Rheumatoid arthritis (polyarthritis progressiva primaria chronica) is a chronic inflammation characterized by synovial hypertrophy with infiltration by inflammatory cells, destruction of articular cartilage and decalcification of bone (osteoporosis). Rheumatoid arthritis is characterized by the production of antibodies (RF - rheumatoid factor, ANF - antinuclear factors) and acute phase proteins. Clinically, rheumatoid arthritis can be described as a symmetrical polyarthritis that predominantly affects the small joints of the hand and radio-carpal joints, with prolonged morning stiffness.
Occurrence[edit | edit source]
Rheumatoid arthritis is 2-3 times more common in women. Symptoms develop most often between the ages of 20 and 40. However, there is also juvenile rheumatoid arthritis, which mainly affects large joints.
Etiology[edit | edit source]
Rheumatoid arthritis is an autoimmune inflammation that is often associated with the HLA-DR 4 or DR 1 immunophenotype. The initiator is thought to be a currently unknown microbial pathogen (EBV, retroviruses, parvoviruses, borrelia, etc. are being considered). It is not exactly known against which antigen the autoimmune reaction is directed - probably against type II collagen or against cartilage glycoprotein 39 (it binds to DR 4). Rheumatoid factor, the antibodies against the Fc fragment of IgG, occurs in 80% of patients.
Pathological-anatomical changes[edit | edit source]
The first changes are in the synovium, then in the fluid, later on the cartilage and finally para-articular involvement. First, serofibrinous intra-articular inflammation occurs, then a panus develops. The panus is a villi-swollen synovial membrane in which connective tissue and blood vessels proliferate excessively. It covers the articular cartilage, separating it from the nourishing synovial fluid. As a result, the chondrocytes die and the subchondral bone mass erodes. If the panus growing from opposite sides of the joint fuse, it can further change fibrotic, ossify, and eventually ankylosis.
Another morphological manifestation of rheumatoid arthritis are rheumatic nodules, which occur mainly in the subcutaneous tissue. Histologically, they consist of three layers:
- centrally there is necrotic tissue
- around it is a layer of palisade fibroblasts and multinucleated cells
- peripherally there is a layer of chronic inflammation
The clinical picture[edit | edit source]
Affection joints[edit | edit source]
Symmetric polyarthritis[edit | edit source]
Initially, involvement of the joints of the hand starts from the periphery.
Proximal interphalangeal → "bottle-shaped fingers"; metacarpophalangeal; radiocarpal.
It usually does not affect the distal interphalangeal. Later, ulnar deviation of the fingers, swan- type deformities (hyperextension in the proximal interphalangeal joint and flexion in the distal interphalangeal joint) and buttonhole - type deformities are typical (flexion in the proximal interphalangeal joint and hyperextension in the distal interphalangeal joint).
The joints are painful at rest, during palpation and movement, morning stiffness occurs (agitation lasts longer than an hour). There are classic signs of inflammation on the joints, except for redness. In more severe cases, chronic inflammation can lead to volar subluxation of the wrists and rupture of the finger tendons. The activity of the process is fluctuating, often depending on the humidity.
Disability of individual joints[edit | edit source]
- Elbow injury - flexion contractures.
- Shoulder joints - rupture of the rotator cuff .
- Hip joints - affected less often.
- Knee joints - angular deformities and flexion contractures. Fluid can penetrate the popliteal bursa - Baker's cyst. Hammer toes and hallux valgus are typical findings on the foot .
Spine[edit | edit source]
Affected mainly in the neck, the atlantoaxial joint is severely affected by subluxation (neck and head pain, spinal cord compression). Sudden death can be a complication of subluxation. An X-ray should be performed prior to each intubation operation if atlantoaxial subluxation is suspected.
Temporomandibular joint involvement[edit | edit source]
It causes chewing pain.
The course of the disease[edit | edit source]
There are 3 types of the course of the disease:
- monocyclic - one cycle of the disease followed by remission lasting more than 1 year;
- polycyclic - gradually progressing with episodes of incomplete remissions (most common);
- progressive - sustained progression without remissions.
Extra-articular involvement[edit | edit source]
The disease may be accompanied by extra-articular disorders:
rheumatic nodules (in the subcutaneous tissue, especially above the elbows and above the proximal edge of the ulna), mostly multiple, usually painful nodules, up to several cm in size;
- tendonsynovitis (mainly in the hands, rupture of tendons with the development of deformities - swan neck, buttonhole);
- osteoporosis (initially periarticular, later diffuse - pathological fractures);
- secondary amyloidosis (AA, especially kidney damage);
- haematological abnormalities (mainly anemia, thrombocytosis);
- eye disorders (iritis, iridocyclitis, keratoconjunctivitis);
- damage to the skin, heart, blood vessels, nerves, lungs, etc.
Diagnosis[edit | edit source]
Laboratory findings[edit | edit source]
- Inflammatory markers: (↑ FW, CRP ).
- Antibodies: rheumatoid factor (RF) - antibody (mostly IgM) against Fc fragments of IgG, detection by latex-fixation test; anti-CCP - antibody against cyclic citrullinated peptide, are more specific for RA than rheumatoid factors; APF - antiperinuclear factors; ANF - antinuclear factors.
- Punctate (biochemically RF, high content of polymorphonuclear cells).
X-ray changes[edit | edit source]
- Early - swelling of the soft tissues near the joints, periarticular osteoporosis, marginal bone erosion.
- Late - narrowing of the joint space, diffuse osteoporosis, deformities, bone ankylosis.
Four Steinbrocker stages were introduced for the evaluation of X-rays.
Stadium I periarticular osteoporosis, no destruction
Stadium II slight signs of destruction, without deformities
Stadium III cartilage and bone destruction, deformities
Stadium IV fibrous or bone ankylosis
Furthermore, scintigraphy can be used in diagnosis (it will show the distribution of disability in individual joints).
Criteria for diagnosis[edit | edit source]
The presence of 4 of 7 criteria is important for the diagnosis of rheumatoid arthritis:
- morning stiffness
- arthritis 3 or more areas
- arthritis of the joints of the hand (RC, MCP, PIP)
- symmetric arthritis
- rheumatoid nodules
- rheumatoid factor (RF)
- X-ray changes
Treatment[edit | edit source]
Regime measures[edit | edit source]
In the acute stage, bed rest, prevention of contractures, analgesic splints, etc.
Physical therapy and rehabilitation[edit | edit source]
Maintaining the range of motion in the joint, preventing muscle weakness.
Pharmacotherapy[edit | edit source]
The basis of pharmacological treatment is disease modifying antirheumatic drugs (DMARDs ).
Disease-modifying drugs (DMARDs)[edit | edit source]
I belong to two groups of drugs:
- biological treatment
- methotrexate : Methotrexate- the most commonly used drug, the drug of first choice,
- leflunomide : leflunomide- a pyrimidine nucleotide inhibitor, has methotrexate-like effects,
- sulfasalazine : sulfasalazine,
- hydroxychloroquine : hydroxychloroquineand chloroquine : chloroquine- have the weakest effect.
- TNFα inhibitors - etanercept : etanercept, infliximab : infliximab, adalimumab : adalimumab, golimumab : golimumab, certolizumab pegol: certolizumab pegol
- rituximab : rituximab- a chimeric monoclonal antibody against the CD20 molecule,
- abatacept : abatacept- blocks T-cell activation by blocking the costimulatory signal,
- tocilizumab National Drug Administration: tocilizumab- an anti-IL-6 receptor antibody,
- anakinra : Anakinra- IL-1 receptor antagonist.
- non-steroidal anti-inflammatory drugs and analgesics - only symptomatic drugs - COX 1 inhibitors - diclofenac : diclofenac, indomethacin : indomethacin, selective COX 2 inhibitors - nimesulide : nimesulide, coxibs ;
- corticoids - systemic (prednisone : prednisone) or intraarticularly (triamcinolone : triamcinolone) - to bridge the period until the onset of action of DMARDs.
Surgical treatment[edit | edit source]
- synovectomy (possibly also radiation application of the isotope yttrium to the joint)
- total endoprosthesis
- arthrodesis (fixation of the joint in an advantageous position, removal of pain, most often the radiocarpal area).
References[edit | edit source]
ČEŠKA, Richard, et al. Internal. 2nd, updated edition edition. Triton, 2015. p. 909. ISBN 9788073878856 .
BEDNÁŘ, Blahoslav, et al. Textbook of pathological anatomy. 2nd edition. Prague: Avicenum, 1975. 760 p.
ŠTORK, Jiří, et al. Dermatovenerology. 1st edition. Prague: Galén, Karolinum, 2008. 502 pp. 238. ISBN 978-80-7262-371-6 .
BENEŠ, Jiří. Study materials [online]. [feeling. 2011]. < http://jirben2.chytrak.cz/ >.