Rheumatoid arthritis (RA) is a chronic, autoimmune disease that mainly affects the joints, although it can also manifest in other organs and systems of the body. It is characterized by persistent inflammation of the joints, which can lead to progressive destruction of cartilage, bone, and other joint tissue.
In RA, the body's immune system, which normally protects against infection, mistakenly begins to attack healthy cells and tissues, especially the synovial membranes that line the joints. This autoimmune reaction triggers a chronic inflammatory response in the joints, resulting in pain, stiffness, swelling, and joint deformity.
RA is a chronic and autoimmune disease that mainly affects the joints.
It is more common in women than in men, with a ratio of approximately 3:1.
It can develop at any age, but it is most common between the ages of 40 and 60.
The prevalence of RA varies by geographic region and ethnicity, ranging from 0.5% to 1% of the general population.
The exact etiology of RA is not yet fully understood, but it is believed to be a multifactorial disease resulting from the interaction between genetic and environmental factors.
Several genes related to susceptibility to RA have been identified, including HLA-DRB1.
Environmental factors, such as tobacco exposure, infections, and hormonal changes, may also play a role in the development of the disease.
RA can present different clinical and pathological phenotypes.
The most common phenotype is symmetric arthritis of the peripheral joints, especially those of the hands and feet.
Other phenotypes may include involvement of large joints, such as the shoulders and knees, or the presence of extra-articular manifestations, such as rheumatoid nodules, lung, cardiac, or renal involvement.
There is no single test for the diagnosis of RA, so it is based on the combination of clinical history, physical examination, and laboratory findings.
The most widely used diagnostic criteria are those of the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR), which require the presence of certain criteria, such as joint involvement, duration of symptoms, and findings in laboratory tests. laboratory.
Laboratory tests may include detection of autoantibodies, such as rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies.
Imaging, such as radiography, ultrasound, and MRI, can help assess joint damage and synovial inflammation.
Pharmacological treatment of rheumatoid arthritis (RA) is based on the use of different categories of drugs that fall into several classes, including classic synthetic disease-modifying antirheumatic drugs (csDMARDs), biologic drugs (bDMARDs), and inhibitors. of Janus kinase (JAK) (tsDMARDs).
Classic synthetic disease-modifying antirheumatic drugs (csDMARDs):
- Methotrexate: It is the most commonly used DMARD and is usually the first choice in the treatment of RA. It works by inhibiting the synthesis of folic acid and decreasing the activity of inflammatory cells.
- Leflunomide: It works by inhibiting the synthesis of pyrimidines and therefore affects cell proliferation and the immune response.
- Hydroxychloroquine: It has immunomodulatory and anti-inflammatory properties. It is used in combination with other DMARDs to improve clinical outcomes.
- Sulfasalazine: It is another DMARD used in the treatment of RA. Its mechanism of action is believed to be related to the inhibition of the activity of inflammatory cells and the reduction of the production of proinflammatory cytokines.
- Tumor necrosis factor (TNF) inhibitors: These include drugs such as etanercept, adalimumab, infliximab, golimumab, and certolizumab pegol. They work by blocking the action of TNF, an inflammatory cytokine involved in the pathogenesis of RA.
- Interleukin-6 (IL-6) inhibitors: Tocilizumab and sarilumab are drugs that block the action of IL-6, a proinflammatory cytokine involved in synovial inflammation and joint damage in RA.
- Interleukin-1 (IL-1) inhibitors: Anakinra is a drug that blocks the action of IL-1, another proinflammatory cytokine implicated in RA.
- Other biologic drugs: These include abatacept, which inhibits T cell activation, and rituximab, which depletes B cells.
Janus kinase (JAK) inhibitors:
- Tofacitinib: It is a Janus kinase inhibitor that blocks the signaling of multiple proinflammatory cytokines involved in the pathogenesis of RA.
- Baricitinib: It is also a Janus kinase inhibitor that works by blocking the signaling of multiple proinflammatory cytokines.
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