The article shows the prevalence and health and social significance of acute rheumatic fever in children in the world and Ukraine. Presents modern approaches to diagnosis, treatment, conduct primary and secondary prevention of this disease are shown.

Currently, about 15.6 million people worldwide suffer from rheumatic fever, of which almost 2.4 million are children aged 5 to 14 years. Annually registering more than 500 thousand new cases of the disease. More than 350 thousand people die from the effects of rheumatic fever. More than 4 million children suffer from chronic rheumatic heart disease.

It should be noted that the incidence of rheumatic fever among children in industrialized countries is 1-5 per 100 thousand a year (0,001–0,005 %), whereas in countries that are developing, is 100-150 per 100 thousand a year (0.1% to 0.15%). The smallest incidence of acute rheumatic fever registered in the US (0.6 per 1,000 children) and Japan (0.7 per 1000). India, Africa, South America and Asia are the incidence of acute rheumatic fever from 0.3 to 21 per 1000 children.

In Ukraine over the last decade there has been a significant decrease in the incidence of acute rheumatic fever. So, as of 2009 the incidence of acute rheumatic fever among children aged 0 to 17 years made up 0.03 per 1,000 children (213 children), as of 2008 0,03 per 1,000 people (268 children). The highest rates were observed in Cherkasy (0.19 per 1,000 children; 43 child) and Kharkiv regions (0,10 per 1000 children; 42 children).

Incidence of acute rheumatic fever without heart disease among children from 0 to 17 for 2009 is 0.01 (54 children), in 2008 — 0,01 (67), respectively. The prevalence of acute rheumatic fever without heart disease for 2009 is 0.02 (134 children) in 2008 to 0.02 (176 children), respectively.

The prevalence of acute rheumatic fever in Ukraine among children aged 0-14 years in 2008 was 0.05 per 1000 children (346 children) in 2009 to 0.04 (263 children). The lowest rates were recorded in Cherkasy (0,24) and Zaporizhia (0,12). In General, according to the MINISTRY of health of Ukraine for 2008, the prevalence of acute rheumatic fever among children aged 0 to 17 years, nearly twice the rates in the group of children from 0 to 14 years is 0.07 (612 children), for 2009 — 0,06 (459 children).

The incidence of chronic rheumatic heart disease among children from 0 to 14 years amounted to 0,03 (178 children) for 2008 and 0.02 (113 children) in 2009, among children aged 0 to 17 years — 0,04 (359 children) and 0.03 (275 children), respectively. Prevalence of chronic rheumatic heart disease among children from 0 to 14 years in 2008 amounted to 0.33 (2127 children) and 0.26 (1674 child) in 2009, among children aged 0 to 17 years — of 0.59 (4876 children) and 0.49 (4003 child) respectively.

The development of acute rheumatic fever are known to be associated with streptococcal infection. Most often associated with rheumatism, so-called rheumatogenic strains of b -hemolytic Streptococcus group A: M1, M3, M5, M6, M14, M18, M19, M24, M27, M29. On the role of streptococcal infection in rheumatoid arthritis indirectly indicates the chronological relationship of the disease with streptococcal infections of the nasopharynx, identifying the vast number of patients of different antistreptococcic antibody — SLA-O (antistreptolysin On), ASG (antistreptokinase), ask (antistreptokinase) in high titres.

Confirmed the role of genetic predisposition in the development of rheumatic fever. Installed polygenic inheritance type of rheumatism. Thus, the definition of genetic markers has proven a propensity for development of rheumatic fever in individuals with blood groups A(II) and(III), and H a A, B35, A11, DR5 and DR7 antigens. Valvular heart lesions most often occur in carriers of HLA A3 and B15. The frequency of rheumatism in the families ranges from 10 to 50 %, which is significantly higher than the prevalence in population (1,5 %). The incidence of rheumatic fever through relatives first-degree relatives does not exceed 15-20 %. Relation of the disease with the inheritance of certain types of haptoglobin and alloantigen b-cells (D8/7).

Recently, acute rheumatic fever was considered one of the diseases that are associated with PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections), but modern data do not find reliable evidence of this fact.

So, acute rheumatic fever occurs after streptococcal infection transferred. You should pay attention to prevalence in Ukraine the so-called peregrinating diseases among children, underscoring the urgency of the problem. Thus, according to the MOH Ukraine (2009), more than 410 thousand children suffer from acute tonsillitis and pharyngitis; more than 27 thousands of children suffer chronic nasopharyngitis and pharyngitis; more than 388 thousand children suffer from chronic diseases of tonsils and adenoids. Predisposing factors are hypothermia, young age, female gender, genetic predisposition.

The modern theory of the pathogenesis of rheumatic fever are toxic and immunological. Poshkodzhennya tissues due to the action of Streptococcus-specific products (toxins), including: M protein (inhibits phagocytosis is antigen cross-reacts with myocardium), Stratoliner O and S, streptokinase, hyaluronidase, proteins, DNase V. Enzyme system of Streptococcus can directly cause tissue damage, as well as due to its monoreactive properties, activate kinin system to assist in the depolymerization of hyaluronic acid, to trigger the production of antitoxic antibodies, to reduce the phagocytic activity of neutrophils.

Circulating antibodies and immune complexes damage the microcirculation with the development of destructive-productive vasculitis. Due to the phenomenon of "antigenic mimicry" (the similarity between Atami microbial cells and structures of the organism — the sarcolemma of cardiomyocytes, cardiac myosin connective tissue of the heart, the glycoprotein of heart valves, vascular wall, cytoplasm of neurons of subthalamic and caudate nuclei of the brain, epithelium and medullare cortical zone of the thymus) there is damage to the structures of the organism with the development of characteristic clinical symptoms of the disease.

Humoral and cellular immunological disorders rheumatism expressed in increasing the credits of ASL-O, ASG, ask, disimmunoglobulinemia, increasing percentage and absolute number of b-lymphocytes by reducing the percentage and absolute number of T-lymphocytes. Significantly disrupted the function of tissue basophils, increasing their degranulation, tissue and blood"wooden track out of biologically active substances — mediators of inflammation: histamine, serotonin, bradykinin and others, contribute to the development of inflammation.

Rheumatic process has a cyclic course. First, reverse phase (Mukono swelling) occurs depolymerization of the main substance of connective tissue, with accumulation of acid mucopolysaccharides. The progression of the disease leads to the development of the second, irreversible phase (fibrinoid necrosis), which is characterized by the disorganization of collagen fibers, their swelling, frequent breakdown of collagen and delay fbrinogen.

Around pathological foci of necrosis, predominantly perivascular, in the interstices of the myocardium, mural endocardium, close to the valves is the formation of specific granulomas (ashoff-talalaevsky granuloma) presented by large basilii by histiocytes, lymphocytes, myocytes, mast and plasma cells. True rheumatic granuloma is localized only in the heart. Gradually developing phase of multiple sclerosis, the site of the granuloma forms a scar. Rheumatic process is the specified cycle for 6 months.

Cardiac involvement occurs in 30-70 % of individuals with a primary attack of acute rheumatic fever and in 73-90 % of individuals with a re-attack. This files most often occurs simultaneous lesion of the myocardium and endocardium (endomyocardial), sometimes in combination with pericarditis (pancardi), possibly isolated lesions of the myocardium (myocarditis). Rheumatic endocarditis begins with valvula with alagana in the process of connective tissue valve stem, which is morphologically manifested by edema and cellular infiltration. Walbolt is characterized by lesions of all connective valve stem with its subsequent deformation.

Further, the process of disorganization of connective tissue leads to deformation of the valve sclerosis and the development of fibrous tissue. At 65-70 % of patients has severe or moderate lesion of the mitral valve. The aortic valve is affected in 25 %, tricuspidal valve is 10 % and is usually associated with lesions of the mitral or aortic valves. The pulmonary valve rheumatism usually remains intact. Severe valvular insufficiency may cause congestive heart failure or even death (1 %).

The severity of myocarditis is determined by the enlargement of the heart, rhythm disorders, ECG changes and the degree of development of heart failure. Inherent pain or discomfort in the heart area, shortness of breath, palpitations, tachycardia, weakening of the tone I at the apex of the heart, murmur at the apex of the heart, the symptoms of pericarditis, enlarged heart, ECG changes (prolonged PQ interval; beats, rhythm atrioventricular pathways; migration pacemaker; ST segment, prolongation of the electrical systole, other arrhythmias), symptoms of circulatory failure.

During the echocardiographic examination with the mitral valve valvular detect club-shaped thickening of the cusps of the mitral valve, it "rough", hypokinesia, rear doors, reducing the total excursion of the valves, the mitral regurgitation. When valvular aortic valve detected by the low-amplitude diastolic tremor flaps of the mitral valve, thickening of echosignal from the cusps of the aortic valve, aortic regurgitation.

Currently, the percentage of cases forming heart defects after undergoing primary rheumatic heart disease is 20-25 %. Among acquired heart disease is dominated by isolated malformations most often mitral insufficiency and rarely the aortic valve, mitral stenosis or combined rtraline-aortal defect. It is known that 99% of the cases of mitral valve stenosis in adults is defined as a consequence of suffering rheumatic heart disease and is associated with risk of atrial fibrillation due to chronic valve disease and enlarged Atria. Approximately 7-10% of children after suffering rheumatic heart disease develops mitral valve prolapse.

It is proved that the frequency of formation of heart defects depends on the severity of rheumatic heart disease. In adolescents who have undergone the first attack, are diagnosed with heart disease in 1/3 of cases (in adults — in 39-45 %). The maximum frequency of the formation of rheumatic heart disease (75 %) was observed within 3 years of onset.

Rheumatoid arthritis is one of the main clinical manifestations and diagnostic criteria of rheumatic fever. The manifestation of arthritis is observed in 70-75 % of cases. The main characteristics of rheumatoid arthritis is symmetric involvement of large joints (usually knee and ankle), the "volatility" of arthritis that is manifested by the rapid appearance and reverse the development (even without treatment), inflammation (migratory joint syndrome), severe pain and limitation of motion in the joints during the attack, with the defeat of the periarticular tissues (local redness of skin, swelling, local rise of temperature), the lack of development of deformation. Lately more frequently recorded MINUCI oligoarthritis, rarely monoartrit.

Chorea is an acute symptom of rheumatic fever. As a rule, small chorea occurs in 12-17 % of patients with rheumatism, mostly girls from 6 to 15 years. The beginning of chorea usually gradual, the child becomes irritable, emotional lability, hyperkinesis occur (usually bilateral, violent movement of various muscle groups, which are enhanced by excitement and disappear during sleep), m"Yazov dystonia with a predominance of hypotonia, increased tendon reflexes, clonus, stato-coordination disorders, vascular reactions, and psychotic symptoms.

Rheumatic nodules — it is a dense, slow-moving, painful education of small size, located in ligaments, aponeurosis, prostalene around joint bags, the subcutaneous tissue on the extensor surfaces of elbow, knee, p"Yashkova-phalangeal joints, the spinous processes of the vertebrae. Usually rheumatoid nodules completely disappear within 1-2 months. Rheumatic nodules are found in 10% of patients.

Erythema annulare is a pale pink, thin, inconspicuous ring-shaped rash with a clear outer and less distinct inner edge. Elements of erythema coalesce into strange shapes located on the surface side, the trunk, rarely on the legs. It should be noted that erythema annulare does not have any subjective sensations and disappears completely. Erythema annulare is diagnosed in 5 % of patients with acute rheumatic fever.

Much less frequently during acute rheumatic fever occurs a lesion of other organs and systems: lungs (rheumatoid pleurisy, pneumonitis, pulmonary vasculitis), kidneys (nephritis with isolated urinary syndrome), gastrointestinal tract (peritonitis), blood vessels (vasculitis), eyes (iritis, iridocyclitis), thyroid gland (thyroiditis).

In childhood frequently observed acute and subacute rheumatism the beginning, together with polyarthritis and carditis observed chorea, erythema annulare and rheumatoid nodules. In the senior school age fall ill mainly girls, usually the disease develops gradually, rheumatic heart disease often has a prolonged duration.

Clinical manifestations of rheumatic fever depends primarily on the activity of the process. With minimal activity the clinical symptoms not expressed. Often there is absolutely no evidence of exudative component of inflammation in organs and tissues. Moderate activity is reumatismo attack with moderate or without fever and a significant exudative component of inflammation is absent. Observed moderate signs of rheumatic carditis, polyarthritis or chorea. With a maximum degree of activity vivid General and local manifestations of the disease with the presence of fever, a predominance of exudative component of inflammation in the affected organs (acute polyarthritis, diffuse myocarditis, pancardi, serositis, pneumonitis, etc.).

The antibody titers were determined in paired sera with an interval of 15 to 20 days. Peak increase in BP noted on the 3rd week of the disease. Normalization of the concentration of at in the blood occurs by the 6th week of the disease. The sensitivity of the definitions of ASLO is 80-85 %, the sensitivity of antikink-In — 90 %. 20% of patients missing at increase in the blood. Some patients with rheumatic heart disease showed increase in the tropomyosin.

So, diagnosis of rheumatism is based on anamnesis, objective clinical examination, laboratory data (WBC, ESR, etc.), the results of serological surveys (titers of ASLO, ASG, ask, ADNK-IN), the data of bacteriological tests (microbiological examination of swabs from the nasopharynx, tonsils), rapid diagnostic methods based on direct detection of streptococcal antigens (D8/17) in smears, and data of instrumental examinations (ECG, EchoCG, x-ray, etc.). The sensitivity of rapid methods (D8/17) is almost 90 %.

Treatment of acute rheumatic fever starts with a stationary phase. Within 2-3 weeks, depending on activity prescribed bed rest. After the disappearance of the manifestations of carditis child transferred to polupostelny mode, then trenyce mode. Assigned a diet containing sufficient amount of proteins, restriction of sodium chloride. Additionally, in the treatment of glucocorticoid drugs prescribed foods rich in potassium and magnesium.