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RHEUMATISM (ACUTE RHEUMATIC FEVER

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Rheumatism (Sokolsky-Bouillaud's disease) - systemic inflammatory disease of
connective tissue with a primary lesion of the cardiovascular system which develops
in predisposed him at a young age (7-15 years) after infection by the ji-haemolytic
streptococcus group A. In the English literature rheumatism often referred to as acute
rheumatic fever.

The incidence of rheumatism in the average is 5 per 100 OOO population, but in
developing countries, according to WHO, it is significantly higher (2.2 per 1000
children). In Russia the incidence of rheumatic fever in the average 0.3 per 1000 child
population. Primary morbidity of children in Moscow is quite low (0.03 in 1000).

Etiology

Acute rheumatic fever develops within 2-4 weeks after previous infection caused by
the p-haemolytic streptococcus group A. We have identified a number of
streptococcus Ar and toxins, in particular the M-cell wall proteins (virulence factors),
streptolysin S and O, streptokinase and gialuro-nidazu. Confirmation of exposure to
the streptococcus organism of rheumatic patients is the detection in most patients
protivostreptokokkovyh AT - antistreptolizina-O antistreptogialuronidazy,
antistreptokinazy, antidezoksiribonukleazy in capable of damaging various tissues and
cells of the body.

In the occurrence of rheumatism important role played by genetic predisposition of
the patient. Rheumatism ill only 0,3-1% of children who have had a streptococcal
infection. At the "family" nature of rheumatism in the early XX century Russia
entered a well-known pediatrician, AA Kissel. The value of the role of genetic factors
in the development of rheumatic fever is confirmed by more frequent its development
in siblings and a higher incidence among monozygotic than among heterozygous
twins. Ar D-8, D-17 B-lymphocytes detected in 98% of patients with carditis and
arthritis, and 75% of patients with rheumatoid trochee genesis.

Pathogenesis

The development of rheumatic fever is determined by several mechanisms. A role can
play a direct toxic damage of components of myocardium cardiotropic enzymes (i-
haemolytic streptococcus group A. However, a leading value add features of cellular
and humoral immune responses to various Ag streptococcus, leading to the synthesis
of protivostreptokokkovyh AT, cross-reacts with Ag infarction (the phenomenon of
molecular mimicry) as well as its cytoplasmic Ag-corona tissue localized in the
subthalamic area and the basal ganglia of the brain. In addition, M protein has the

Rheumatic carditis. joints and nervous system. Rheumatoid polyarthritis occurs. Typically. In the pathological process involved also microvasculature vessels. plasma and mast cells. as well as from lymphoid. . fibrinoidnye changes. in the early stages of the disease to distinguish myocarditis and endocarditis clinically is often very difficult. abdominal syndrome (rheumatic peritonitis) is now practically not observed. Classically divided into four stages of pathological process in rheumatic disease: Muko-idnoe swelling. in 40-60% of cases.properties of "superantigens". Parents have noticed that after 2-3 weeks recovering from a sore throat in a child persist lethargy. endocardium and pericardium. serous membranes. The defeat of the heart (rheumatic heart disease) is a leader in the clinical picture of disease and determine its course and prognosis. pain and swelling mainly of large. Proliferative stage is characterized by the formation of rheumatic granuloma composed of large basophilic cells gistiotsitarnogo origin of giant polynuclear cells. volatility and the rapid regression of the process. The most widely considered to be the defeat of the myocardium .myocardium. rheumatic heart disease patients do not complain. It is characterized by acute onset on the background of a low rise in body temperature. Clinical picture Rheumatic fever usually occurs in children of school age and much less frequently in preschool children. However. In 70-85% of cases the disease occurs primary rheumatic heart disease.the defeat of cells of the subcortical nuclei. Changes in the skin and subcutaneous tissue are also due to vasculitis and focal inflammatory infiltration. fatigue. the most important of which are polyarthritis. Lesions of the internal organs in the form of rheumatic pneumonia. Rheumatoid arthritis can be attributed to the group of reactive arthritis that have arisen as a result of infection. nephritis. In Rheumatic heart disease can attack all the shell of the heart . it requires a comprehensive clinical and instrumental examination. Pathomorphology For rheumatism is characterized by preferential damage of connective tissue. carditis and the defeat of the subcortical nuclei of the brain. that is able to induce activation of T-and B- lymphocytes. sometimes medium- sized joints. Typical rheumatic granulomas reveal only in the heart (now quite rare).diffuse myocarditis. without prior processing of Ar . The disease is characterized by polymorphism of symptoms. Rheumatoid polyarthritis. In the stage mucoid swelling may reverse the development process. according to different authors. while chorea . proliferative reaction and sclerosis. The basis of the defeat of the nervous system is you-rheumatic Kulit.presenting cells and interaction with molecules of class II major histocompatibility complex.

rarely . Flow chorea is often protracted and recurrent nature. Considerable difficulties is the clinical diagnosis of valvular lesions in the early stages of the disease. mood instability). This form of rheumatic disease occurs in 7-10% of cases. Calling the knee-jerk reaction. Hyperkinesis increase with excitement. it usually manifests intensification of pre-existing or new noise. irritability.aortic valve insufficiency. slowing atriovent-rikulyarnoy conductivity (sometimes up to atrioventricular dissociation). The main symptoms caused by lesion of the subcortical nuclei of the brain. Any damage to the aortic valve at echocardiography identify melkoamplitudnoe diastolic flutter of his wings. violent movements of individual muscle groups) lead to inaudibility speech. which is of great prognostic value. X-rays visible aortic configuration of the heart with a predominant increase in the left ventricle. When radiography in children with a lesion of the mitral valve detected "mitral" configuration of the heart. less often bradycardia.Characteristic emotional disorders (tearfulness. mitral-aortic defect. Chorea. Most commonly affects the mitral valve. the muffled tones of the heart. The ECG may identify various arrhythmias. Thus on echocardiography reveal thickening and "shaggy" echo of the valve leaflets and chords. mitral stenosis. broadening and depletion of high-frequency oscillations predominantly tone I. there are clinical signs of rheumatic heart disease in the form of tachycardia. change in handwriting slovenly eating. The outcome of rheumatic heart disease with the duration of the acute period of 1. it is possible to identify a symptom Gordon (tonic reduction quadriceps). is a positive symptom "flabby shoulders": when lifting a patient standing for armpits from behind his head deeply immersed in the shoulders. the active phase lasts up to 2 months. Can complete patient immobility ( "soft" chorea). enlargement of the heart. nekoordi-niruemye. Auscultation listen systolic sound. During this period. enlargement of the left chambers. When PCG exhibit reduced amplitude distortion. are attached to motor disturbances accompanied by decreasing muscle tone. and sometimes the impossibility of self-service. In these patients. limiting the mobility of the back of his sash. mainly girls of school age. Relapsing Rheumatic heart disease usually develops on the background of acquired heart disease. the development of circulatory failure. . Typically. pacemaker migration. Clinically. The most common forms of mitral valve insufficiency. Hyperkinesis (promiscuity. Important role in the diagnosis is echocardiography.subfebrile. Hypotonia of muscles impedes normal life.5 up to 2 months depending on the formation of heart disease (20-25%). are more often bilateral.

a rash in the form of pale-pink rings on the skin of the chest and abdomen. General. fatigue. 5. Rheumatic nodules. Chorea. weakness. "Rheumatoid" history (contact with the transferred epipharungeal streptococcal infection. Currently. Ring-shaped erythema . 6. Adynamia. complemented the AI Nesterov (1963). does not rise above the surface of the skin. the presence of cases of rheumatism in the family). Jones (1944). in the occipital region. Proof ex juvantibus . babies are extremely rare. 2. Increased body temperature. Rheumatic nodules .rounded dense formations of up to 0.Ring-shaped erythema. Ring-shaped erythema. Diagnosis Criteria for diagnosing rheumatic fever developed AA Kissel (1940).5-1 cm. Additional manifestations of A. rapidly disappearing without pigmentation and desquamation. clinical and anatomical organ damage. 4.improving the patient's condition after the 2-3-week course of specific therapy. The classification is based on the phase of illness. Classification The generally accepted at present is the classification and nomenclature of rheumatism AI Nesterova (Table 13-1). The main manifestations 1. defined in the place of attachment of tendons. Cardia. . 2. 7. The rash is not accompanied by itching. Subcutaneous nodules. 3. the nature of the disease and the state of circulation. 1. Polyarthritis.

cerebral vasculitis. 5. nephritis. pneumonia. peritonitis. 1. III Rheumatic heart disease without primary valvular Rheumatic heart disease with relapsing (how) Rheumatic fever without obvious changes in the heart • Polyarthritis • Serozity (pleurisy. Pale skin. B. neuro-psychiatric disorders • Vasculitis. Working classification and nomenclature of rheumatism Phase and the degree of activity of rheumatism Clinical and anatomic characteristics of lesions Heart Other organs and systems Nature of flow Circulatory failure Active • The degree of activity I. hepatitis. thyroiditis Acute • H. meningo-encephalitis. 6. Abdominal syndrome. II.3. iritis. Subacute • H. Table 13-1. Nosebleeds. Sweating. Leukocytosis (neutrophil). encephalitis. abdominal syndrome) • Chorea. skin lesions. iridocyclitis. Special (laboratory findings). 4. Protracted • H 11A Continuously • H 11E recurrent Latent Inactive Miokardioskleroz rheumatic heart disease (a) .

. Clinical Rheumatology. Criteria diagnosis rheumatism * More criterion Minor criteria Cardio Clinical Polyarthritis Previous rheumatic fever or rheumatic Chorea disease Ring-shaped erythema Arthralgia Subcutaneous rheumatic nodules Fever Laboratory indicators of acute phase ESR C-reactive protein Leukocytosis Daiiye confirming streptococcal infection Increased titer protivostreptokokkovyh AT. newly transferred angina * From: Nasonova VA et al. seeding throat group A streptococcus.Implications and residual effects of deferred exocardial lesions th N I (K about X £ about £ S Table 13-2. . 1989 The presence of the patient's two large or one large and two small criteria indicates a high probability of acute rheumatic fever. especially if confirmed by data on past infection caused by group A streptococci .M. antistreptolizina-O.

Diclofenac: 2-3 mg / kg / day in 2-3 doses for 1-1. . Treatment Complex method of treatment of primary rheumatism includes the simultaneous appointment of small doses (0.Indomethacin: 2-3 mg / kg / day in 2-3 doses for 1 -1.25 g depending on the age of 1 times per day after dinner. 5 months. PMK. thyrotoxicosis. hyperkinesis in SLE. increasing titers antistreptolizina-O. fibrinosis. 2. NSAIDs combined with glucocorticoids and one of the basic drugs. the debut of Jura and juvenile spondylitis. Increased permeability of capillaries. hemorrhagic Vasco-cast. UPU. increased concentration of serum mukoproteinov. do Lago) in a dose of 0. prednisolone at a dose of 15-25 mg / day.Differential Diagnosis Rheumatoid polyarthritis differentiate from reactive arthritis. -. 3. SLE. Changes serological indicators: the emergence of Ar streptococci in the blood.7 mg / kg / day) of glucocorticoids and NSAIDs. the duration of treatment for several months to several years. • Of the NSAIDs most frequently prescribed indomethacin and diclofenac. Horeyu differentiate the functional tics. -. infective endocarditis. with 1/2-1/3 of the daily dose prescribed in the morning. antistreptokinazy.5-0. the most common criteria of WHO (1989). tumors of the brain. 5 months.chloroquine (hingaminom. the appearance of C-reactive protein.5 months. especially with a protracted course of disease and the formation of heart disease. Currently. 4. developed by the American Association of rheumatological (Table 13-2). Rheumatic heart disease should be distinguished from non-rheumatic carditis. • As a basic therapy using quinoline derivatives: -. Al-tistreptogialuronidazy. increased the concentration of ss 2 and y-globulin. Initial dose is gradually reduced until the complete abolition of an average of 1. Dysproteinemia: increased ESR.06-0.

75-1 million U / day. Secondary prevention is aimed at preventing relapse and pro-disease progresses. • bitsillin-5 in a dose of 0.dentists (smallpox). scarlet fever). during the first 10-14 days of therapy prescribed benzylpenicillin or its analogs on 0.2 g depending on the age of 1 times per day after dinner.75 million ED 1 time in 2 weeks to patients of preschool age. In the complex therapy also includes the reorganization of foci of chronic infection. With decompensated chronic tonsillitis tonsillectomy is needed.05-0.hydroxychloroquine (Plaquenil) in a dose of 0. The most optimal year-round prevention is carried out every month for at least 5 years. In 6-8 months after the acute period recommended spa treatment.5 million ED 1 time in 4 weeks to school age children. 1.Recommended preparation . particularly chronic tonsillitis. appoint: • Benzathine benzylpenicillin + benzylpenicillin procaine (bitsillin-5) in a dose of 1.All children who have suffered rheumatism.75-1. Prevention Recommendations of the WHO (1989) Prevention of rheumatism and its recurrence include the following activities. • rational physical education and sport. including prescriptions penicillin dose 0. Forecast Weather in recent years has improved thanks to the measures of primary and secondary prevention. • good nutrition with adequate vitamins.-. The primary rheumatic heart disease leads to the formation of .activities that ensure the proper development of the child: • Quenching with the first months of life. 2. Primary prevention . Given the nature of streptococcal rheumatism. • control of infection caused by group A streptococcal (sore throat.5 million U / day for 10-14 days. the duration of treatment for several months to several years.

1%.heart defects only at 20-25% of patients. Rarely have cases of severe course of rheumatism.4-0. . Mortality rate decreased from 11.12 to 0.