With the help of additional drugs-inhibitors of FNP (apfa-etanercept, infliximab), forms of the disease that were resistant to therapy can be cured, signs of arthritis, spondylitis, and acute uveitis are relieved.
The introduction of stovburov klitins for reactive arthritis helps to renew the structure of damaged cartilage, normalize metabolism, and relieve inflammation in the cartilage.
When the ignition is released, it will be evacuated from the empty load. Anti-inflammatory creams, ointments, gels, and applications with dimexide are used locally. Physiotherapy methods for reactive arthritis include phonophoresis, hydrocortisone, sinusoidal modulating struma (SMS), cryotherapy, and exercise therapy.
After the acute stage of ignition has been stopped, procedures aimed at restoring the function of the dryers are prescribed - licorice baths (with Dead Sea salts, sulphurous water, hydrogen sulphide), mud baths.
The long-term prognosis for reactive arthritis is variable. In 35% of patients, the symptoms persist for a short period of time, and the illness does not recur later. The same number of patients experience relapses with symptoms of arthritis, enteritis, and systemic reactions. In 25% of cases, arthritis progresses to a primarily chronic nature with a tendency to progress slightly. Another 5% of patients suffer from an important form of reactive arthritis, which can lead to destructive and ankylous changes in the joints and spine.
The main approach to preventing reactive inflammation of the joints is the prevention of primary intestinal (salmonella, yersiniosis, campylobacteriosis, dysentery) and sechostatic (chlamydia) infections.
Yu.V. Marushko , Doctor of Medical Sciences, Professor, Head of the Department, E.Yu. Marushko , Department of Pediatrics No. 3 of the National Medical University named after. O.O. Bogomoltsya, m. Kiev
Reactive arthritis (code MKH-10 M02) is an illness that is accompanied by aseptic inflammation of the mouth, and is caused by an extra-articular infection, in which the primary infectious agent is not visible from the area. This is the case with the choice of standard piece housing media.
The need for the availability of medicines for the treatment of illness is due to the significant increase in reactive arthritis in the structure of rheumatic diseases in children and the need for differential diagnosis of such a serious pathology as septum genic arthritis, acute rheumatic fever, systemic inflammation of the tissue and juvenile rheumatoid arthritis (JRA).
Terminology. Today there are two terms in use: “reactive arthropathy” and “reactive arthritis”. “Arthropathy” means “secondary inflammation of joints due to other illnesses and pathological conditions.” “Arthritis” can be defined as arthropathy of the inflammatory genesis. Clinically, arthritis most often manifests itself as synovitis (inflamed synovial membrane from effusion in an empty joint - synovial hypertrophy), as a rule, the diagnosis is made for the presence of swelling in the joint, pain the “starting” character and early poverty. However, in children, the inflammation of the sore throat can go beyond the pronounced incompatibility of the pain syndrome with objective changes in them (so-called “dry” sore throat), or it can even go beyond arthralgia, especially in HLA-B27-positive children. Itey. In this case, the term “arthritis” can be better replaced with the term “arthropathy”. MKH-10 coined the term “reactive arthropathy”. In rheumatological terminology and in scientific research, the term “reactive arthritis” has traditionally been used, so this term itself has become familiar, just as in clinical practice, doctors have learned MKH-10 more accurately establishes the diagnosis of “reactive arthropathy.”
All types of arthritis that are associated with infection are divided into three large groups: septic, parainfectious and post-infectious. In case of septic arthritis, the infectious agent can be used directly in the area. As a rule, there are bacterial pathogens that cause purulent arthritis (pioarthritis), draining hematogenous path, or when draining the cavity, osteomyelitis into an empty drain. This type of arthritis may cause a “Vibuchian” clinical transition and, in case of inappropriate treatment, lead to destruction of the joint. Parainfectious is arthritis, which usually develops against the background of a viral infection and is accompanied by alteration of the tissues of the throat by the virus, which may result in a “slurry” transition and passes from apnea to the main illness. The group of post-infectious arthritis is formed by pathological conditions, in which arthritis occurs within an hour after an infectious process, associated with the immune mechanism of infection and/or mediating the action of lifestyle products Nosti of microorganisms on the surface. Classic examples of post-infectious arthritis are acute rheumatic fever and reactive arthritis.
The term “reactive arthritis” was coined in 1969. R. Ahvonen, K. Sievers and K. Aho for arthritis that developed after suffering from ersiniosis enterocolitis. Today, it is understood that only episodes of post-infectious arthritis, which are due to the inheritance of a previous infection, caused by Salmonella, Shigella, Campylobacter, Yersinia, Chlamydia trachomatis, Ureaplasma urea, are used to rectify alyticum, β-hemolytic streptococcus group A, Chlamydophila pneumoniae and Mycoplasma pneumoniae. It is necessary to strengthen the “reactive” from the group of post-infectious arthritis, which is due to the high frequency of carriage of the HLA-B27 antigen in this subgroup of patients, which is a risk factor for recurrent inflammation of the joints or development enthesitis-associated form of JRA.
Epidemiology. The incidence of illness and the prevalence of reactive arthritis among children is 32.7 and 86.9 cases per 100 thousand. children are similar, and in the structure of children's rheumatic diseases, the incidence of reactive arthritis becomes 57.5% among children up to 14 years of age and 41.8% among children. Thus, reactive arthritis is a major part of the structure of illness due to rheumatic diseases in the child population.
The pathogenesis of reactive arthritis is still unclear. In the genesis of reactive subglobular inflammation, a major role is played by immune complexes - their accumulation in the synovial membrane on aphids of the expressed immune type of macroorganism on the antigens of arthritic microorganisms leads to ignition infiltration of the synovial membrane and exudation into the empty sinus. The delay in the development of arthritis following infection is due to the time required for seroconversion and the increase in titers of antimicrobial antibodies of the IgG class, which subsequently create immune complexes.
The presence of the HLA-B27 antigen is of great importance. It is important that certain antigens of arthritic microorganisms are structurally similar to HLA-B27, which leads to the development of a crossover immune type as a result of the phenomenon of molecular mimicry of the tissues of the kidneys in which this antigen is widely expressed [3]. The connection between illnesses and the presence of HLA-B27 is explained by the fact that in carriers of the designated antigen, after suffering an intestinal and urogenital infection, reactive arthritis develops 50 times more often, less especially in of which HLA-B27 is daily. On the other hand, 40-80% of patients with reactive arthritis show a positive association with HLA-B27. When the connection between the presence of the antigen and various pathogens varies. Thus, in reactive arthritis after infection with Salmonella or Chlamydia, association with HLA-B27 is detected in less than 50% of cases, and in cases of shigella infection - in approximately 80% [1].
Clinical picture. It is characterized by asymmetrical oligoarthritis (? 4 angles) with a tendency to develop the greater angles of the lower ends, debuting 10-30 days after a causative infection. The most common signs of synovitis are: swelling of the cyst, of a “starting” nature, external flatness, looseness, redness after pressing on the cyst. In addition to JRA, the transition from reactive arthritis is non-destructive, regardless of the severity of illness and the number of relapses, which, as a rule, does not lead to disability. You may sometimes be wary of arthralgia (pain in the throat without objective signs of pain).
The anamnesis may reveal signs of a recent arthritic infection: fever, diarrhea, sore throat, signs of respiratory illness, dysuria, vision from arterial organs, etc. These often causative illnesses can be erased or flared up subclinically.
The group of reactive arthritis is commonly seen as Reiter's syndrome. VIN is characterized by the classic trigeline of the asymmetric aligoarthritis, Consterus, Urethritis/Cervical Ta -ilkoli in a quarter of the familiarization - keratoderma -like visipannia on the Schikiri Dolone I STOP (Fig. 1). Sickness develops after chlamydial or intestinal infection and most often occurs as a recurrent or chronic disorder. Arthritis in Reiter's disease is characterized by a large amount of effusion in the joints with minor pain and stiffness in them [3]. In children, illness is extremely rare.
In addition, HLA-B27-positive patients with reactive arthritis may exhibit symptoms characteristic of seronegative spondyloarthropathy. Before them there is enthesitis (inflamed area of attachment of ligaments and tendons to the cysts). The most typical are plantar fasciitis, enthesitis of the Achilles tendon and achilles bursitis (Fig. 2), enthesitis of the hump of the magnum. Dactylitis (inflammation of the tissue of each finger with the “sausage-like” toe), tarsitis (inflammation of the joints and ligaments of the metatarsus, which manifests itself as diffuse swelling of the back side of the foot), tenosynovitis and deformity painless aphthae on the mucous membranes of the oral cavity and body organs [15 ]. This will complicate the differential diagnosis of reactive arthritis and the enthesitis-associated form of JRA (an analogue of seronegative spondyloarthropathy in adults).
Laboratory quilting. Depending on the severity of the shift, changes in laboratory tests may be daily, or minor leukocytosis may be avoided due to a change in the leukocyte formula to the left, increased fluidity of erythrocyte sedimentation and equal to C-reactive protein. The appearance of autoantibodies (rheumatoid factor, anti-cyclic citrullinated peptide antibodies, antinuclear antibodies and their types) is not typical. HLA-B27 is positive in approximately 80% of cases. The presence of an arthritogenic infectious agent is significant during acute illness. Remnants of chlamydia and salmonella carriage, in case of arthritis, which is not reactive, seeing signs of alarms can lead to an incorrect diagnosis. Serological diagnosis with bark to identify past arthritogenic infection.
Puncture of the affected joint is important for differential diagnosis, especially in cases of monoarthritis. Normally, the synovial level is <2000 leukocytes/ml (in most cases <500 leukocytes/ml), neutrophils are less than 25%, the glucose level is similar to the serum level. When analyzing the synovial tissue of patients for reactive arthritis, the concentration of leukocytes should become 2000 - 25,000/ml and contain 25-75% of neutrophils. The level of synovial glucose is found to be equal to blood plasma. With bacterial inoculation, the microflora of the day, although on aphids of post-chlamydial arthritis, the polymerase Lanzug reaction can detect the genetic material of Chlamydia trachomatis. It is important that the herb does not attack the joint directly, but consumes it intra-articularly, visiting the macrophages that migrate there.
Change research methods. Korisniy is to conduct an X-ray examination of the affected cyst to exclude acute hematogenous osteomyelitis. In case of reactive arthritis, beware of strengthening of the tissues around the subglobulus, widening of the subglobular cleft and darkening of the physiological spaces, so that indirect radiological signs of swelling in the empty tendon.
Ultrasound examination reveals exudative synovitis of an affected cyst (violent in an empty cyst). Proliferative changes in the synovial membrane are not typical for reactive arthritis. MRI and computer tomography, rather, serve to exclude other illnesses, but not to diagnose reactive arthritis.
Diagnostic criteria. The diagnosis of reactive arthritis is based on diagnostic criteria adopted in 1996. in Berlin at the 3rd International Conference dedicated to the problems of this disease:
2. Infectious manifestations (the term appears – 2-4 years before the development of arthritis):
b) liability for the presence of typical clinical manifestations of infection.
4. Exclusion criteria – identification of the cause of mono-oligoarthritis:
b) septic arthritis;
c) Lyme disease;
d) streptococcal arthritis;
e) microcrystalline arthritis.
Classification. Over time, reactive arthritis can be divided into acute (up to 2 months), protracted (up to 1 month), chronic (up to 1 month), relapsing (at least 6 months between arthritis episodes). Due to the number of symptoms, illness is divided into monoarthritis/monoarthropathy (from one joint), oligoarthritis/oligoarthropathy (2-4 joints), polyarthropathy (?5 joints). It is important to understand that the concept of “protracted” and “chronic” overflow of reactive arthritis is used only for seizures, if there is an underlying reason for reactive arthritis, which cannot be eliminated for a long time. Since the evidence of such a cause has not been established, the diagnosis of protracted/chronic reactive arthritis is incorrect, and the child is classified as having JRA disease.
Poststreptococcal reactive arthritis. From the group of reactive arthritis, we can see post-streptococcal reactive arthritis, an inheritance of its etiological similarity with acute rheumatic fever and in view of the need for antibiotic prophylaxis in addition to anti-inflammatory therapy Yu. This illness is similar to other post-infectious arthritis to asymmetric oligoarticular lesions of the greater angles of the lower ends, which develops after acute tonsillopharyngitis caused by β-hemolytic strep. shock of group A (GABSA). In contrast to acute rheumatic fever, arthritis is not migratory, inflammation develops even earlier - on average 11 days after tonsilitis, synovitis does not significantly improve due to nonsteroids. them anti-inflammatory drugs (NSAIDs). The important point is that the patient does not meet the criteria for acute rheumatic fever. Current research suggests that there are two clinical patterns of poststreptococcal reactive arthritis: one more similar to acute rheumatic fever and may be accompanied by carditis, the other to HLA-B27-positive reactive arthritis.
Ayoub et al. (1997) established the following criteria for poststreptococcal reactive arthritis:
1. Arthritis of the cob, asymmetrical (although it can be symmetrical), not migratory, it can affect any swelling or persistent or recurrent disorder.
2. Confirmation of previous GABHS infection.
3. Inconsistency with the Jones criteria for acute rheumatic fever.
Confirmation of GABHS infection can be microbiological or through a rapid test for the detection of streptococcal antigens. These methods cannot eliminate the current infection from GAB-carrying, which can be expected in 15% of school-aged children. Serological diagnosis reveals a significant level of antistreptolysin O (ASLO), which normally begins to rise after 1 day and then decreases at the 3-6th day after the previous GABHS infection. For diagnostic purposes, it is important to increase the level of ASLO two times above the upper limit of the laboratory norm, or at least its increase will last 2-3 days with the vicoristic method of male sirens. Since the child does not clinically suffer from tonsilitis, the diagnosis cannot be based solely on the advanced level of ASLO. In this case, it is necessary to monitor the patient for clinical and echocardiographic signs of carditis and repeat the analysis after 2-4 days. In case of signs of heart disease, and with increasing titers, the child is more likely to be diagnosed with “post-streptococcal reactive arthritis.” If the patient's heart is recovered, the patient is diagnosed with acute rheumatic fever. Due to the presence of a sign of carditis and an increase in ASLO titers in male patients, the diagnosis of “post-streptococcal reactive arthritis” is unlikely.
Septic arthritis/acute hematogenous osteomyelitis. Particular concern for septic arthritis may result from the presence of monoarticular disease in the patient. For those who receive antibacterial treatment in the first 4 days after the first symptoms appear, the prognosis for the patient’s functional capacity is satisfactory. The manifestations of this type of arthritis are swelling of the cyst, expression of pain in passive arms, blackened skin over it, and increased thermoactivity. Pain in osteomyelitis is characterized by widening of the cyst between the projections of the angle. Children under the age of 1 are at a high risk of transition from osteomyelitis to septic arthritis, since their vascular mesh is damaged, which causes metaphases and epiphysis. In 50% of cases in children under 12 months of age, acute hematogenous osteomyelitis turns into septic arthritis.
Kocher et al. (1999) developed such an algorithm for the differential diagnosis of septic arthritis based on 4 criteria: fever; intolerance to any kind of obsession with the sun (the child cannot stand on his leg); erythrocyte sedimentation rate (SSE) using the Westergren method ?40 mm/year; blood leukocytosis ?12?10 9 /l. If four criteria are present, the likelihood of diagnosing septic arthritis is 99.6%, and three criteria – 93%.
Changed methods of investigation are of little use in excluding septic arthritis, since puncture of the pulp with bacteriological investigations is no longer the gold standard for diagnosing this disease. The concentration of synovial leukocytes is ≥50,000/ml (and especially ≥100,000/ml), the number of neutrophils is ≥90% and are indicators for the diagnosis of “septic arthritis”. In this case, the concentration of glucose in the synovial fluid is reduced to an average of 30% of that in the synovial fluid. Bacteriological testing is positive in 70% of cases. The diagnosis of septic arthritis is low-grade when the concentration of synovial leukocytes is ≥25,000/ml, the number of neutrophils is <75%, but this picture does not include arthritis of other etiologies. The interval between these intervals (the number of leukocytes in the synovial range is 25,000-50,000/ml, the number of neutrophils is 75-90%) indicates a “gray” interval, if there is any evidence of septic arthritis should be based on the results of complex clinical-laboratory treatment and clinical examination of a doctor.
Tuberculous arthritis. At the time of illness, up to 5% of all cases of extralegal tuberculosis in children occur. For tuberculosis of the musculoskeletal system, the indicator is destructive damage to the bodies of the transverse ridges. When it comes to arthritis, the classic version is to avoid chronic monoarthritis from inflammation of the knee or knee joint. The medical history may reveal exposure to tuberculosis. Exudative processes and pain syndrome of weak expressions are important. It is characterized by the creation of cystic sequestration and marginal defects of the cysts, which are formed into a corner, which are revealed by radiography or computed tomography of the affected area. A positive Mantoux test, Diaskin test and interferon gamma test confirm the diagnosis. DNA can be detected using the PLR method in the synovial region of the affected tendon due to a decrease in glucose level in line with serum concentration, the importance of lymphocytes over neutrophils during cytology to the best of our knowledge.
Lyme disease is a systemic borelosis (boreliasis - Borrelia burgdorferi - transmitted by the bite of an ixodid tick). The first manifestations disappear after a few days: at the site of the bite there is a migratory erythema, before the appearance of subsidiary elements is possible. The underlying symptoms are fever, weakness, myalgia, arthralgia. In the late phase, chronic atrophic acrodermatitis occurs (the burning phase - erythema of the vermilion/purple color - is gradually replaced by the phase of skin atrophy), myositis, carditis, arthritis. The SOE is moved in 77% of cases. Lyme arthritis is characterized by monoarthritis (64.2%), oligoarthritis (29.4%), polyarthritis (6.4%); The acquisition of other suglobs is not in power. The most commonly affected areas are the knee joint (90%), the culinary joint (14%), the gomilk-foot joint (10%), the carpal joint (9%), the elbow joint (7%) and others (7%). For diagnosis, it is necessary to carefully take a history of tick bites and evidence of migratory erythema in the past. Corysnym emphasizes the presence of antibodies to Borrelia burgdorferi.
Gostra rheumatic fever. This illness is characterized by migratory non-destructive polyarthritis with significant damage to the great and middle slopes. The ignition of one slug lasts for about 3-4 days. In addition, acute rheumatic fever is characterized by heart disease with development of valvulitis of the mitral ± aortic valve, and in severe cases - pericarditis and pancarditis. Significantly, other specific manifestations of illness become more common: minor chorea, annular erythema, rheumatic nodules. Characteristic is an hour-long contraction (on average 21 days) with the transfer of GABHS-tonsylopharyngitis, elevated ASLO titer and anti-DNase serum. To establish a diagnosis of acute rheumatic fever, illness may meet the modified Johnson criteria.
Juvenile rheumatoid arthritis. The complexity of differential diagnostics lies in the possibility of overrunning JRA in the appearance of oligoarthritis, serving as an infectious disease triggering the onset of JRA, a significant overlap in the spectrum of clinical and laboratory manifestations of reactive arthritis and enthesitis-associated forms of JRA (including enthesitis and positivity for the HLA-B27 antigen). The main factor in differential diagnosis is the follow-up of illness. If all possible causes of arthritis are excluded and eliminated, regardless of the anti-inflammatory treatment, the disease affects more than 6 categories, such a disease can be classified as the one that may be JRA.
Systemic ignition diseases of healthy tissue. This group of patients, in addition to arthritis, is characterized by other specific clinical manifestations and laboratory indicators. Thus, the systemic red shepherd is characterized by photosensitiveness, erythema on the appearance of the “blizzard” type, a high level of color, the presence of antinuclear antibodies and antibodies to double-stranded DNA, etc. In juvenile dermatomyositis/polymyositis, myopathic ± skin syndromes come to the fore. Juvenile systemic sclerosis is not characterized by sclerodermic skin lesions or Raynaud's syndrome.
Hemarthrosis. Hemorrhage in an empty stomach is characterized by swelling, increased temperature, looseness in the joint and pain and is accompanied by traumatic injuries or coagulopathy/thrombocytopenia. The first episode is characterized by a history of trauma and signs of a traumatic injury to the skin above the ridge (wound, soreness, blue). Detection of defects in the cystic structures is usually aided by radiography and computer tomography, and destruction of the soft tissue structures by ultrasound and MRI. In case of coagulopathies/thrombocytopenias, establish a clear history of spontaneous bleeding; A coagulogram, a measured platelet count and an analysis of the activity of blood coagulation factors can confirm the diagnosis. Ultrasound diagnostics helps to diagnose hemarthrosis in reactive arthritis. Hemarthrosis is characterized by spontaneous contrast of the subglobular effusion with the dissolved suspension, but there are often signs of clot organization, just as in reactive arthritis the appearance of an anechogenic homogeneous fluid appears (Fig. 3). A spot in the diet for the diagnosis of “hemarthrosis” can be made either by puncture of the joint with aspiration and analysis instead.
Pigmented volonodular synovitis. The pathogenesis of this pathology remains unclear, the disease is a benign villous proliferation of the synovium due to its discoloration in the brown/brown color of the inheritance of hemosiderin and the creation of hemorrhagic (“and rusty color) in an empty pile. Subglobular syndrome has a severe monoarticular localization (in 95% of cases, the patellar tendon is affected, and sometimes the patellar tendon, the knee joint, the elbow joint, and the carpal joint). Manifestations of illness include swelling with mild pain syndrome, loss of laxity due to increased thermoactivity of the joint; wound tightness on a daily basis. Laboratory changes that indicate inflammation (advancement of CRE and level of C-reactive protein) are not typical. Anti-inflammatory therapy practically has no effect. Diagnostic is a puncture of the joint when removing the “rusty” one. MRI can reveal lesions containing hemosiderin in proliferated synovies. The only reliable diagnostic method is a synovial biopsy with histological examination. The treatment is performed in surgical synovectomy.
Likuvannya. If we suffer from reactive arthritis, we prescribe NSAIDs. Among them are non-selective (block cyclooxygenase type 1 and type 2): ibuprofen (from 3 months of age 5-10 mg/kg per dose up to 3 times per dose), diclofenac (children over 8 years old 2-3 mg/kg/day maximum 100 mg/day), naproxen (for daily doses over 16 days, 250 mg daily/day); and selective (it is important to block cyclooxygenase type 2): nimesulide (children over 12 years of age, 2 mg/kg/day), meloxicam (children over 16 years of age 7.5-15 mg/day in 1 hour 2 doses). It should be noted that the analgesic effect of most NSAIDs manifests itself from the first dose, since the maximum anti-inflammatory effect occurs on the 10-12th day of the course, so the pain of treatment begins in the middle 2-4 days. In cases of severe arthritis, step-by-step therapy can be used: for the first 5 days, the drug is administered internally, such as diclofenac sodium, with a subsequent transition to oral administration. The main side effects of NSAIDs with trival use are the development of gastroduodenitis, schuta and duodenum, which are more typical for non-selective anti-inflammatory drugs, and can also prevent hepatitis and nephrotoxicity.
You can locally apply ointments or gels based on NSAIDs (ointments for ibuprofen, diclofenac, ointments containing nimesulide), which are recommended to be applied during the acute period of the day before.
Systemic administration of glucocorticoids is not recommended. Effective is the intraglobular administration of long-acting glucocorticoids.
For reactive arthritis associated with chlamydia and ureaplasmosis, antibiotic therapy is indicated. In case of detection of chlamydia in the urogenital tract, respiratory chlamydia, a 10-14-day course of treatment with clarithromycin (15 mg/kg/dose) or a 5-day course of treatment with azithromycin (10 mg/kg/dose) is carried out. We do not allow preventive infusion of antibiotic therapy to prevent the development of reactive arthritis in patients with gastrointestinal infection.
Based on the evidence of severe heart disease in patients with poststreptococcal reactive arthritis, the American Heart Association recommends antibiotic prophylaxis with benzathine benzylpenicyline for 1 day per day in such patients. and a sign of a strong heart in 12 months - change it. In case of heart disease, the diagnosis is changed to chronic rheumatic heart disease and secondary prevention is indicated. Benzathine benzylpenicyline is administered to children with a body weight of ≥27 kg at 600,000 Od, >27 kg – at 1,200,000 Od once every 4 days of internal administration.
Medical examination. The child, who has suffered reactive arthritis, undergoes dispensary examination by a pediatric cardio-rheumatologist for the period of 1 year. A series of therapeutic procedures lasting 3 months, and then – once every 3 months, clinical and laboratory tests are carried out to monitor the growth of the child and the effectiveness of the treatment.
The list of references is available in the editorial office.
On 1-3 February, a scientific and practical conference with international participation “Another academic symposium in pediatrics” was held in Truskavtsi. Within the framework of a research program, research has been developed on the problems of gastroenterological, nephrological, endocrine, hematological and allergic diseases of the child’s eyelid. Zokrem, the testimony of the duet format was presented by the head of the Department of Childhood and Adolescent Diseases of the National Medical Academy of Postgraduate Education (NMAPO) named after P. L. Shupik (m. Kiev), Doctor of Medical Sciences, Professor Galina Volodymyr Ivna Beketova is a professor at the Department of Pediatric Dentistry at the National Medical Academy of Postgraduate Education named after P. L. Shupika, Doctor of Medical Sciences Natalia Olegivna Savichuk.
At the discussion club, held as part of the scientific and practical conference with international participation “Academic Symposium on Pediatrics” (March 1-2, Truskavets), the head of the Department of Pediatrics No. 1 and Medical Genetics of the State University spoke about the advantages of cefixime, a third-generation cephalosporin. Dnepropetrovsk Medical Academy of the Ministry of Health of Ukraine,” Doctor of Medical Sciences, Professor Alexander Evgenievich Abaturov.
The problem of urticarial vasculitis in children remains one of the most pressing in pediatrics due to the chronic course of the disease and the possibility of developing systemic manifestations with damage to internal organs. Therefore, knowledge of the diagnostic criteria for urticarial vasculitis is necessary in pediatric practice. .
On the pages of this thematic issue, we continue to familiarize pediatricians with the practical aspects and diagnostic capabilities of the electrocardiography (ECG) method. This publication will report on the ECG diagnosis of cardiac conduction disorders in children.
Reactive arthritis becomes a group of inflammatory diseases of the lungs. The smell is associated with arthritis infections, which include parainfectious (usually viral), septic and post-infectious (reactive) arthritis. For the treatment of septic (infectious) arthritis, with Rheumatoid arthritis, every day. It is a classic case of HLA-B27-associated disease, which develops after urogenital and intestinal infections and is associated with the group of seronegative spondyloarthropathy.
The term “reactive arthritis” was coined in 1969. R. Ahvonen, K. Sievers and K. Aho for arthritis that developed after suffering from ersinious enterocolitis. The most common form of reactive arthritis is Reiter's syndrome, which is characterized by asymmetric arthritis, urethritis/cervicitis, swelling of the eyes, skin/mucous membrane lesions (balanitis, oral mucosal lesions or keratoderma).
The frequency of ReA, according to the literature, is 30-40 episodes per 100,000 population.
Before ReA, there are ignition non-infectious congestion of the throats, which develop as a result of immune changes in aphids of intestinal and urogenital infections, resulting from the following Infectious agents: Yersinia, Salmonella, Shigella, Campylobacter, Chlamydia. In 80% of cases, ReA develops in children after gastroenteritis infections. In this case, ReA develops 10-30 days after the infection, clinical manifestations of which may be daily. The specific pathogenesis of the “classical” forms of ReA is the persistence of internal cellular debris in the patient’s body. The fungus can persist both at the entrance gates of infection and in the peripheral areas, where DNA and RNA fragments of microorganisms can be detected. The human body is designed to control the infection, but cannot eliminate the alarm, which results in the development of a weak, protracted ignition reaction. In patients with ReA, expressions of connections between the presence of the genes of the molecules of the head molecules of the histosuiciency complex and the development of this illness were established. Thus, there is evidence that in the carriers of HLA-B27 antigens after intestinal and urogenital infections, ReA develops 50 times more often, less so in those with HLA-B27 every day. 40-80% of patients with ReA show a positive association with HLA-B27. The results of the new research indicate that the connections with HLA-B27 also occur in the same type. With Salmonella and Chlamydia -induced arthritis, association with HLA-B27 is found in less than 50% of cases, and with Shigella -induced diseases - in approximately 80%. It has been shown that antibodies to certain microorganisms cross-react from HLA-B27, which is explained by the phenomenon of molecular mimicry, realized through the structural similarity of the cell wall of neighboring bacteria with neighboring bacteria. females HLA-B27. Antibodies that over-react can damage hair cells, on the surface of which HLA-B27 is expressed. Overreaction causes inadequate implementation of the immune response and promotes persistence and chronicity of infection.
One of the prototypes of ReA is chlamydia-associated arthritis . After a urogenital infection, called Chlamydia trachomatis , the fungus probably spreads through infected monocytes to the synovial membrane of the great tendons, provoking the local immune system. Go, the inheritance of each host cell suppresses apoptosis and the expression of HLA molecules. At the same time, chlamydia causes the expression of a specific heat shock protein, which relieves chronic arthritis.
P. Toivanen and A. Toivanen divide ReA into two groups: HLA-B27-associated and HLA-B27-unassociated.
ReA develops more often in children. Boys and girls are getting sick with the same frequency.
The main symptom in the classic case of ReA is asymmetrical oligoarthritis with levels of less than five joints, especially at the lower ends, which manifests itself several days or even after the infection. In 25% of trigger cases, the infection resolves subclinically. In many cases, the diagnosis of ReA is supported by the presence of discharge disorders and infections of the sinus ducts in partners. Columns and carpal-foot tendons are most often affected; arthritis of the carpal-carpal joints can be prevented. The appearance of arthritis may be accompanied by fever. In post-infectious arthritis, the clinical manifestation is extremely variable – ranging from mono- to polyarthritis. In patients with ReA, a typical manifestation of periarticular inflammation is dactylitis, which is the inflammation of every finger or foot (“sausage-like” deformities), which is registered in 5-10% of children. Following the articular manifestation of ReA, episodes of illness due to enthesitis and tenosynovitis are described. Enthesopathies are often detected along the spinous ridges, at the insertion site of the Achilles tendon and the plantar aponeurosis to the heel hump. In particular, pain in the heel area (talalgia) is noted. About 40% of patients with ReA suffer from pain, tightness and interconnection of the vertebrae in the cervical and transverse parts of the ridge, in the area of the ridge-club joints. In 20% of patients, most importantly HLA-B27-positive, ankylosing arthritis develops within a few years.
ReA may appear due to damage to the eyes of the anterior uveitis in one or both eyes, which without care can cause loss of vision.
The skin often shows signs of pustulosis, balanitis, or swelling of the mucous membrane of the mouth. Infrequent extra-articular manifestations of ReA include carditis and glomerulonephritis.
Reiter's disease is considered a special form of ReA, which is characterized by a triad of symptoms - urethritis (cervicitis), conjunctivitis (keratoconjunctivitis) and arthritis, associated with chlamydial infection. For the evidence of keratoderma, refer to Reiter's tetralogy. Reiter's syndrome debuts as a sign of deterioration of the urogenital tract 2-4 years after suffering a chlamydial or intestinal infection. In Reiter's syndrome, the most common cause of infection is Shigella flexneri and Chlamydia trachomatis .
In the acute phase of ReA, laboratory tests reveal positive indicators of the acute phase of inflammation, increased erythrocyte sedimentation fluidity, neutrophilic leukocytosis, elevated levels of C-reactive protein and feritin. Test results for antinuclear antibodies and rheumatoid factor were negative. The detection of HLA-B27 may be of great diagnostic and prognostic value for the diagnosis of ReA.
To establish an accurate diagnosis of ReA, it is important to identify the alarm that caused the development of ReA. To identify trigger infections, microbiological, serological and molecular biological methods are used.
An infection in a person can be detected using a smear from an oral cavity during microbiological investigations or through an additional polymerase lanciug reaction during an acute infection or during further persistence and microorganisms at the entrance gates of infection.
In case of chronic overabundance of ReA, early infection can be detected using additional serological tests using specific antibodies. However, the interpretation of the results of serological tests is subject to maternal clinical considerations. In the absence of clinical signs of this or other infection, positive results of serological tests are not informative. Zocrema, the prevalence of chlamydial etiology in a patient with symptoms of infection of the urogenital tract when indicating antibodies before chlamydia becomes 50-77%, and after the number of symptoms of infection is less than 12-31%. If anti-chlamydial antibodies are detected in a patient with diffuse arthralgia, the likelihood of a causal link becomes less than 1-3%.
The diagnosis of ReA is made based on diagnostic criteria adopted in 1996. in Berlin at the 3rd International Conference dedicated to the problems of ReA:
1. Peripheral arthritis (more important than the severity of the joints):
2. Infectious manifestations (the term appeared 2-4 years before arthritis):
3. Laboratory confirmation of infection:
a) necessary for the detection of typical clinical manifestations of infection;
4. Exclusion criteria - identification of the cause of mono- and oligoarthritis:
e) crystalline arthritis.
S. Pacheco-Tena established the following diagnostic criteria for ReA:
1. Global diagnosis of ReA:
a) signs of arthritis and extra-articular illness;
b) clinical signs of infectious disease 4-6 days before the onset of arthritis without bacteriological identification of the disease.
2. Reliable diagnosis of ReA:
a) identification of the bacterium that caused arthritis (positive results of microbiological or serological investigations);
b) identification of bacteria that were the cause of the illness that began 4-6 years before the onset of arthritis.
3. Bacteria associated with non-differentiated oligoarthritis or spondyloarthritis.
Differential diagnosis of ReA traces is carried out with other juvenile arthritis.
Among arthritis associated with infection, it is necessary to differentiate from post-streptococcal arthritis, the diagnostic criteria for which are as follows: the appearance of arthritis 1-2 days after suffering a streptococcal infection ї nasopharynx, contusion of the great sinuses, lack of effectiveness of non-steroidal anti-inflammatory drugs and detection of elevated titer of antistreptococcal antibodies .
Another type of arthritis associated with infection is viral arthritis. Viruses that can cause the development of parainfectious arthritis include the worm virus, parvovirus B19, adenoviruses, hepatitis B and C virus, herpes viruses of various types, mumps virus, enteroviruses, Coxsackie virus. Arthritis, associated with a viral infection, develops during the course of the infection. The severity of viral arthritis increases every day or every day. Either virus or parvovirus B19 can cause chronic arthritis. Children aged 3-10 years often suffer from acute transient arthritis of the cervical tendons, which, most likely, may be viral and develops after an infection of the upper respiratory tract. Transient coxitis has a good prognosis and will end in a child's wet clothes.
Lyme disease is diagnosed in patients with minor changes in the skin, appearance of migratory erythema, impairment of the nervous system with signs of lymphocytic meningitis and arthritis. In addition, the diagnosis of boreliasis is based on the history of the patient’s stay in an endemic area and the presence of a tick bite. The diagnosis is confirmed by the results of serological studies based on the detection of antibodies to Borrelia burgdorferi .
When carrying out differential diagnosis in a patient with manifestations of arthritis, it is necessary to terminally exclude purulent arthritis, since antibacterial therapy is immediately available to avoid the development of irreversible changes in the affected area. The residual diagnosis of septic arthritis is established after tracing the synovial tissue with microbiological identification of the organism.
Tuberculous arthritis is rarely observed. It develops as a result of early generalization or late reactivation of pulmonary tuberculosis. Tuberculous arthritis is recorded in patients of various risk groups: immunocompromised, patients on HIV/AIDS, etc. Tuberculosis infection often causes osteomyelitis of the spine. There are several possible types of monoarthritis of the great thighs without signs of pulmonary tuberculosis and with various risk factors for this disease. In such cases, there is arthritis of one part of the lower end, which is characterized by acute cob with fever, positive gastrophase indicators, as well as a positive Mantoux reaction. The diagnosis is confirmed by identifying mycobacteria in the synovial tissue using a microbiological method or a polymerase lancin reaction.
It is most difficult to differentiate from juvenile idiopathic arthritis, which overlaps with signs of oligoarthritis of the lower ends in girls of preschool age and may be accompanied by scorched eyes. The diagnosis of juvenile idiopathic arthritis is established on the basis of progressive arthritis, detection of antinuclear antibodies and characteristic genetic markers of this variant of the disease (HLA-A2, -DR5, -DR8).
Juvenile sacroiliitis can develop as a result of chronic overload of ReA in HLA-B27-positive individuals. The main diagnostic sign of juvenile spondyloarthritis is radiological confirmation of sacroiliitis.
The eradication of persistent infection is theoretically responsible for the development of ReA. However, there is now little evidence to support the use of antibacterial therapy to overcome arthritis caused by Enterobacteriaceae. Indications for antibacterial therapy are subject to reliable identification of the infectious agent. J. Sieper et al. reported on the results of a multicenter, single-blind clinical follow-up study on the use of ciprofloxacin in rheumatoid arthritis, which shows that it has a significant impact on overcoming arthritis. The follow-up did not include chlamydia-associated arthritis. Only in cases of chlamydia-associated rheumatoidosis can a positive effect be achieved by continued antibiotic therapy. If chlamydia is detected in the urogenital tract, a 10-14-day antibacterial treatment is carried out. We do not provide a preventive injection for the development of ReA antibiotic therapy in patients with gastrointestinal infection and arthritis in the chronic phase.
All illnesses on ReA are caused by non-steroidal anti-inflammatory drugs, such as diclofenac, naproxen, ibuprofen. Systemic administration of corticosteroids is not recommended. Internal administration of these medications is effective. If the effect is not achieved after treatment for 6 months or if the arthritis is recurrent, the basic medications should be completely stopped, sulfasalazine zocrem. In case of chronic overload of ReA, methotrexate or azathioprine is prescribed.
ReA in children, as a rule, has an favorable prognosis. In patients with ReA, illness lasts for several days to one day. In 20% of patients, there is a chronic overload of ReA; relapses of illness are often avoided. A prognostic factor for overcoming ReA is detection of the HLA-B27 antigen. In 40% of patients with ReA, spondyloarthropathy subsequently develops.
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