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EXTRA-ARTICULAR MANIFESTATIONS OF RHEUMATOID ARTHRITIS
Tolibov Farrux Farhodivich
Asia International University, Bukhara, Uzbekistan.
https://doi.org/10.5281/zenodo.15478727
Abstract. Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease of
connective tissue with predominant joint involvement in the form of erosive-destructive
progressive polyarthritis. Felty's syndrome is a variant of RA that includes chronic polyarthritis,
splenomegaly, and leukopenia.
Keywords: Rheumatoid arthritis (RA), polyarthritis, Joint damage, inflammation.
Introduction:
Epidemiology: incidence 0.5-1% of the population, peak incidence in the
5th decade of life; the most disabling lesion of the joints - after 10 years from the onset of the
disease 50% of patients are disabled, after 20 years - all 100%.
The etiology is unknown, the involvement of the following factors is discussed:
a) genetic predisposition (correlates with HLA DR4, Dw4 and other HLA antigens)
b) infectious agents (Epstein-Barr virus (increased titres to it are detected in 80% of
patients), retroviruses, rubella, herpes viruses, mycoplasmas, mycobacteria are considered to be
the etiological factor).
Pathogenesis of RA:
1. It is based on genetically determined autoimmune processes arising due to deficiency
of T-suppressor function of lymphocytes under the influence of an unknown etiological factor. In
the debut of the process is characterised by AG-specific activation of T-helper cells with
hyperproduction of pro-inflammatory (ФНО - the most important factor, IL-1, IL-8, etc.) and
relative deficiency of anti-inflammatory (IL-4, etc.) mediators, stimulation of synovial B-
lymphocytes with synthesis of rheumatoid factor - altered IgM, sometimes IgG or IgA to IgG
fragment of own tissues (is an autoantigen).
2. Joint damage starts with inflammation of the synovial membrane (synovitis) producing
synovial fluid, then due to autoimmune inflammation panus is formed - granulation tissue
originating from the inflamed synovial membrane, consisting of actively proliferating
fibroblasts, macrophages, lymphocytes and very rich in blood vessels; panus grows intensively,
sprouts into cartilage and destroys it with the help of a number of enzymes
3. cartilage is gradually destroyed and disappears, it is replaced by granulation tissue with
the development of ankylosis, deformity of the joint, formation of bone erosions (usuras),
inflammation of periarticular tissues.
Classification of RA:
a) according to the degree of seropositivity: seropositive and seronegative
b) according to the degree of activity: minimal, moderate, high
c) according to joint X-ray data: I - periarticular osteoporosis, II - osteoporosis + slight
narrowing of the articular gap, there may be single nodules, III - osteoporosis + sharp narrowing
of the articular gap + multiple nodules, IV - osteoporosis + narrowing of the articular gap +
multiple nodules + there may be bone ankyloses.
d) depending on the functional insufficiency of the joint: 0 - no functional insufficiency, I
- restriction of professional ability to work, II - loss of professional ability to work, III - loss of
ability to self-care.
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RA clinic:
- several weeks to months of RA may be preceded by a prodromal period (malaise,
fatigue, depression, etc.)
(a) Joint syndrome
- the disease begins subacutely with a gradual increase in pain and stiffness in small
peripheral
joints
(wrist,
metacarpophalangeal,
proximal
interphalangeal,
ankle,
metatarsophalangeal); almost never affect the joints of the spine, distal interphalangeal joints and
joints of the big toe, proximal interphalangeal joint of the little finger (joints-exceptions).
- bilateral, symmetrical joint involvement (inflammatory synovitis)
- pain in the area of the joints for a long time, increasing with exertion and decreasing at
night, stronger in the morning than in the evening
- morning stiffness of joints for more than 1 hour,
b) extra-articular manifestations of RA:
- constitutional: weakness, malaise, weight loss, subfebrile temperature
- rheumatoid nodules - accumulations of immune complexes over the affected joints or in
the area of the extensor surface of the elbow bone; nodule size from 2-3 mm to 4-5 cm, painless,
can be both mobile (located in the subcutaneous tissue) and immobile (located under the
subcutaneous tissue).
- Cardiovascular: pericarditis, ‘early atherosclerosis’, digitalis arteritis (up to Raynaud's
syndrome).
- pulmonary: dry pleurisy, interstitial pulmonary fibrosis
- CN lesions: compression neuropathy (compression of nerve trunks due to joint
deformity), symmetrical neuropathy, multiple mononeuritis (vasa nervorum), cervical myelitis.
- Renal: amyloidosis, renal tubular acidosis, interstitial nephritis (more often due to LS)
- Haematological: anaemia, moderate leucocytosis, thrombocytosis; neutropenia in Felty's
syndrome
Diagnostic criteria for RA:
At least 4 of the following criteria must be present to make a diagnosis of RA:
1. morning stiffness for more than 1 hour
2. arthritis of ≥ 3 joints (polyarthritis)
3. arthritis of the joints of the hands
4. symmetrical arthritis
5. rheumatoid nodules
6. rheumatoid factor
7. characteristic radiological changes.
These signs should last for at least 6 weeks as sometimes other arthritis can manifest in
the same way.
Treatment of RA.
1. treatment should be permanent (lifelong), complex (medication + physiotherapy +
sanatorium-resort + surgery as indicated), individual, stage-by-stage.
2. Drug therapy:
А. Basis therapy (slow acting drugs):
- Arava (leflunamide) (ranked 1st in efficacy, used > 5 years)
- methotrexate (2nd most effective, used > 20 years)
- gold preparations (turedone) (3rd most effective, used > 60 years)
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- sulfasalazine (4th most effective, used > 50 years)
- D-penicillamine (5th most effective, used > 40 years)
- Azathioprine (6th most effective, used > 30 years)
- aminoquinoline drugs (Plaquenil) (7th most effective, used > 40 years);
All these drugs are effective in 40% of cases, 30% have side effects, and another 30%
have no effect; on average, the effect of baseline therapy occurs after 2 months (Arava - 1
month). It is possible to combine baseline drugs (methotrexate + sulfasalazine + plaquenil, etc.),
but only if they are pathogenetically combined.
Б. Anti-inflammatory therapy:
1) NSAIDs: traditional, classical (indomethacin, diclofenac 75-150 mg/day in 2-3 doses,
ibuprofen 1.2-3.2 g/day in 3-4 doses, etc.) and selective COX-2 inhibitors (less side effects:
meloxicam / movalis 7.5-15 mg/day, nimesulide / nimesil / nimesil / nayz 100 mg/day in 2 doses,
celecoxib / celecbrex).
CONCLUSION:
Extra-articular manifestations of rheumatoid arthritis (RA) represent a significant aspect
of the disease's systemic nature, affecting multiple organs and contributing to increased
morbidity and mortality. These manifestations, including rheumatoid nodules, pulmonary
involvement, cardiovascular complications, vasculitis, and ocular or hematologic disorders, often
indicate a more severe disease course. Early recognition and comprehensive management of
extra-articular features are essential to improve patient outcomes, prevent irreversible damage,
and tailor individualized treatment strategies. Understanding the full spectrum of RA beyond
joint involvement underscores the importance of multidisciplinary care in achieving optimal
disease control and quality of life for patients.
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