27.1. Rheumatoid arthritis
Rheumatoid Arthritis (RA) - chronic autoimmune inflammatory systemic connective tissue disease with progressive lesion of mainly peripheral (synovial) joints by the type of erosive-destructive polyarthritis.
Epidemiology
Prevalence of RA among the adult population in different geographical areas of the world ranges from 0.5 to 2%. The ratio of women to men is 3:1. The disease occurs in all age groups. Peak incidence falls on the most active working age - 50-60 years. RA causes permanent disability in half of patients during the first 3-5 years from the disease onset.
After 10-15 years from the disease onset, approximately 90% of patients lose their ability to work, one third becomes completely disabled, and more than 25% require expensive conservative or surgical treatment.
Etiology
Until now, no exact causes of the RA development are known, but significant risk factors for the disease development should not be excluded.
Hypothermia, injuries, nervous or physical fatigue, occupational hazards, smoking, bacterial or viral infections may provoke RA. The development of RA is also promoted by periods of hormonal adjustment (puberty, postpartum and menopausal periods). There is also a certain seasonality of exacerbations (more often in spring and autumn).
The role of genetic factors and heritability of the disease are highlighted.
Human leukocyte antigen (HLA - DRB1) is considered one of the main risk factors - one of the tissue compatibility antigens.
Attention is often paid to the role of multifactorial RA causes, for example, the interaction of genetic and environmental factors that potentiate each other's effects.
Pathogenesis and pathomorphology
The pathogenesis is based on immunopathological disorders resulting from an imbalance in the T- and B-lymphocyte functions, which leads to uncontrolled synthesis of antibodies by B-lymphocytes, in particular IgG. Great importance is attached to the role of monocytes and macrophages synthesizing cytokines (tumor necrosis factor α, interleukins 6 - IL6, IL1, etc.).
In RA, any joint may be affected, but more often, small joints of the hands and feet are involved.
The synovial membrane of the joint undergoes changes first: proliferative-exudative inflammation occurs (synovitis). The synovial membrane thickens, becomes hyperemic, abundantly injected with vessels, a large number of tufts is formed. In addition to proliferation, the production of inflammatory mediators by activated mast cells also occurs. Subsequently, its enlargement occurs, "pannus" is formed - an aggressive granulation tissue that grows from the side of the synovial membrane to the cartilage surface, leading to its inevitable destruction due to the release of proteolytic enzymes, development and progression of secondary arthrosis in the affected joint.
Proliferating vessels are one of the most important sources of proteolytic enzymes, which are able to cause cartilage tissue destruction. Active vascular proliferation (angiogenesis) is considered an important sign of rheumatoid synovitis. It has been proven that angiogenesis promotes pannus formation and the development of destructive arthritis, contributing to constant presence of large amounts of activated macrophages and other blood cells in the inflamed synovial membrane. This explains the well-known phenomenon of the continuous erosive process progression, despite the clinical improvement (decrease in inflammatory activity).
The following changes may be distinguished among the main changes occurring with RA.
- Osteoporosis (local or systemic) is noted already in the early stages of the disease due to the activation of osteoclasts under the influence of proinflammatory cytokines.
- Periarticular tissues are involved in the inflammatory process; as a result, foci of fibrinous necrosis may occur in tendons, leading to their rupturing. The joint capsule and ligaments are stretched. The inflammatory process progression leads to the development of subluxations and contractures.
- Rheumatoid nodules (a characteristic feature of RA) represent a necrosis zone surrounded by large histiocytes, followed by lymphoid and plasma cells, fibroblasts, neutrophils. A fibrous capsule is formed around the nodule.
- Vasculitis develops primarily in small cutaneous vessels, skeletal muscles, and internal organs, although vessels of all sizes are generically affected in RA. Immune complex vasculitis is likely to develop during the production of autoantibodies, for example, rheumatoid factor.
- With RA progression, articular surfaces move closer forming fibrous-bone ankylosis, which leads to immobility of the affected joint.
Classification
By the presence of rheumatoid factor and/or antibodies to cyclic citrullinated proteins (AB-CCP) in the blood, seropositive and seronegative (or, respectively, AB-CCP-positive and AB-CCP-negative) RA are distinguished.
Clinical stages of the disease are distinguished by the duration of the course:
- immediate-early - less than 6 months;
- early - from 6 months to 1 year;
- extensive - more than 1 year in the presence of typical RA symptoms;
- late - 2 years or more in combination with pronounced destruction (radiological stage III-IV) of small and large joints, the presence of complications.
RA activity rate
To determine the RA activity rate, it is necessary to consider not only clinical (morning stiffness, joint hyperthermia, exudative changes, etc.) but also laboratory (ESR, globulins, C-reactive protein, seromucoid, etc.) parameters. For a more accurate determination of activity, the use of DAS 28 index (disease activity score) is recommended, the calculation formula of which includes the number of affected and the number of swollen joints out of 28 (glenohumeral, ulnar, radiocarpal, genicular and hand joints), ESR and the patient's well-being assessment score on a visual analog scale. There are 3 activity rates: