RA is associated with inflammation of the synovium, autoantibody production, progressive cartilage and bone destruction, early morbidity, and other systemic consequences in which many include cardiovascular events. Although structural changes can be visualized by conventional imaging techniques, joint damage is rarely apparent in early stages of disease, but rather accumulates over time (4). Various immune modulators and signalling pathways are involved in the pathophysiology of RA. The influx of mononuclear cells, including T and B cells results in synovitis, which is inflammation of the synovial joint. The synovial lining becomes hyperplastic and the membrane expands and destroys bone, due to osteoclast-rich regions. Cartilage is also degraded by enzymes secreted from synoviocytes and chondrocytes (4).
RA patients produce autoantibodies which are specific for RA. They can produce Anti-Citrullinated Protein antibodies (ACPAs) which target citrullinated proteins/peptides found within the synovium. Similarly, they can also produce Anti-Homocitrullinated Protein Antibodies (AHCPAs) which target homocitrullinated proteins/peptides. These autoantibodies in addition to the classical rheumatoid factor
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Due to the irreversible damage that occurs in RA, there is a need to improve the identification and diagnosis of early RA. The primary serological tests for RA used to be assays detecting rheumatoid factor; however, nowadays ACPA assays are being used clinically. The most widely known autoantibody is the rheumatoid factor (RF). These IgM autoantibodies are directed against the Fc portion of IgG molecules. RF can be detected in about 75% of RA patients; however, it is also found in the healthy elderly population (5). Thus, it is not very specific. In addition, false positive RF results occur in patients with chronic infections and other rheumatic and inflammatory
Rheumatoid Arthritis or “RA” is an autoimmune disorder where the immune system mistakenly attacks its own body tissues. This disease affects the lining of joints causing pain and swelling. Eventually the swelling can lead to bone erosion and joint deformity. RA can happen to anyone at any age, but the majority of people who have to endure this disease are women over the age of 40.
Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic inflammation of the joints. While inflammation of the tissue around the joints and inflammatory arthritis are characteristic features of rheumatoid arthritis, the disease can also cause inflammation and injury in other organs in the
Rheumatoid Arthritis(RA) is the most common type of autoimmune arthritis. RA is a progressive and debilitating musculoskeletal disorder that affects the joints symmetrically, causing a range of systemic effects. What it causes is still not well known; nevertheless, findings of new research points towards a believe that it is triggered by a defective immune system, which causes the release of inflammatory chemicals. These chemicals cause damage to cartilage and bone, usually affecting the wrists, the joints of the hand, including the knuckles, the middle joints of the fingers and feet. While this condition can affect any joints, besides, important body organs such as the eyes and the lungs can also be affected by the inflammation that occurs as a result of this chronic condition. Only in America 1.3 million of people are affected by this ailment, and 75 % of them are mainly women. Its onset usually occurs between fourth and sixth decades; however, RA can occur at any age("Diseases And
Rheumatoid Arthritis has been subject of numerous studies and researches in the look for a better understanding of how it effects the individuals diagnosed with it. There is a higher incident of females diagnosed with RA than male as well as a relationship with genetic and environmental factors involved. Around one percent of the world population is affected by RA; therefore, diverse studies have been performed to understand how the lives of the diagnosed patients can be impacted by the disease. For example, how RA affects the mobility, safety and activities of daily living in general as well as the development of interventions to better approach RA. On
Rheumatoid arthritis is a chronic syndrome that is characterized by inflammation of the peripheral joints, but it may also involve the lungs, heart, blood vessels, and eyes. The prevalence of this autoimmune disease is between 0.3% to 1.5% of the population in the United States (Feinberg, pp 815). It affects women two to three times more often than men, and the onset of RA is usually between 25 and 50 years of age, but it can occur at any age (Reed, pp 584). RA can be diagnosed by establishing the presence of persistent joint pain, swelling in a symmetric distribution, and prolonged morning stiffness. RA usually affects multiple joints, such as the hands, wrists, knees, elbows, feet, shoulders, hips, and small
20 patients with active RA in 1992 were first to be treated with infliximab. There was a dramatic drop in C-reactive protein (CRP and ethrocyte sedimentation rate. However patients relaped with 3-8 week demonstrating that they require another dose of
Rheumatoid arthritis frequently affects the wrists and fingers; it rarely presents anywhere else in the body. It is associated with significant and prolonged morning stiffness of the affected joints, which are often overtly warm and swollen. Radiographs show bone erosion as opposed to formation. If it is still difficult to differentiate between rheumatoid arthritis and OA, laboratory findings, like elevated erythrocyte sedimentation rate, positive serologies (such as for rheumatoid factor), or elevated white blood cell count are great indicators for rheumatoid arthritis versus
Along with the physical exam, a rheumatologist will ask several questions regarding the patient's symptoms and health history. Then, may perform several diagnostic tests. Some of these diagnostic tests include blood tests which are used to look for biomarkers like antibodies what are linked with RA as well blood tests in order to measure inflammation levels. Some of these blood tests include ones to detect anemia which is a red blood cell deficiency; the rheumatoid factor, an antibody found in about 80% of people with RA, however isn’t definitive because it can show up in other inflammatory diseases; an antibody known as anti-cyclic citrullinated peptide (anti-CCP), which is primary only seen in RA, even before symptoms start, but only seen in about 60-70% of patients with the disease; elevated red blood cell
Rheumatoid Arthritis or (RA) is an autoimmune disease that attacks the joints and connective tissue. The result is inflammation that produces permanent damage in the joints. Rheumatoid arthritis is a chronic syndrome that tends to be progressive and destructive as compared to Osteoarthritis or (OA), which is more of an age related disease caused by “wear and tear” of the joints. In contrast to (OA), rheumatoid arthritis is characterized by inflammation mostly of the joints, but is a general body disease.
Advances in the treatment of RA have shown that active drugs should be given as soon as possible [1, 2]. This idea has been framed in the concept of a window of opportunity for the best results, window that extends only for the first months since symptoms onset [3-6]. The benefits of treatment in this window include increased response rates, decreased disease activity, prevention of bone erosions, less disability, increased rates of remission, even of drug-free remission, and larger improvement in health quality scores [3-6]. These benefits are of large significance, but are demanding for the rheumatologist because often it is difficult to diagnose RA when the first symptoms appear. This task has been facilitated by the development of new RA classification criteria in 2010 [2]. These criteria aim to define patients earlier in the disease course than the 1987 ACR criteria [7].
Only if symptoms and signs strongly suggest of a connective tissue or autoimmune rheumatologic disorder, testing for a broad range of autoantibodies (antinuclear antibodies and rheumatoid factor, extractable nuclear antigens) should be done. [1, 2, 3, 4]
Synovitis is a result of inflammation of the synovium. This can be caused by an autoimmune disorder, an infection, or from gout. Transient synovitis is characterized by sudden onset and is typically self-limiting. This process is self-limiting due to the structural stability of the joint and the overall health of the patient. It should be noted that if infection is present in the joint, that would exclude transient synovitis. Transient synovitis is absent any other disease process. If there was infection in the joint, damage to the joint structures, or an autoimmune component causing inflammation, transient synovitis would not be
Genetic factors are relatively contributed about 50 % of the risk of the pathogenesis of RA (Aho et al., 1986; MacGregor et al., 2000). MHC encoding HLA-DRB1 gene is one of greater risk posing allele responsible for the 1/3rd of genetic basis (Deighton et al., 1989; Rigby et al., 1991). These alleles further subdivided and defined by the presence or absence of Anti-citrullinated protein antibodies (ACPA), also termed as ACPA positive RA and ACPA negative RA (Seegobin et al., 2014). ACPA positive RA more worsens the condition with severe erosive damage (Silman and Pearson, 2002). However, the non-genetic factors such as pregnancy, lifestyle, and obesity have been implicated in the development of RA (Colebatch
The detection of autoantibodies against intracellular targets called antinuclear antibodies (ANA) is important in the diagnosis of systemic autoimmune rheumatic diseases (SARD) such as systemic lupus erythematosus (SLE), Sjögren's syndrome (SjS), mixed connective tissue diseases (MCTD), systemic sclerosis (SSc) and idiopathic inflammatory myopathies (IIM). Testing for ANA is therefore a logical first step in the differential evaluation of patients when systemic autoimmune etiology is suspected. Timely diagnosis of SARD is challenging due to the wide spectrum of overlapping symptoms. Furthermore, while the frequency of ANA is highest in patients with SARD, these antibodies are also found in