Rheumatoid arthritis ( RA ) is a long-term autoimmune disorder that primarily affects joints. It usually produces a warm, swollen, and painful joint. Pain and stiffness often worsen after rest. Most often, the wrist and hand are involved, with the same joint usually involved on both sides of the body. The disease can also affect other parts of the body. This can lead to low red blood cell count, inflammation around the lungs, and inflammation around the heart. Fever and low energy can also be present. Often, symptoms appear gradually from week to month.
While the cause of rheumatoid arthritis is unclear, it is believed to involve a combination of genetic and environmental factors. The underlying mechanism involves the immune system attacking the joints. This causes inflammation and thickening of the joint capsule. It also affects the bones and cartilage underneath. Diagnosis is made largely based on the signs and symptoms of a person. X-rays and laboratory testing may support diagnosis or exclude other diseases with similar symptoms. Other diseases that may arise also include systemic lupus erythematosus, psoriatic arthritis, and fibromyalgia among others.
The goal of treatment is to reduce pain, reduce inflammation, and improve one's overall function. This can be helped by balancing rest and exercise, the use of splints and braces, or the use of tools. Pain medications, steroids, and NSAIDs are often used to help treat symptoms. Disease-modifying antirheumatic drugs (DMARDs), such as hydroxychloroquine and methotrexate, may be used to try to slow the progression of the disease. Biological DMARD can be used when the disease does not respond to other treatments. However, they may have a higher rate of side effects. Surgery to repair, replace, or put together joints can help in certain situations. Most alternative medicine treatments are not supported by evidence.
RA affects approximately 24.5 million people by 2015. This is between 0.5 and 1% of adults in developed countries with 5 and 50 per 100,000 newly developing conditions each year. Onset is most common in middle age and women are exposed to 2.5 times more often than men. By 2013, it resulted in 38,000 deaths rising from 28,000 deaths in 1990. The first description recognized by RA was made in 1800 by Dr. Augustin Jacob LandrÃÆ' Â © -Beauvais (1772-1840) from Paris. The term rheumatoid arthritis is based on Greek for watery and inflamed joints.
Video Rheumatoid arthritis
Signs and symptoms
RA mainly attacks the joints, but also affects other organs in over 15-25% of individuals.
Sendi
Arthritis of the joints involves inflammation of the synovial membrane. The joints become swollen, tender and warm, and the rigidity limits their movement. Over time, several joints are affected (polyarthritis). The most commonly involved are small joints in the hands, legs and cervical spine, but larger joints such as the shoulder and knee can also be involved. Synovitis can cause tissue withdrawal with loss of movement and erosion of the joint surface leading to deformity and loss of function.
RA usually manifests with signs of inflammation, with swollen, warm, painful and stiff joints, especially in the early morning waking or following prolonged activity. Increased stiffness in the morning is often a hallmark of the disease and usually lasts for more than an hour. Gentle movements can relieve symptoms in the early stages of the disease. These signs help differentiate rheumatoid from joint non-inflammatory problems, such as osteoarthritis. In non-inflammatory arthritis causes, signs of inflammation and morning stiffness are less prominent with stiffness usually less than an hour, and movement inducing pain caused by mechanical arthritis. The pain associated with RA is induced in the site of inflammation and is classified as nociceptive as opposed to neuropathic. Joints are often influenced quite symmetrically, although these are not specific, and the initial presentation may be asymmetrical.
As pathology develops, inflammatory activity causes the tendon to be blocked and erosion and destruction of joint surfaces, which interfere with various movements and cause deformity. The fingers may suffer from almost any disorder depending on which joint is most involved. Specific deformities, which also occur in osteoarthritis, include ulnar deviation, boutonniere deformity (also "buttonhole deformity", proximal interphalangeal joint flexion and extension of the distal interphalangeal joints of the hand), goose neck deformity (hyperextension of the proximal interphalangeal joint and flexion in the distal interphalangeal joint ) and "Z-thumb." "Z-thumb" or "Z-deformity" consists of interphalangeal joint hypertension, fixed flexion and subluxation of metacarpophalangeal joints and gives the appearance of "Z" on the thumb. Deformity of the toe hammer can be seen. In the worst case, joints are known as arthritis mutilans because of the mutilation nature of the deformity.
Skin
Rheumatoid nodules, which are occasionally in the skin, are the most common non-joint feature and occur in 30% of people who experience RA. This is a type of inflammatory reaction known to pathologists as "necrotizing granuloma". The initial pathological process in the formation of nodules is unknown but may be essentially synovitis, since similar structural features occur in both. The nodule has a central area of ​​fibrinoid necrosis which may be ruptured and corresponding to the fibrin-rich necrotic material found in and around the affected synovial space. Approximately necrosis is a layer of macrophages and palisading fibroblasts, corresponding to the intima layers of the synovium and cuff connective tissue containing a collection of lymphocytes and plasma cells, corresponding to the subintimal zone of synovitis. A typical rheumatoid nodule may be several millimeters in diameter up to a few centimeters and is usually found on top of bony bulge, such as elbows, heels, knuckles, or other areas that support recurrent mechanical stress. Nodules are associated with positive RF (rheumatoid factor) titer, ACPA, and severe erosive arthritis. Rarely, this can occur in internal organs or on various sites in the body.
Some forms of vasculitis occur in RA, but most are seen with old and untreated diseases. The most common presentations are due to the involvement of small and medium-sized vessels. Rheumatoid vasculitis can thus often present with skin ulceration and nerve vasculitic infarction known as multiplex mononeuritis.
Other, less common, skin-related symptoms include pyoderma gangrenosum, Sweet syndrome, drug reactions, erythema nodosum, lobe panniculitis, finger skin atrophy, palmar erythema, and skin fragility (often worsened by corticosteroid use).
Lung
Pulmonary fibrosis is a known complication of rheumatoid arthritis. This is also a rare but well-recognized consequence of therapy (eg with methotrexate and leflunomide). Caplan syndrome describes pulmonary nodules in individuals with RA and additional exposure to coal dust. Exudative pleural effusions are also associated with RA.
Heart and blood vessels
People with RA are more susceptible to atherosclerosis, and the risk of myocardial infarction (heart attack) and stroke is significantly increased. Other possible complications are: pericarditis, endocarditis, left ventricular failure, valvulitis and fibrosis. Many people with RA do not experience the same chest pain that other people experience when they experience angina or myocardial infarction. To reduce cardiovascular risk, it is important to maintain optimal control of inflammation caused by RA (which may be involved in causing cardiovascular risk), and to use proper exercise and medication to reduce other cardiovascular risk factors such as blood lipids and blood pressure.. Physicians treating people with RA should be sensitive to cardiovascular risk when prescribing anti-inflammatory drugs, and may want to consider prescribing routine use of low-dose aspirin if gastrointestinal effects are tolerated.
Blood
Anemia is the most common disorder of blood cells that can be caused by various mechanisms. Chronic inflammation caused by RA causes elevated hepcidin levels, which leads to anemia of chronic diseases in which iron is poorly absorbed and also sequestered into macrophages. The red cells have normal size and color (normocytic and normochromic). Low white blood cell counts usually occur only in people with Felty syndrome with enlarged liver and spleen. The mechanism of neutropenia is very complex. Increased platelet count occurs when inflammation is uncontrolled.
More
- Kidney
Renal amyloidosis may occur as a consequence of untreated chronic inflammation. Treatment with penicillamine and gold salts is known as the cause of membranous nephropathy.
- Eyes
- The eye can be directly affected in the form of episcleritis or scleritis, which, when severe, can rarely develop into scleromalacia perforation. Somewhat more commonly is the indirect effect of keratoconjunctivitis sicca, which is the dryness of the eyes and mouth caused by lymphocyte and salivary lymphocyte infiltration. When severe, corneal dryness can cause keratitis and loss of vision. Severe drought prevention treatment with measures such as nasolacrimal blockage is important.
- Liver
- Liver problems in people with rheumatoid arthritis may be due to the underlying disease process or as a result of drugs used to treat the disease. Autoimmune liver disease that accompanies, such as primary biliary cirrhosis or autoimmune hepatitis can also cause problems.
- Neurological
- Peripheral neuropathy and multiplex mononeuritis may occur. The most common problem is carpal tunnel syndrome caused by compression of the median nerve by swelling around the wrist. Rheumatoid disease of the spine can cause myelopathy. Axial subluxation of Atlanto can occur, due to erosion of the odontoid process and/or the transverse ligament at the cervical spine connection to the skull. Such erosion (& gt; 3mm) can cause vertebrae to slip from one another and suppress the spinal cord. Awkwardness is initially experienced, but without caution, this can develop into quadriplegia or even death.
- Constitutional symptoms
- Constitutional symptoms including fatigue, low grade fever, malaise, morning stiffness, loss of appetite and weight loss are common systemic manifestations seen in people with active RA.
- Bone
- Local osteoporosis occurs in RA around the inflamed joint. Postulated for some is caused by inflammatory cytokines. More common osteoporosis may be caused by immobility, the effects of systemic cytokines, the release of local cytokines in bone marrow and corticosteroid therapy.
- Cancer
- Incidence of lymphomas is increasing, although rare and associated with chronic inflammation, not RA treatment.
Maps Rheumatoid arthritis
Risk factors
RA is a systemic autoimmune disease (whole body). Several genetic and environmental factors affect the risk of RA.
Genetic
The family history of RA increases the risk by about three to five times; in 2016 it is estimated that genetics can reach between 40 and 65% of seropositive RA cases, but only about 20% for seronegative RA. RA is strongly associated with genes of histocompatibility complex (MHC) inherited histocompatibility complex (MHC) HLA-DR4 major tissue is the major genetic factor involved - the relative importance varies among ethnic groups. Genome association studies that examined single nucleotide polymorphisms have found about a hundred genes associated with RA risk, with most involving HLA (especially HLA-DRB1) systems that control self-recognition versus nonself molecules; other mutations affecting the co-stimulatory immune pathway, eg CD28 and CD40), cytokine signaling, lymphocyte receptor activation threshold (eg, PTPN22), and innate immune activation appear to have fewer effects than HLA mutations.
Environment
There are epigenetic and environmental risk factors established for RA. Smoking is an established risk factor for RA in Caucasian populations, increasing risk three times compared to non-smokers, especially in men, heavy smokers, and those with a positive rheumatoid factor. Simple alcohol consumption may be protective.
Silica exposure has been associated with RA.
Negative findings
No infectious agents are consistently associated with RA and there is no evidence of a disease classification to indicate the cause of the infection, but periodontal disease has been consistently associated with RA.
Many negative findings indicate that either the trigger varies, or that it may, in fact, be an event that can not be separated by the immune response.
Pathophysiology
RA is primarily initiated as a state of persistent cell activation leading to autoimmunity and immune complexes in joints and other organs in which it manifests. The site of disease is a synovial membrane, where swelling and congestion cause infiltration by immune cells. The three phases of RA development are the initiation phase (due to non-specific inflammation), the amplification phase (due to T cell activation), and the chronic inflammatory phase, with tissue injury resulting from cytokines, IL-1, TNF-alpha and IL-6.
Non-specific inflammation
Factors that allow an abnormal immune response, once started, become permanent and chronic. These factors are genetic disorders that alter the setting of adaptive immune responses. Genetic factors interact with environmental risk factors for RA, with smoking being the most obvious risk factor.
Other environmental and hormonal factors may explain a higher risk for women, including postnatal onset and hormonal drugs. The likelihood of increased susceptibility is that negative feedback mechanisms - which normally maintain tolerance - are followed by positive feedback mechanisms for certain antigens, such as IgG Fc bound by rheumatoid factor and citrullinated fibrinogen bound by antibodies to citricular peptides (ACPA - anti-citrate protein antibody). The debate about the relative role of B cells produces immune complexes and T cell products in inflammation in RA has been going on for 30 years, but no cells are needed at the site of inflammation, only autoantibodies to IgGFc, known as rheumatoid factor and ACPA, with ACPA having specificity 80% to diagnose RA. Like other autoimmune diseases, people with RA have abnormal glycosylated antibodies, which are believed to increase joint inflammation.
Amplification in synovium
Once a common abnormal immune response has been established - which may take several years before symptoms appear - plasma cells derived from B lymphocytes produce rheumatoid factor and ACPA from IgG and IgM classes in large numbers. It activates macrophages through Fc receptors and complement binding, which is part of intense inflammation in RA. Binding autoreactive antibodies to Fc receptors is mediated through N-glycans antibodies, which are altered to promote inflammation in people with RA.
This contributes to local inflammation of the joints, particularly synovium with edema, vasodilation and the inclusion of activated T cells, especially CD4 in microscopic nodular aggregates and CD8 in microscopic diffuse infiltrates. Synovial macrophages and dendritic cells act as cells presenting antigens by expressing a class II MHC molecule, which forms an immune response in the tissues.
Chronic inflammation
This disease develops by forming granulation tissue on the edges of the synovial layer, pannus with angiogenesis and enzymes that cause extensive tissue damage. Sinovium thickens, cartilage and bones are boiling, and joints worsen, with elevated levels of calprotectin that serves as a biomarker of this event.
Cytokines and chemokines attract and accumulate immune cells, ie activated T and B cells, monocytes and macrophages of activated fibroblasts, in joint space. By signaling through RANKL and RANK, they eventually trigger the production of osteoclasts, which decrease bone tissue.
Tumor necrosis factor (TNF alpha) plays a major role and some theories exist on how TNF release occurs in RA. Tumor necrosis factor-alpha (TNF-?) Is a proinflammatory cytokine that plays an important role in regulating the inflammatory response in rheumatoid arthritis (RA). If TNF release is stimulated by B-cell products in the form of immunity containing RF or complex ACPA, through activation of Fc immunoglobulin receptor, RA can be seen as a type III hypersensitivity. In 1999, if TNF release stimulated by T cell products such as interleukin-17 may be closer to type IV hypersensitivity even though this terminology may be somewhat outdated and unhelpful.
Although TNF appears to be a dominant chemical mediator, other cytokines are involved in inflammation in RA, because blocking TNF is not beneficial to all people and all tissues, especially lung and nodule diseases can get worse. Blocking IL-1, IL-15 and IL-6 has beneficial effects and IL-17 may be important.
Diagnosis
Imaging
X-rays from the hands and feet are generally done when many joints are affected. In RA, there may be no change in the early stages of the disease or x-rays can show near osteopenia joints, soft tissue swelling, and smaller joint space than normal. As the disease progresses, there may be bone erosion and subluxation. Other medical imaging techniques such as magnetic resonance imaging (MRI) and ultrasound are also used in RA.
Technical advances in ultrasonography such as high frequency transducers (10 MHz or higher) have increased the spatial resolution of ultrasound images that represent 20% more erosion than conventional radiography. Doppler color and ultrasound Doppler power are useful in assessing levels of synovial inflammation because they can show active vascular synovitis signals. This is important, because in the early stages of RA, the synovium is severely affected, and synovitis appears to be the best predictive marker of future joint damage.
Blood tests
When RA is clinically suspect, a doctor can test for rheumatoid factor (RF) and antibacterial protein antibodies (ACPAs measured as anti-PKC antibodies). This is positive in 75-85%, but negative RF or CCP antibodies do not rule out RA, more precisely, arthritis is called seronegative , which is in about 15-25% of people with RA. During the first year of disease, the rheumatoid factor is more likely to be negative with some individuals becoming seropositive over time. RF is a non-specific antibody and is seen in about 10% of healthy people, in many other chronic infections such as hepatitis C, and chronic autoimmune diseases such as SjÃÆ'¶gren syndrome and systemic lupus erythematosus. Therefore, this test is not specific to RA.
Therefore, a new serological test examines antibacterial anti-citrullinated ACPAs antibodies. This test is positive again in 61-75% of all RA cases, but with a specificity of about 95%. Like RF, ACPA is repeatedly present before symptoms begin.
The most common clinical test for ACPA is the anti-cyclic citrullinated peptide (anti CCP) ELISA. In 2008, a point-of-care serological test for early detection of RA combined RF and anti-MCV detection with 72% sensitivity and 99.7% specificity.
Other blood tests are usually done to differentiate from other causes of arthritis, such as blood sedimentation rate (ESR), C-reactive protein, complete blood count, renal function, liver enzymes and other immunological tests (eg, antinuclear antibodies/ANA) done at this stage. High levels of ferritin may reveal hemochromatosis, mimic RA, or be a sign of Still disease, a seronegative rheumatoid arthritis variant, usually juvenile.
Classification Criteria
In 2010, the Rheumatoid Acid Criteria of ACUL/EULAR 2010 Rheumatoid was introduced.
The new criterion is not a diagnostic criterion but a classification criterion for identifying diseases with high chances of developing a chronic form. However a score of 6 or more expressly classifies a person with a diagnosis of rheumatoid arthritis.
This new classification criterion rejected the "old" ACR criterion of 1987 and adjusted for initial RA diagnosis. The "new" classification criteria, published jointly by the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR) set a point value between 0 and 10. The four areas covered in the diagnosis:
- joint involvement, pointing metacarpophalangeal joints, proximal interphalangeal joints, interphalangeal joints of the thumb, second to fifth metatarsophalangeal joints and wrists as small joints, and shoulders, elbows, hip joints, knees , and ankle as big joint :
- Large 1-joint involvement gives 0 points
- Large 2-10 joint involvement gives 1 point
- The involvement of 1-3 small joints (with or without large joint involvement) gives 2 points
- The involvement of 4-10 small joints (with or without large joint involvement) gives 3 points
- Involvement of more than 10 joints (with involvement of at least 1 small joint) gives 5 points
- serological parameters - including rheumatoid factor and ACPA - "ACPA" stands for "anti-citrullinated protein antibody":
- Negative RF and ACPA negatively gives 0 points
- Low-positive RF or low-ACPA gives 2 points
- High-positive RFI or high ACPA gives 3 points
- acute phase reactants: 1 point for increased blood sedimentation rate, ESR, or increased CRP value (c-reactive protein) Duration of
- arthritis: 1 point for symptoms lasting six weeks or longer
The new criteria accommodate the growing understanding of RA and improvement in diagnosing RA and treatment of disease. In serologies the "new" criteria and autoimmune diagnostics carry the major weight, because ACPA detection is appropriate to diagnose the disease at baseline, before joint damage occurs. The joint destruction seen in radiological images is an important point of the ACR criterion from 1987. This criterion is no longer considered relevant, as this is just the kind of damage that should be avoided by care.
In clinical practice, the following criteria apply:
- two or more swollen joints
- morning stiffness lasts more than an hour for at least six weeks
- the detection of rheumatoid or autoantibody factors against ACPA such as autoantibodies to mutated citrullinated vitrins may confirm RA suspicion. Results of negative autoantibodies do not exclude the diagnosis of RA.
Differential diagnosis
Some other medical conditions may resemble RA, and need to be distinguished from it at the time of diagnosis:
- Crystallally induced arthritis (gout, and pseudogout) - usually involves certain joints (knee, MTP1, heel) and can be distinguished from joint fluid aspiration in doubt. Redness, asymmetric distribution of affected joints, pain occurs at night and initial pain less than an hour with gout.
- Osteoarthritis - differentiated by X-rays from affected joints and blood tests, older age, initial pain less than an hour, asymmetric distribution of affected joints and worsening pain when using joints for longer periods.
- Systemic lupus erythematosus (SLE) - differentiated with specific clinical symptoms and blood tests (antibodies against double-stranded DNA)
- One of several types of psoriatic arthritis resembles RA - nail changes and skin symptoms differentiate between them
- Lyme disease causes erosive arthritis and is very similar to RA - this can be distinguished by blood tests in endemic areas
- Reactive arthritis (previous Reiter disease) - asymmetric involving the heel, sacroiliac joints and large joints on the feet. Usually associated with urethritis, conjunctivitis, iritis, painless buccal ulcers, and keratoderma blennorrhagica.
- Axial spondyloarthritis (including ankylosing spondylitis) - this involves the spine, although a symmetric polyetritis of a small joint similar to RA may occur in the context of this condition.
- Hepatitis C - RA such as symmetric small symmetric polyarthritis may occur in the context of this condition. Hepatitis C can also cause auto-antibodies Rheumatoid Factor
The causes of rarer usually behave differently but can cause joint pain:
- Sarcoidosis, amyloidosis, and Whipple disease can also resemble RA.
- Hemochromatosis can cause arthritis of the hands.
- Acute rheumatic fever can be distinguished by the pattern of joint involvement migration and evidence of antecedent streptococcal infection.
- Bacterial arthritis (as by Streptococcus ) is usually asymmetrical, whereas RA usually involves both sides of the body symmetrically.
- Gonococcal arthritis (bacterial arthritis) also initially migrates and may involve tendons around the wrist and ankle.
Sometimes arthritis in the stage is not different (ie no criterion above positive), even if the synovitis is witnessed and assessed with ultrasound imaging.
Monitor progress
Many tools can be used to monitor remission in rheumatoid arthritis.
- DAS28
- The disease activity score of 28 joints ( DAS28 ) is widely used as an indicator of RA disease activity and response to treatment. The included joints are (bilateral): the proximal interphalangeal joint (10 joints), the metacarpophalangeal joint (10), the wrist (2), the elbow (2), the shoulder (2) and the knee (2). When looking at these joints, both the number of joints with touching tenderness (TEN28) and swelling (SW28) is calculated. The rate of sedimentation of the blood (LED) was measured and the affected person made a subjective assessment (SA) of disease activity for the previous 7 days on a scale between 0 and 100, where 0 was "no activity" and 100 was the "highest possible activity. With this parameter, DAS28 is calculated as:
From this, the disease activity of the affected person can be classified as follows:
It is not always a reliable indicator of the effects of treatment. One of the major limitations is that low-grade synovitis may be missed.
- More
- Other tools to monitor remission in rheumatoid arthritis are: ACR-EULAR Temporary Definition Remission of rheumatoid arthritis, Simplified Disease Activity Index (SDAI) and Clinical Disease Activity Index (CDAI). Some scores do not require input from health care professionals and allow for self-monitoring by such persons, such as HAQ-DI.
Prevention
No known precautions for conditions other than risk factor reduction.
Management
There is no cure for RA, but treatment can improve symptoms and slow the progression of the disease. Disease-modification treatments have the best results when started early and aggressively.
The goal of treatment is to minimize symptoms such as pain and swelling, to prevent bone deformity (eg, bone erosion seen in X-rays), and to maintain daily functioning. It is primarily aimed at disease-modifying antirheumatic drugs (DMARDs); analgesics can be used to help manage pain. RA should generally be treated with at least one specific anti-rheumatic drug. The use of benzodiazepines (such as diazepam) to treat pain is not recommended because it does not seem to help and is associated with risk.
Lifestyle
Regular exercise is recommended as it is safe and useful for maintaining muscle strength and overall physical function. It is uncertain whether certain dietary actions have an effect. Physical activity is beneficial for people with rheumatoid arthritis who complain of fatigue. Occupational therapy has a positive role to play in improving the functional ability of people with rheumatoid arthritis.
Disease modifying agents
The disease-modifying antirheumatic drugs (DMARDs) are the main treatment for RA. They are a diverse collection of medicines, grouped by usage and convention. They have been found to improve symptoms, reduce joint damage, and improve overall functional ability. The DMARD should start early in the disease because they produce remission of the disease in about half of the people and the results are improved overall.
The following medications are considered as DMARDs: methotrexate, hydroxychloroquine, sulfasalazine, leflunomide, TNF-alpha inhibitors (certolizumab, infliximab and etanercept), abatacept, and anakinra. Rituximab and tocilizumab are monoclonal antibodies as well as DMARDs.
The most commonly used agents are methotrexate with other frequently used agents including sulfasalazine and leflunomide. Sodium aurothiomalate (gold) and cyclosporin are less commonly used because of more common side effects. Agents can be used in combination. Methotrexate is the most important and useful DMARD and is usually the first treatment. Side effects should be monitored regularly with toxicities including gastrointestinal, hematologic, lung, and liver. Side effects such as nausea, vomiting or abdominal pain can be reduced by taking folic acid.
The Cochrane 2015 review found rituximab with methotrexate effective in improving symptoms compared with methotrexate alone. Rituximab works by describing the levels of B-cells (immune cells involved in inflammation). People taking rituximab have increased pain, function, reduced disease activity and reduced joint damage based on x-ray images. After 6 months, 21% more people experienced improvements in their symptoms using rituximab and methotrexate.
Biological agents are generally only used if methotrexate and other conventional agents are not effective after a three month trial. They are associated with a higher rate of serious infections compared to other DMARDs. Biologic DMARD agents used to treat rheumatoid arthritis include: tumor necrosis factor alpha (TNF?) Blocker such as infliximab; interleukin 1 blockers such as anakinra, monoclonal antibodies against B cells such as rituximab, and tocilizumab inhibitors of T-cell stimulation such as abatacept. They are often used in combination with methotrexate or leflunomide. Abatacept should not be used at the same time as other biologics. In those with well-controlled TNF-blockers, dose reduction did not appear to affect overall function. People should be screened for latent tuberculosis before starting TNF blocker therapy to avoid reactivation.
TNF blockers and methotrexate appear to have the same effectiveness when used alone and better results are obtained when used together. TNF blockers seem to have the same effectiveness as etanercept that appears to be the safest. Abatacept appears to be effective for RA with 20% more people getting better with treatment than without but long-term safety studies are not yet available. However, there is a lack of evidence to distinguish between the biology available for RA. Problems with biologics include high costs and relationships with infections including tuberculosis.
Anti-inflammatory and analgesic agents
Glucocorticoids can be used in the short term and at the lowest possible doses for flare-ups and while awaiting slow-onset drugs start to take effect.
Non-NSAID drugs for pain relief, such as paracetamol can be used to help relieve pain symptoms; they do not change the underlying disease.
NSAIDs reduce both pain and stiffness in those with RA but do not affect the underlying disease and appear to have no effect on the long-term disease course of people and thus are no longer the first-line agents. NSAIDs should be used with caution in those with gastrointestinal, cardiovascular, or renal problems. Use of methotrexate together with NSAIDS is safe, if adequate monitoring is performed. COX-2 inhibitors, such as celecoxib, and NSAIDs are equally effective.
Surgery
Especially for the affected fingers, hands, and wrists, synovectomy may be necessary to prevent pain or tendon rupture when drug treatment has failed. Severely affected joints may require joint replacement surgery, such as knee replacement. Postoperatively, physiotherapy is always needed.
Alternative medicine
In general, there is not enough evidence to support a complementary health approach to RA, with security issues for some of them. Some practice of the mind and body and dietary supplements can help people with symptoms and therefore may be of additional benefit to conventional treatments, but there is not enough evidence to draw conclusions. A systematic review of CAM modalities (excluding fish oil) found that "Available evidence does not support its current use in RA management." Studies showing the beneficial effects on RA on various modalities of CAM are often influenced by publication bias and are generally not high quality evidence such as randomized controlled trials (RCTs).
A Cochrane review in 2005 stated that low-level laser therapy can be tried to improve morning pain and stiffness due to rheumatoid arthritis because there are some side effects.
There is some evidence that Tai Chi increases the range of joint motion in people with rheumatoid arthritis. The evidence of acupuncture is inconclusive with it seems to be equivalent to fake acupuncture.
Dietary supplements
- Fatty acids
- Gamma-linolenic acid, omega-6 fatty acids, can relieve pain, calculate soft joints and stiffness, and are generally safe. For omega-3 polyunsaturated fatty acids (found in fish oil), meta-analyzes report beneficial effects on pain, although confidence in the effect is considered moderate. The same review reported less inflammation but no difference in joint function. A review examined the effects of omega-3 fatty oils on marine oils on pro-inflammatory eicosanoid concentrations; leukotriene 4 (LTB 4 ) is inherited in people with rheumatoid arthritis but not in those with non-autoimmune chronic disease. (LTB 4 ) increases vascular permeability and stimulates other inflammatory substances. The third meta-analysis analyzed fish consumption. The result is an inverse relationship that is not statistically significant and non-statistically between fish consumption and RA. The fourth review was limited to experiments in which people ate> = 2.7 g/day for more than three months. The use of painkillers decreased, but improvements in soft or swollen joints, morning stiffness and physical function were unchanged. Collectively, the current evidence is not strong enough to determine that supplementation with omega-3 fatty acids or regular fish consumption is an effective treatment for rheumatoid arthritis.
- Herbs
- The American College of Rheumatology states that no herbal medicines have health claims backed by high-quality evidence and therefore they do not recommend their use. There is no scientific basis to suggest that herbal supplements that are advertised as "natural" are safer to use than conventional medicines because they are chemicals. Herbal medicines, although labeled "natural", may be toxic or fatal if taken.
Due to the false belief that herbal supplements are always safe, there are sometimes doubts to report their use that may increase the risk of adverse reactions.
The following are being investigated for treatment for RA, based on preliminary promising results (not recommended for clinical use): boswellic acid, curcumin, devil's claw, Euonymus tool, and thunder god vine (Tripplegium wilfordii ). NCCIH has noted that, "In particular, the herb of the herbal lightning god (Tripterygium wilfordii) can have serious side effects."
There is conflicting evidence about the role of erythropoiesis-stimulating agents for the treatment of anemia in people with rheumatoid arthritis.
Pregnancy
Over 75% of women with rheumatoid arthritis have improved symptoms during pregnancy but may have worsening symptoms after childbirth. Methotrexate and leflunomide are teratogenic (harmful to the fetus) and not used in pregnancy. It is recommended that women of childbearing age should use contraception to avoid pregnancy and to discontinue use if pregnancy is planned. Low doses of prednisolone, hydroxychloroquine and sulfasalazine are considered safe in pregnant people with rheumatoid arthritis.
Vaccinations
People with RA have an increased risk of infection and death and recommended vaccinations can reduce this risk. Inactivated influenza vaccine should be accepted every year. The pneumococcal vaccine should be given twice for people under age 65 and once for those over 65. Lastly, live-attenuated zoster vaccine should be given once after age 60, but is not recommended in people with alpha blocker tumor necrosis factor.
Prognosis
The course of this disease varies greatly. Some people have mild short-term symptoms, but in most of these diseases are progressive for life. About 20% -30% will have subcutaneous nodules (known as rheumatoid nodules); this is associated with a poor prognosis.
Prognostic factors
Poor prognostic factors include,
- Persistent synovitis
- Early erosive disease
- Extra-articular findings (including subcutaneous rheumatoid nodules)
- Positive RF serum findings
- A positive serum anti-CCP autoantibody
- Introduction to the HLA-DR4 "Shared Epitope" alleles
- RA family history
- Poor functional status
- Socio-economic factors
- Increased acute phase response (rate of sedimentation of blood (LED), C-reactive protein [CRP])
- Increased clinical severity.
Mortality
RA reduces the average age from three to twelve years. According to the National Rheumatoid Arthritis Society in the United Kingdom, young age at onset, long duration of the disease, the presence of other co-morbidities together, and severe RA characteristics - such as poor functional ability or overall health status, x-rays, the need for hospitalization or involvement of non-joint organs - has been shown to be associated with higher mortality. "A positive response to treatment may indicate a better prognosis.A 2005 study by the Mayo Clinic noted that RA sufferers have doubled the risk heart disease, independent of other risk factors such as diabetes, alcohol abuse, and elevated cholesterol, blood pressure and body mass index.RA mechanisms that cause this increased risk are still unknown: Chronic inflammation has been suggested as contributing factors. biological drug therapy s new extend the life of people with RA and reduce the risk and progress of sion atherosclerosis. It's based on cohort studies and the registry, and still remains hypothetical. It is still uncertain whether biology enhances vascular function in RA or not. There was an increase in total cholesterol and HDLc levels and no increase in the atherogenic index.
Epidemiology
RA affects between 0.5 and 1% of adults in the developed world with between 5 and 50 per 100,000 newly developed conditions each year. In 2010 it resulted in about 49,000 deaths globally.
Onset is rare under the age of 15 years and since then incidence has increased with age up to the age of 80 years. Women are affected three to five times more often than men.
The age at which the disease most often begins is in women between 40 and 50 years, and for men rather later. RA is a chronic disease, and although rare, spontaneous remission can occur, natural journey is almost always one of the persistent symptoms, waxing and fading in intensity, and the progressive breakdown of joint structures leading to deformation and disability.
History
The traces of arthritis are first known back at least as far back as 4500 BC. A text dated the first 123 AD describes a symptom very similar to RA. It was recorded in the remains of a skeleton of Native Americans found in Tennessee. In Europe, the disease became increasingly rare before the 17th century. The first description recognized by RA in modern medicine was in 1800 by the French physician Dr Augustin Jacob Landrà © © -Beauvais (1772-1840) based in the famous SalpÃÆ'ªtriÃÆ'¨re Hospital in Paris. The name "rheumatoid arthritis" itself was created in 1859 by the English rheumatologist Dr Alfred Baring Garrod.
Anomalies have been observed from Pre-Columbian bone investigations. The bones from the Tennessee site showed no signs of tuberculosis even though it was prevalent at times across America.
The art of Peter Paul Rubens may illustrate the effects of RA. In his later paintings, his hand shows, in the opinion of some doctors, the increase in deformity is consistent with the symptoms of the disease. RA seems to have been partially portrayed in 16th century paintings. However, it is generally recognized in the art history circle that hand paintings of the 16th and 17th centuries follow certain conventions, most clearly seen in the Mannerism movement. It is conventional, for example, to show Christ's righteous hand enforced in what now appears as a flawed posture. These conventions are easily misinterpreted as illustrative.
Historical treatments for RA also include: rest, ice, compression and elevation, apple diet, nutmeg, some light exercise every now and then, nettle, bee venom, copper bracelets, rhubarb diet, tooth extraction, fasting, honey, vitamins, insulin, magnetism, and electroconvulsive therapy (ECT).
Etymology
Rheumatoid arthritis comes from the Greek word ????? - rheuma (nom.), ???????? - rheumatos (gen.) ("flow, current"). Suffix - oid ("resembles") provides translation as inflammation of the joint that resembles rheumatic fever . Rhuma which means the release of water may refer to the fact that the joints are swollen or that the disease may be aggravated by wet weather.
Research
Meta-analysis found an association between periodontal disease and RA, but the mechanism of this association remains unclear. Two species of bacteria associated with periodontitis are involved as a mediator of protein citrullination in people's gums with RA.
Vitamin D deficiency is more common in people with rheumatoid arthritis than in the general population. However, whether vitamin D deficiency is the cause or consequence of the disease is still unclear. One meta-analysis found that vitamin D levels were low in people with rheumatoid arthritis and that vitamin D status was inversely correlated with the prevalence of rheumatoid arthritis, suggesting that vitamin D deficiency is associated with susceptibility to rheumatoid arthritis.
References
External links
- Rheumatoid arthritis di Curlie (berdasarkan DMOZ)
- Charles Weber. "Sejarah rheumatoid arthritis". < rentang>
Source of the article : Wikipedia
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