Rheumatoid arthritis is a chronic autoimmune disease causing inflammation in the lining of the joints and leading to long-term joint damage. According to the Arthritis Foundation and the NIH, 1.3 million Americans have rheumatoid arthritis, while in the UK, more than 350,000 people are affected. This month, Special Topics revisits an analysis we did two years ago by looking at the research trends in rheumatoid arthritis over the past decade and over the past two years.
Drug treatment trials dominate the 10-year list. Treatments investigated include rofecoxib, celecoxib, inflimixab alone or with methotrexate, entanercept alone or with methotrexate, anti-TNF antibodies, rituximab, adalimumab, leflunomide, sulphasalazine, and interleukin-1 receptor antagonists. The long-term gastrointestinal toxicity of rofecoxib and celecoxib are examined, as are the role of cytokine pathways in the mechanisms of joint inflammation and the diagnostic value of rheumatoid arthritis autoantibodies. Compared with our 2006 analysis, etanercept appears to be taking on a larger therapeutic role; in addition, studies into the mechanisms of disease are increasing.
Rheumatoid arthritis can be a painful and disabling condition that can result in significant loss of mobility and function if not treated adequately. Its causes are still not known. There is no evidence indicating that emotional and physical effects could cause the disorder. Smoking is one of the most significant risk factor among the non-genetic risks. The disease can be diagnosed through various techniques: imaging and blood tests among others.
The course of RA varies significantly. Some individuals might have mild short-term signs and symptoms. However, in many people the disease is progressive for life. Approximately 20 to 30 per cent of the patients have rheumatoid nodules, which is linked to poor prognosis. Some of the prognostic factors include positive serum RF findings, early erosive disease, persistent synovitis, family history, socioeconomic factors, poor functional status, C-reactive protein (CRP) and positive serum anti-CCP autoantibodies, The disease is known to reduce the lifespan by about 3 to 12 years. However, the use of biologic drug therapies extends the lifespan of people suffering from the disease (Cush, Weinblatt, & Kavanaugh, 2010).
Post-traumatic arthritis can be treated by losing weight, exercising to strengthen the muscles, and using NSAIDs. In addition, arthritic joints can also be injected with hylamers or cortisone that act as artificial fluid for the joint. Surgical treatment might be used where the above medications are not effective in relieving the pain and maintain the function. Surgical treatment might include debriding, replacing or reconstructing the joint surfaces (Cush, Weinblatt, & Kavanaugh, 2010).
Juvenile Rheumatoid Arthritis (JRA), or sometimes called juvenile chronic arthritis, is a disease that affects children causing joint inflamation which makes the joints stiff and painful.
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.
Drug therapy also dominates the two-year list. Named trials include the PREMIER, TEMPO, and ASPIRE studies, as well as the British Society for Rheumatology Biologics Register. Drug treatments include anti-TNF antibodies, adalimumab, rituximab, abatacept, B-cell targeting, tocilizumab, etanercept, and glucocorticoids. Like the 10-year list, there are more papers speculating on the etiology of rheumatoid arthritis compared with the 2006 analysis, as well as more papers examining the diagnostic value of specific autoantibodies. Other concerns, such as the reconstitution of peripheral blood B cells after certain types of therapy and predictors of joint damage, are also addressed.
In some patienst with rheumatoid arthritis, chronic inflammation leads to the destruction of the cartilage, bone and ligaments causing deformity of the joints.
Papers: To construct the top 20 papers lists for the past decade and the past two years, the papers were further narrowed down by the title keywords "rheumatoid arthritis." This adjustment resulted in the top 20 papers being selected from a pool of 8,898 (10 years) and 2,504 (2 years) papers.
Rheumatoid Arthritis (RA) refers to an autoimmune illness resulting from chronic and systemic inflammatory, which might affect various organs and tissues, though it primarily attacks synovial or flexible joints. Rheumatoid arthritis can be a painful and disabling condition that can result in significant loss of mobility and function if not treated adequately. The condition involves the inflammatory reaction of the capsules around the synovium due to the swelling of the synovial cells or turgenscence, development of fibrous tissue in the synovium and excess synovial fluid. The pathology of AR frequently results in fusion of the joints and destruction of articular cartilage. According to Cush, Weinblatt, & Kavanaugh (2010), rheumatoid arthritis can also produce inflammation in the membrane around the heart, lungs and white of the eye. Despite the cause of the illness not well-know, autoimmunity seems to play a crucial role in its progression and chronicity. RA is a clinical diagnosis made based on the symptoms, radiographs, physical exams and labs. In this regard, this paper discusses the RA by paying attention to the following: incidence, etiology, risk factors, clinical manifestations, and medical treatments.
Rheumatoid Arthritis is one of autoimmunity. Its causes are still not known. According to Goronzy & Weyand (2001), it is a disorder that affects the whole body, that is why it is referred to as systemic illness. There is no evidence indicating that emotional and physical effects could cause the disorder. The various negative findings argue that either the causes varies among individuals, or that it might be a an event inherent in the immune response. About half of the Rheumatoid Arthritis is believed to be genetic. The disorder is significantly linked to the inherited tissue type major histocompatibility complex (MHC) antigen. It is also associated with genes PAD14 and PTPN22. As a result, the history of the family is a significant factor. The inheritance of the PTPN22 gene has been said to increase the vulnerability of the disease. PAD14 has been detected to be a primary risk factor in individuals of Asian descent, and not in people of European descent. The prevalence rate of disease in first-degree relative is estimated to be about 2-3 per cent.
Epidemiological researches have affirmed a possible link between the two herpes virus that are Human Herpes Virus 6 (HHV-6) and Epstein-Barr virus (EBV) and rheumatoid arthritis. Individuals suffering from rheumatoid arthritis are most likely to show an abnormal unnube reaction to EBV. In addition, they have high levels of anti-Epstein-Barr virus antibodies. According to Goronzy & Weyand (2001), the deficiency of vitamin D is popular in individuals with rheumatoid arthritis and might causally be linked to the disorder. Some studies have revealed that there is reduced risk with supplemental, whereas others have not.