Rheumatoid Arthritis--A Separate World, Personal Account of Living with Rheumatoid Arthritis
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Blood tests may include a blood count looking for anemia or signs of infection and other tests for markers of inflammation. Osteoarthritis , damage to cartilage in the joints, is a different disease process. Osteoarthritis is not an autoimmune disease but is related to wear and tear on cartilage, which causes joint pain. Osteoarthritis does not have effects on the heart, lungs, or the body's immune system. Anti-inflammatory medications ease pain and reduce inflammation within joints.
Steroids are often used in RA treatment. Because of adverse side effects of steroids, it is important to find the smallest effective dose for each individual. DMARDs are medications that act on the body's immune response. Biologic products, such as monoclonal antibody medications, may be used as part of treatment for RA. Lifestyle changes, such as gentle daily exercise and eating a healthy diet, can improve overall well-being, maintain muscle strength and joint motion, and help with mood. Quitting smoking may improve symptoms. Joint replacement may be offered to persons with RA when joint pain, stiffness, and deformity become limiting factors in an individual's life.
Consultation with an orthopedic surgeon may be recommended when joint damage is present. Many are available in English and Spanish. The information and recommendations appearing on this page are appropriate in most instances, but they are not a substitute for medical diagnosis. For specific information concerning your personal medical condition, JAMA suggests that you consult your physician. This page may be photocopied noncommercially by physicians and other health care professionals to share with patients. Torpy, MD ; Gabriela D. Perazza, MS ; Robert M.
Sign in to access your subscriptions Sign in to your personal account. Create a free personal account to download free article PDFs, sign up for alerts, and more. Purchase access Subscribe to the journal. Macrophage activation syndrome is a life-threatening complication of juvenile idiopathic arthritis JIA that necessitates immediate treatment with high-dose steroids and cyclosporine.
The following guidelines on treating RA to therapeutic target were issued in by an international task force of rheumatologists, patient representatives, and a rheumatology nurse [ 7 , 8 ]:.
The pathogenesis of RA is not completely understood. An external trigger eg, cigarette smoking, infection, or trauma that sets off an autoimmune reaction, leading to synovial hypertrophy and chronic joint inflammation along with the potential for extra-articular manifestations, is theorized to occur in genetically susceptible individuals.
Synovial cell hyperplasia and endothelial cell activation are early events in the pathologic process that progresses to uncontrolled inflammation and consequent cartilage and bone destruction. Genetic factors and immune system abnormalities contribute to disease propagation. CD4 T cells, mononuclear phagocytes, fibroblasts, osteoclasts, and neutrophils play major cellular roles in the pathophysiology of RA, whereas B cells produce autoantibodies ie, rheumatoid factors. Ultimately, inflammation and exuberant proliferation of the synovium ie, pannus leads to destruction of various tissues, including cartilage see the image below , bone, tendons, ligaments, and blood vessels.
Although the articular structures are the primary sites involved by RA, other tissues are also affected. The cause of RA is unknown. Genetic, environmental, hormonal, immunologic, and infectious factors may play significant roles. Socioeconomic, psychological, and lifestyle factors eg, tobacco use, the main environmental risk [ 9 ] may influence disease development and outcome.
Genes other than those of the major histocompatibility complex MHC are also involved. Juvenile idiopathic arthritis JIA , also known as juvenile rheumatoid arthritis JRA , is a heterogeneous group of diseases that differs markedly from adult RA. JIA is known to have genetically complex traits in which multiple genes are important for disease onset and manifestations, and it is characterized by arthritis that begins before the age of 16 years, persists for more than 6 weeks, and is of unknown origin.
Some investigators suggest that the future of treatment and understanding of RA may be based on imprinting and epigenetics. RA is significantly more prevalent in women than in men, [ 15 , 16 ] which suggests that genomic imprinting from parents participates in its expression. Epigenetics is the change in DNA expression that is due to environmentally induced methylation and not to a change in DNA structure.
Clearly, the research focus will be on environmental factors in combination with immune genetics. For many decades, numerous infectious agents have been suggested as potential causes of RA, including Mycoplasma organisms, Epstein-Barr virus EBV , and rubella virus. This suggestion is indirectly supported by the following evidence:. The inducibility of arthritis in experimental animals with different bacteria or bacterial products eg, streptococcal cell walls.
The disease-modifying activity of several agents that have antimicrobial effects eg, gold salts, antimalarial agents, minocycline. Emerging evidence also points to an association between RA and periodontopathic bacteria. For example, the synovial fluid of RA patients has been found to contain high levels of antibodies to anaerobic bacteria that commonly cause periodontal infection, including Porphyromonas gingivalis. Sex hormones may play a role in RA, as evidenced by the disproportionate number of females with this disease, its amelioration during pregnancy, its recurrence in the early postpartum period, and its reduced incidence in women using oral contraceptives.
Hyperprolactinemia may be a risk factor for RA. All of the major immunologic elements play fundamental roles in initiating, propagating, and maintaining the autoimmune process of RA. The exact orchestration of the cellular and cytokine events that lead to pathologic consequences eg, synovial proliferation and subsequent joint destruction is complex, involving T and B cells, antigen-presenting cells eg, B cells, macrophages, and dendritic cells , and various cytokines.
Rheumatoid Arthritis: Practice Essentials, Background, Pathophysiology
Aberrant production and regulation of both proinflammatory and anti-inflammatory cytokines and cytokine pathways are found in RA. T cells are assumed to play a pivotal role in the initiation of RA, and the key player in this respect is assumed to be the T helper 1 Th1 CD4 cells. These cells may subsequently activate macrophages and other cell populations, including synovial fibroblasts.
Experimental models suggest that synovial macrophages and fibroblasts may become autonomous and thus lose responsiveness to T-cell activities in the course of RA. B cells are important in the pathologic process and may serve as antigen-presenting cells. The hyperactive and hyperplastic synovial membrane is ultimately transformed into pannus tissue and invades cartilage and bone, with the latter being degraded by activated osteoclasts. The major difference between RA and other forms of inflammatory arthritis, such as psoriatic arthritis , lies not in their respective cytokine patterns but, rather, in the highly destructive potential of the RA synovial membrane and in the local and systemic autoimmunity.
Whether these 2 events are linked is unclear; however, the autoimmune response conceivably leads to the formation of immune complexes that activate the inflammatory process to a much higher degree than normal.
This theory is supported by the much worse prognosis of RA among patients with positive RF results. First-degree relatives of individuals with RA are at 2- to 3-fold higher risk for the disease. Because the worldwide frequency of RA is relatively constant, a ubiquitous infectious agent has been postulated to play an etiologic role. Women are affected by RA approximately 3 times more often than men are, [ 15 , 16 ] but sex differences diminish in older age groups. Time elapsed since pregnancy is also significant.
In the 1- to 5-year postpartum period, a decreased risk for RA has been recognized, even in those with higher-risk HLA markers. The Danish study also found a higher risk of RA among women with a history of preeclampsia, hyperemesis during pregnancy, or gestational hypertension. Outcome in RA is compromised when diagnosis and treatment are delayed.
The clinical course of RA is generally one of exacerbations and remissions. Nonetheless, predicting the long-term course of an individual case of RA at the outset remains difficult, though the following all correlate with an unfavorable prognosis in terms of joint damage and disability:.
In a retrospective study that used logistic regression to analyze clinical and laboratory assessments in patients with RA who took only methotrexate, the authors found that measures of C-reactive protein CRP and swollen joint count after 12 weeks of methotrexate administration were most associated with radiographic progression at week The prognosis of RA is generally much worse among patients with positive RF results.
For example, the presence of RF in sera has been associated with severe erosive disease. Other laboratory markers of a poor prognosis include early radiologic evidence of bony injury, persistent anemia of chronic disease, elevated levels of the C1q component of complement, and the presence of ACPA see Workup. In fact, the presence of ACPA and antikeratin antibodies AKA in sera has been linked with severe erosive disease, [ 28 ] and the combined detection of these autoantibodies can increase the ability to predict erosive disease in RA patients.
RA that remains persistently active for longer than 1 year is likely to lead to joint deformities and disability. A study by Mollard et al of women in a US-wide observational cohort who developed RA before menopause found greater functional decline in postmenopausal women than in premenopausal ones; furthermore, the trajectory of functional decline worsened and accelerated after menopause. However, ever-use of hormonal replacement therapy, ever having a pregnancy, and longer length of reproductive life were associated with less functional decline. Most data on RA disability rates derive from specialty units caring for referred patients with severe disease.
Little information is available on patients cared for in primary care community settings. RA is associated with traditional and nontraditional cardiovascular risk factors. The leading cause of excess mortality in RA is cardiovascular disease, followed by infection, respiratory disease, and malignancies.
Symptoms and risk factors
The effects of concurrent therapy, which is often immunosuppressive, may contribute to mortality in RA. However, studies suggest that control of inflammation may improve mortality. Nontraditional risk factors appear to play an important role in cardiovascular morbidity and mortality. Myocardial infarction , myocardial dysfunction, and asymptomatic pericardial effusions are common; symptomatic pericarditis and constrictive pericarditis are rare. Myocarditis, coronary vasculitis, valvular disease, and conduction defects are occasionally observed.
A large Danish cohort study suggested the presence of an increased risk of atrial fibrillation and stroke in patients with RA. The overall mortality in patients with RA is reportedly 2. In the s, mortality among those with severe articular and extra-articular disease approached that among patients with 3-vessel coronary disease or stage IV Hodgkin lymphoma. Much of the excess mortality derives from infection, vasculitis, and poor nutrition.
With the exception of lymphoma, mortality from cancer is unchanged. Patient education and counseling help to reduce pain, disability, and frequency of physician visits. These may represent the most cost-effective intervention for RA. With a potentially disabling disease such as RA, the act of informing the patient of the diagnosis takes on major importance. Telling patients more than they are intellectually or psychologically prepared to handle a common practice risks making the experience so intense as to trigger withdrawal.
Conversely, failing to address issues of importance to the patient compromises the development of trust.
The patient needs to know that the primary physician understands the situation and is available for support, advice, and therapy as the need arises. Encouraging the patient to ask questions helps to communicate interest and caring. Patients and families do best when they know what to expect and can view the illness realistically. Many patients fear crippling consequences and dependency.
Accordingly, it is valuable to provide a clear description of the most common disease manifestations. Without encouraging false hopes, the physician can point out that spontaneous remissions can occur and that more than two thirds of patients live independently without major disability. In addition, emphasize that much can be done to minimize discomfort and to preserve function. A review of available therapies and their efficacy helps patients to overcome feelings of depression stemming from an erroneous expectation of inevitable disability.
Even in those with severe disease, guarded optimism is now appropriate, given the host of effective and well-tolerated disease-modifying treatments that are emerging. Several common misconceptions regarding RA deserve attention. Explaining that no known controllable precipitants exist helps to eliminate much unnecessary guilt and self-recrimination. Dealing in an informative, evidence-based fashion with a patient who expresses interest in alternative and complementary forms of therapy can help limit expenditures on ineffective treatments. Another misconception is that a medication must be expensive to be helpful.
Physical Examination
Active participation of the patient and family in the design and implementation of the therapeutic program helps boost morale and to ensure compliance, as does explaining the rationale for the therapies used. The family also plays an important part in striking the proper balance between dependence and independence.
Allowing the patient with RA to struggle with a task is sometimes constructive. Abandonment is a major fear in these individuals. With occupational therapy, the treatment effort is geared toward helping the patient maintain a meaningful work role within the limitations of the illness. Persons with long-standing severe disease who have already sustained much irreversible joint destruction benefit from an emphasis on comfort measures, supportive counseling, and attention to minimizing further debility. Such patients need help in grieving for their disfigurement and loss of function.
An accepting, unhurried, empathic manner allows the patient to express feelings. The seemingly insignificant act of touching does much to restore a sense of self-acceptance. Attending to pain with increased social support, medication, and a refocusing of attention to function is useful. A trusting and strong patient-doctor relationship can do much to sustain a patient through times of discomfort and disability.
Rheumatoid arthritis disease activity measures: American College of Rheumatology Recommendations for use in clinical practice. Arthritis Care Res Hoboken. Arthritis Care and Research. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: Agency for Healthcare Research and Quality.
Choosing Medications for Rheumatoid Arthritis. May 28, ; Accessed: Treating rheumatoid arthritis to target: Smoking, use of moist snuff, and risk of chronic inflammatory diseases. Barton A, Worthington J. Genetic susceptibility to rheumatoid arthritis: A missense single-nucleotide polymorphism in a gene encoding a protein tyrosine phosphatase PTPN22 is associated with rheumatoid arthritis. Am J Hum Genet. Influence of gender on assessments of disease activity and function in early rheumatoid arthritis in relation to radiographic joint damage. Areskoug-Josefsson K, Oberg U.
A literature review of the sexual health of women with rheumatoid arthritis. Joint linkage and imprinting analyses of GAW15 rheumatoid arthritis and gene expression data. Antibodies to porphyromonas gingivalis are associated with anticitrullinated protein antibodies in patients with rheumatoid arthritis and their relatives. Autopathogenic correlation of periodontitis and rheumatoid arthritis. Does rheumatoid arthritis remit during pregnancy and relapse postpartum?
Results from a nationwide study in the United Kingdom performed prospectively from late pregnancy. National cohort study of reproductive risk factors for rheumatoid arthritis in Denmark: Does pregnancy provide vaccine-like protection against rheumatoid arthritis?.
Harrison's Principles of Internal Medicine. Very early rheumatoid arthritis as a predictor of remission: Factors associated with radiographic progression in patients with rheumatoid arthritis who were treated with methotrexate. Autoantibodies in rheumatoid arthritis: Autoantibodies can be prognostic markers of an erosive disease in early rheumatoid arthritis.
Work disability in rheumatoid arthritis 10 years after the diagnosis. The impact of menopause on functional status in women with rheumatoid arthritis. Risk of atrial fibrillation and stroke in rheumatoid arthritis: Danish nationwide cohort study. Psycho-educational interventions in the treatment of arthritis. Tucker M, Kirwan JR. Does patient education in rheumatoid arthritis have therapeutic potential?. Practical aspects of therapeutic intervention in rheumatoid arthritis.
Cost-effectiveness of combination nonbiologic disease-modifying antirheumatic drug strategies in patients with early rheumatoid arthritis. An algorithm to identify rheumatoid arthritis in primary care: Views Read Edit View history. Cochrane Database of Systematic Reviews. Quality of life measures: Autoimmune diseases induced by TNF-targeted therapies.
Pneumocystis jiroveci pneumonia in patients with rheumatoid arthritis treated with infliximab: Predictors for remission in rheumatoid arthritis patients: Is routine viral screening useful in patients with recent-onset polyarthritis of a duration of at least 6 weeks? Results from a nationwide longitudinal prospective cohort study. Rheumatoid factor determines structural progression of rheumatoid arthritis dependent and independent of disease activity.
Precipitating and perpetuating factors of rheumatoid arthritis immunopathology: Best Pract Res Clin Rheumatol. Mutation and citrullination modifies vimentin to a novel autoantigen for rheumatoid arthritis. Anti-citrullinated protein antibodies in rheumatoid arthritis: Clin Rev Allergy Immunol. Novel biomarkers improve diagnosis in early RA. New autoantibodies as biomarkers for early and seronegative rheumatoid arthritis [abstract OP]. Imaging in rheumatoid arthritis.
Emerging role of ultrasonography in rheumatoid arthritis: Ultrasound of Rheumatoid Arthritis. Advanced Imaging of Arthritis. Reliability of ultrasonography to detect synovitis in rheumatoid arthritis: Rheumatoid and psoriatic knee synovitis: Role of magnetic resonance imaging in the diagnosis and prognosis of rheumatoid arthritis. Doppler ultrasonography and dynamic magnetic resonance imaging for assessment of synovitis in the hand and wrist of patients with rheumatoid arthritis.
Change of synovial vascularity in a single finger joint assessed by power doppler sonography correlated with radiographic change in rheumatoid arthritis: Do non-steroidal anti-inflammatory drugs have a significant effect on detection and grading of ultrasound-detected synovitis in patients with rheumatoid arthritis?
Results from a randomised study. Lateral mass screw fixation of complex spine cases: Cervical spine involvement in rheumatoid arthritis: A good response to early DMARD treatment of patients with rheumatoid arthritis in the first year predicts remission during follow up. Disease activity early in the course of treatment predicts response to therapy after one year in rheumatoid arthritis patients. Predictors of remission, normalized physical function, and changes in the working situation during follow-up of patients with early rheumatoid arthritis: Pregnancy and rheumatoid arthritis.
Pregnancy in patients with rheumatic disease: Rheumatoid arthritis and pregnancy: Parke A, West B.
Living With Rheumatoid Arthritis
Hydroxychloroquine in pregnant patients with systemic lupus erythematosus. Antirheumatic drugs in pregnancy and lactation. Safety of anti-tumor necrosis factor therapy during pregnancy in patients with inflammatory bowel disease. British Society for Rheumatology and British Health Professionals in Rheumatology guideline for the management of rheumatoid arthritis after the first 2 years.
Rheumatoid arthritis
Effects of home-based exercise program on the functional status and the quality of life in patients with rheumatoid arthritis: Effectiveness of aquatic exercise and balneotherapy: A Randomized, Controlled Trial. Effects of high-intensity resistance training in patients with rheumatoid arthritis: Surgical principles and planning for the rheumatoid hand and wrist.
Functional and work outcomes improve in patients with rheumatoid arthritis who receive targeted, comprehensive occupational therapy. Feasibility and outcomes of a home-based exercise program on improving balance and gait stability in women with lower-limb osteoarthritis or rheumatoid arthritis: Arch Phys Med Rehabil. Impact of biologic therapy on functional status in patients with rheumatoid arthritis--a meta-analysis.