Rheumatic (collagen) diseases are a group of diseases which includes rheumatism, lupus erythematosus, rheumatoid arthritis, scleroderma, nodular periarteritis and dermatomyositis as well as Bechterew's disease (spondylitis deformans).As connective tissue involvement is the main link in the morphogenesis of the diseases, «systemic diseases of connective tissue with immune disturbances or rheumatic diseases» which are also frequently used replaced the term «collagen diseases», suggested by G. Klempererinl942.

At present, the following signs of rheumatic diseases are distinguished:

1) early systemic changes of microcirculation;

2) systemic and progressive deorganization of the connective tissue consisting of 4 phases: a) mucoid swelling, b) fibrous changes, c) cellular reactions, d) sclerosis;

3) combination of different phases of connective tissue deorganization which indicated the chronic character of the disease;

4) marked disturbance of immune homeostasis with immune organs hyperplasia;

5) involvement of synovial membranes;

6) visceral disturbances. Peculiarities of each nosological form: l)involvement of the connective tissue of a

particular organ: heart in rheumatism; joints in rheumatic arthritis; joints and ligaments of the spinal column in Bechterew's disease; skin in scleroderma; vessels in nodular periarteritis; skin, vessels and kidney in lupus erythematosus; striated muscles in dermatomyositis; 2) genetic and environmental factors are important for development of theses diseases. Thus, rheumatic arthritis has less severe course in the residents of Africa than in those of Europe. Lupus erythematosus is more frequent in continental Europe and the USA than in Great Britain.


Rheumatism (Sokolsky-Boiiillaiid disease)is an

acute relapsing chronic disease of infectious allergic character which involves mainly the heart and vessels. Etiology: beta-hemolytic streptococcus of group A. The pathogenesis is very complicated and is not clear. However, it is known that streptococcus invades tonsils causing angina. The organism sensibilization occurs and antibodies to streptococuss antigens are produced. Gradually under the influence of streptococcus antigens and their enzymes, immune reaction becomes inverted (autoaggression) because the anti-

genie properties of the human connective tissue are similar to those of beta-hemolytic streptococcus. It means that the proper connective tissue turns into autoantigen to which autoantibodies are produced. Autoantigen + autoantibody complexes precipitate in microcirculatory bed and connective tissue causing its damage namely increase of vascular permeability (hyalouronidase of streptococcus increases it) and deorganization of the connective tissue.

There are several morphological signs of rheumatism:

1) systemic progression of connective tissue deorganization (mucoid swelling, fibrous changes, cellular reaction, sclerosis); 2) damage of the vessels; 3) immunopathological processes. Specific cellular reaction is rheumatic granuloma (Aschoff — Tala-laev's). Structure: in the center, there is a focus of fibrinoid necrosis with macrophages with hypertrophic nuclei, epithelial cells located in the fan-like manner later a crown of lymphocytes appears.

Unspecific cellular reactions are interstitial diffuse or focal lymphohistiocytic infiltration as well as vasculitis.

Heart In rheumatism, endocarditis, myocarditis, pericarditis and pancarditis may develop.

Endocarditis is inflammation of the endocardium. Depending on localization it can be valvular, chordal, parietal. The most prominent changes develop in the mitral and aortic valves.

According to A.I. Abrikosov, valvular endocarditis is classified as follows: 1) diffuse or valvulitis, 2) acute warty; 3) fibroplastic; 4) relapsing warty.The outcome of endocarditis is heart defect. Myocarditis is inflammation of myocardium. It can be: 1) nodular productive, 2) diffuse interstitial exudative, 3) focal interstitial exudative.

The outcome is unfavorable (cardiosclerosis).

Pericarditis is inflammation of the pericardium. It can be 1) serous, 2) serofibrinous, 3) fibrinous. The outcome is unfavorable: obliteration of the pericardial cavity and calcification of the connective tissue formed in it with development of so-called armored heart.

When all layers are involved it is termed pancarditis.

Vessels. Rheumatic vasculitis with fibrinoid changes of the walls. In the capillaries, there is endothelium proliferation followed by desquamation, so-called rheumatic endotheliosis. Vascular permeability increases sharply. The disease results in vascular sclerosis (arteriolosclerosis, arteriosclerosis, capil-larosclerosis).

Joints. Polyarthritis with marked changes in the synovial membrane and preservation of the articular cartilage.

Nervous system. The damage is connected with rheumatic vasculitis. Nervous cells degeneration, brain destruction and hemorrhages occur in the brain. If these changes are clearly marked, they may cause chorea minor (in children).

Rheumatic glomerulonephritis, rheumatic pneumonia are visceral changes. Hyperplasia of lymphatic tissue, marked plasmatization are observed in the immune system.

Clinico-anatomical forms of rheumatism: 1) cardiovascular, 2) polyarthritic, 3) nodular (nodules around vessels in dermis), 4) cerebral. Complications: heart defects, thromboembolism, cardiosclerosis, armored heart. Death is caused by thromboembolism, heart defect.

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