Inflammatory Arthritis - RA

Onset RA

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Public RA

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In RA for reasons scientists don't understand,maybe genetics are part of it,and maybe there's something in the environment that triggers this off--the lining of the joint becomes inflamed. And these pus-like inflammatory cells,accumulate in the lining,and they make the synovial tissue lining of the joint thick,and extra fluid is made in the joint. The inflammation,tissue thickening,and joint fluid (pannus)  are why the RA patient feels the warmth and the swelling and redness.
 
In the synovial tissue,cytokine cells in the joint (there are many different types) communicate with each other. The important cells we are interested in, is the macrophage and the T-cell,they talk to each other,inside the lining of the joint. The first thing that happens is that they meet and they touch each other through through the T cell receptor,and then other types of cytokines or costimulatory molecules,and there are several of them,meet,and that's when cell messengers like TNF-alpha,IL-1s (among others) are released from the macrophage (white blood cells) and these little substances are recognized on the surface of the T-cell,and that sends messages into the T-cell,and the DNA (of the T-cell) allows other messages to occur, Current biologic medication are targeted against these inflammatory cytokines.

Early diagnosis of RA is critically important because of the very rapid progression of the disease, particularly in its early stages.  For example, research  found that 70% of 90 patients with RA showed radiographic damage after 3 years and that these patients could be identified 1 year after diagnosis. The rate of progression in the first year was significantly higher than in the second and third years. Overall, approximately 20% of the joints were affected after 3 years.
 
Another research team carried out a quantitative radiographic analysis of the hands and wrists of 200 patients with RA and noted that 93% of the 42 patients who had been diagnosed for <2 years had evidence of radiographic damage, including 35 with joint space narrowing and 28 with erosions.
 
Still,another research team used magnetic resonance imaging (MRI) to evaluate 42 patients with early RA (median symptom duration, 4 months). Erosions were detected in 45% of scans, bone marrow edema in 64%, synovitis in 93%, and tendonitis in 79%. Importantly, only 15% of patients had erosions that were detectable on plain film radiographs. These investigators concluded that a high percentage of RA patients develop MRI-detectable erosions very early in their disease, when plain radiography is frequently normal.
 
Despite the availability of new, highly effective, targeted therapies that provide unprecedented opportunities to treat rheumatoid arthritis, major obstacles still stand in the way of a cure. These include:
 
I) A lack of knowledge of the etiology of the disease. Although data have long hinted that bacteria, viruses, nonspecific inflammation, and autoantibodies might be pathogenic factors in at least some cases of RA, the basic mechanisms that initiate and sustain this disease remain elusive.
 
II) A lack of means to intervene in the most relevant disease processes. Even the most advanced therapies currently available appear to suppress relatively peripheral pathways of inflammation and not central abnormalities of cell function that underlie the disease.
 
III) The considerable clinical, pathological, and immunological heterogeneity of RA may also influence the capacity to induce remission.
 
IV) The inability to make an early diagnosis. By the time physicians are able spot clinical signs of the disease, it is probably too late to bring the tissue back to normal.
 
V)  Limited ability to recognize those at risk. One of the most important obstacles is an inability to detect the earliest events that lead to the development of persistent, destructive synovitis.
 
The development of a clearly defined set of clinical criteria would facilitate early referral of the patient with suspected RA to a rheumatologist for definitive diagnosis and initiation of therapy when it is most likely to have a significant positive impact on the long-term outcome.
 
Research associates developed a clinical guide for rapid referral to a rheumatologist of patients with suspected RA. Criteria for referral include: 1) less than or equal to 3 swollen joints  2) Metatarsophalangeal (MTP) and/or metacarpophalangeal (MCP) involvement (with positive squeeze test) 3) Morning stiffness for greater than 30 minutes
 
These investigators also noted that patients who are positive for RF, have an acute phase response, or show erosions on x-ray should be referred to a rheumatologist regardless of presenting symptoms, and that nonsteroidal anti-inflammatory drug use can mask RA symptoms
 
There are difficulties in making an accurate diagnosis of RA in its early stages. A principal problem is that RAs most defining feature is chronicity, which, by definition, takes time to identify. An important question in the consideration of "early" RA is how this term should be defined.
 
Early RA can be defined chronologically; anatomically, by the distribution of involved joints; functionally, by responses to the HAQ or Arthritis Impact Measurement Scales (AIMS); radiographically, by evidence of erosions, narrowing, and changes in alignment; or pathophysiologically, by synovial biopsy, measurement of cytokine levels, or assessment of genetic markers.
 
Aggressive early treatment of patients with RA has a significant positive effect on disease progression.  Research studies compared disease progression in two cohorts of RA patients. Patients in the first group (n = 109), the delayed-treatment group, were diagnosed with probable or definite RA between 1993 and 1995 and initially were treated with analgesics. If they had persistent active disease, they were treated subsequently with the DMARDs chloroquine or salazopyrine. A second cohort of patients (n = 97), the early-treatment group, diagnosed between 1996 and 1998, were promptly treated with either chloroquine or salazopyrine.
 
The median lag time from the initial presentation of symptoms to the initiation of DMARD therapy was 15 days in the early-treatment group and 123 days in the delayed-treatment group. There was less radiologic joint damage after 2 years in the early-treatment group (median Sharp score, 3.5) compared with the delayed-treatment group (median Sharp score, 10; p < 0.05).  The median area under the curve of the 2-year disease activity score was lower in the early-treatment group (64 units) compared with the delayed-treatment group (73 units; p = 0.002).
 
 Research, studies compared disease progression in two cohorts of RA patients. Patients in the first group (n = 109), the delayed-treatment group, were diagnosed with probable or definite RA between 1993 and 1995 and initially were treated with analgesics. If they had persistent active disease, they were treated subsequently with the DMARDs chloroquine or salazopyrine. A second cohort of patients (n = 97), the early-treatment group, diagnosed between 1996 and 1998, were promptly treated with either chloroquine or salazopyrine.
 
The median lag time from the initial presentation of symptoms to the initiation of DMARD therapy was 15 days in the early-treatment group and 123 days in the delayed-treatment group. There was less radiologic joint damage after 2 years in the early-treatment group (median Sharp score, 3.5) compared with the delayed-treatment group (median Sharp score, 10; p < 0.05).
 
The median area under the curve of the 2-year disease activity score was lower in the early-treatment group (64 units) compared with the delayed-treatment group (73 units; p = 0.002).

If a person's had more than six weeks of "just a little arthritis," they really do need to talk to a physician to find out a couple of answers. One, they would like to know, "What is my diagnosis?" Two, if the diagnosis is rheumatoid arthritis or another form of arthritis, they want to know what their prognosis is: what to expect in the near future as well as the long-term future.
 
Then they really need to sit down with the primary care physician or rheumatologist to discuss treatment options, both what's available currently that will make them feel better, what's available currently that will slow or stop the disease from progressing and causing the disability that can happen with rheumatoid arthritis, and then what the side effects and the risks are of the treatment.
 
Rheumatoid arthritis can be very aggressive and has been shown even to shorten one's life expectancy. The other important point is that rheumatoid arthritis is not a benign disease. It's really a disease that can be very aggressive. It can limit not only one's ability to do things, but it's been shown at a study by researchers even to shorten one's life expectancy.
 
If the physician makes the diagnosis of rheumatoid arthritis early and responds to that with the appropriate aggressive therapy to slow the disease down, the prognosis becomes much, much better. The patient's ability to live a full and useful life is extended.
 
Since arthritis is viewed,as less serious than heart disease or cancer, people will live with some of the pain. The other thing is that patients with arthritis and arthritis symptoms will get advice, and they'll get advice from many of their friends about what to do, which foods they should eat, and which foods they shouldn't eat - advice which really has no basis in science, but everyone seems to have an opinion about arthritis
 
If someone had more than six weeks of minor arthritis pains, and they've been persistent for six weeks, and especially if they've been in more than one or two or three joints, this is something that they need to see their physician about. If there's difficulty in nailing down a diagnosis, this is the time to consider a referral to a rheumatologist for an opinion.
 
If the general practitioner knows your symptoms are not rheumatoid arthritis and may just be due to some local infection or something else, and he or she is confident in that diagnosis and can tell you the prognosis, the therapy, and the side effects, that would be fine.  But if the diagnosis is unclear or the primary care physician or internist is not really sure whether to intervene with big-league, potent medicines, then a consultation with a rheumatologist would be appropriate.
 
The diagnosis is primarily made by a history and a physical examination; then ancillary, or secondary, blood tests and x-rays are done. The medical history and the physical examination of the patient will give us the diagnosis in about 95 percent of the patients.  The history is one of inflammation - again, pain and swelling - of small joints, namely the finger joints and the joints in the feet. The joint swelling and the pain is usually symmetric, meaning if it's on the right side, it's usually on the left side, as well.
 
That kind of history points the doctor or the rheumatologist to a diagnosis of rheumatoid arthritis. Then when the doctor or the rheumatologist examines the patient, they can actually feel the inflammation and feel some of the nodules or the bumps that rheumatoid arthritis can make. Rheumatologist are trained in a two-year program to feel the inflammation of rheumatoid arthritis.
 
Once they've done that, then they'll do some blood tests. The two most important blood tests check for inflammation, and there are actually two of those. One is called the ESR (erythrocyte sedimentation rate) or "sed" rate, and the other is called the CRP or C-reactive protein.  They're very similar tests, and they really just tell physicians that the patient has inflammation in the system, but these tests don't tell them that it's actually rheumatoid arthritis.
 
In 50 percent of patients with rheumatoid arthritis, the rheumatoid factor in early disease is negative. Physicians will look for the "rheumatoid factor," but the rheumatoid factor test can both be important and unimportant - because in 50 percent of patients with rheumatoid arthritis, the rheumatoid factor in early disease is negative.
 
The patient can have rheumatoid arthritis by history and exam, but the blood test could be negative. Twenty percent of patients with rheumatoid arthritis still have a blood test that's negative for the rheumatoid factor,it's a helpful piece of information if it's positive but not necessarily if it's negative.
 
Another important piece of information that the doctors and rheumatologists have to put together is that rheumatoid factor is just an abnormal protein, and it actually can occur in other diseases, so even people with diabetes or chronic infections will have a positive rheumatoid factor and not have rheumatoid arthritis. It has to be used very judiciously. X-rays are very important because if doctors see rheumatoid arthritis on the x-ray, they know that the patient has it, and they also know that the prognosis is not very good and one has to be very aggressive in therapy.
 
Currently there is no cure for RA. The diagnosis is primarily made by a history and a physical examination; then ancillary, or secondary, blood tests and x-rays are done. The medical history and the physical examination of the patient will give physicians the diagnosis in about 95 percent of the patients.

There is no known cure for rheumatoid arthritis. To date, the goal of treatment in rheumatoid arthritis is to reduce joint inflammation and pain, maximize joint function, and prevent joint destruction and deformity. Early medical intervention has been shown to be important. Optimal treatment for the disease involves a combination of medications, rest, joint strengthening exercises, joint protection, and patient (and family) education.
 
Treatment is customized according to many factors such as disease activity, types of joints involved, general health, age, and patient occupation. Treatment is most successful when there is close cooperation between the doctor, patient, and family members.
 
Two classes of medications are used in treating rheumatoid arthritis: fast-acting "first-line drugs," and slow-acting "second-line drugs (also referred to as Disease-Modifying Antirheumatic Drugs or DMARDs)." The first-line drugs, such as aspirin and cortisone (corticosteroids), are used to reduce pain and inflammation.  The slow-acting second-line drugs, such as gold, methotrexate and hydroxychloroquine (Plaquenil) promote disease remission and prevent progressive joint destruction, but they are not anti-inflammatory agents.
 
The degree of destructiveness of rheumatoid arthritis varies from patient to patient. Patients with less destructive forms of the disease can be managed with rest and anti-inflammatory agents only. In general, however, patients fair better when treated earlier with second-line drugs (disease-modifying antirheumatic drugs), even within months of the diagnosis.  Patients with more aggressive disease require second-line drugs, such as methotrexate, in addition to anti-inflammatory agents. Sometimes these second-line drugs are used in combination. In some patients with severe joint deformity, surgery may be necessary.
 
"First-line" Drugs: Acetylsalicylate (Aspirin), naproxen (Naprosyn), ibuprofen (Advil, Medipren, Motrin), and etodolac (Lodine) are examples of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs are medications that can reduce tissue inflammation, pain and swelling. NSAIDs are not cortisone.  Aspirin, in doses higher than that used in treating headaches and fever, is an effective antiinflammatory medication for rheumatoid arthritis. Aspirin has been used for joint problems since the ancient Egyptian era.
 
The newer NSAIDs are just as effective as aspirin in reducing inflammation and pain, and require fewer dosages per day. Patients' responses to different NSAID medications vary. Therefore, it is not unusual for a doctor to try several NSAID drugs in order to identify the most effective agent with the fewest side effects.  The most common side effects of aspirin and other NSAIDs include stomach upset, abdominal pain, ulcers, and even gastrointestinal bleeding. In order to reduce stomach side effects, NSAIDs are usually taken with food. 
 
Additional medications are frequently recommended to protect the stomach from the ulcer effects of NSAIDs. These medications include antacids, sucralfate (Carafate), protein-pump inhibitors (Prevacid, and others), and misoprostol (Cytotec).
 
While "first-line" medications (NSAIDs and corticosteroids) can relieve joint inflammation and pain, they do not necessarily prevent joint destruction or deformity. Rheumatoid arthritis requires medications other than NSAIDs and corticosteroids to stop progressive damage to cartilage, bone, and adjacent soft tissues.
 
 The medications needed for ideal management of the disease are also referred to as Disease-modifying Anti-rheumatic Drugs or DMARDs. They come in a variety of forms and are listed below. These "second-line" or "slow-acting" medicines may take weeks to months to become effective. They are used for long periods of time, even years, at varying doses. If effective, DMARDs can promote remission, thereby retarding the progression of joint destruction and deformity.
 
Sometimes a number of second-line medications are used together as combination therapy. As with the first-line medications, the doctor may need to use different second-line medications before treatment is optimal.
Hydroxychloroquine (Plaquenil) is related to quinine, and is also used in the treatment of malaria. It is used over long periods for the treatment of rheumatoid arthritis. Possible side effects include upset stomach, skin rashes, muscle weakness, and vision changes. Even though vision changes are rare, patients taking Plaquenil should be monitored by an eye doctor (ophthalmologist).
 
Sulfasalazine (Azulfidine) is an oral medication traditionally used in the treatment of mild to moderately severe inflammatory bowel diseases, such as ulcerative colitis and Crohn's colitis. Azulfidine is used to treat rheumatoid arthritis in combination with antiinflammatory medications. Azulfidine is generally well tolerated. Common side effects include rash and upset stomach. Because Azulfidine is made up of sulfa and salicylate compounds, it should be avoided by patients with known sulfa allergies.
 
Methotrexate has gained popularity among doctors as an initial second-line drug because of both its effectiveness and relatively infrequent side effects. It also has an advantage in dose flexibility (dosages can be adjusted according to needs). Methotrexate is an immune suppression drug. It can affect the bone marrow and the liver, even rarely causing cirrhosis. All patients taking methotrexate require regular blood test monitoring of blood counts and liver function blood tests.
 
Gold salts have been used to treat rheumatoid arthritis throughout most of the past century. Gold thioglucose (Solganal) and gold thiomalate (Myochrysine) are given by injection, initially on a weekly basis for months to years. Oral gold, auranofin (Ridaura) was introduced in the 1980's. Side effects of gold (oral and injectable) include skin rash, mouth sores, kidney damage with leakage of protein in the urine, and bone marrow damage with anemia and low white cell count. Patients receiving gold treatment are regularly monitored with blood and urine tests. Oral gold can cause diarrhea. These gold drugs have lost such favor that many companies no longer manufacture them.
 
D-penicillamine (Depen, Cuprimine) can be helpful in selected patients with progressive forms of rheumatoid arthritis. Side effects are similar to those of gold. They include fever, chills, mouth sores, a metallic taste in the mouth, skin rash, kidney and bone marrow damage, stomach upset, and easy bruising. Patients on this medication require routine blood and urine tests. D-penicillamine can rarely cause symptoms of other autoimmune diseases.
 
Immunosuppressive medicines are powerful medications that suppress the body's immune system. A number of immunosuppressive drugs are used to treat rheumatoid arthritis. They include methotrexate (Rheumatrex, Trexall) as described above, azathioprine (Imuran), cyclophosphamide (Cytoxan), chlorambucil (Leukeran), and cyclosporine (Sandimmune).
 
Because of potentially serious side effects, immunosuppressive medicines are generally reserved for patients with very aggressive disease, or those with serious complications of rheumatoid inflammation, such as blood vessel inflammation (vasculitis).  The exception is methotrexate, which is not frequently associated with serious side effects and can be carefully monitored with blood testing. Methotrexate has become a preferred second-line medication as a result.
 
Immunosuppressive medications can depress bone marrow function and cause anemia, a low white cell count and low platelets counts. A low white count can increase the risk of infections, while a low platelet count can increase the risk of bleeding.  Methotrexate can also lead to liver cirrhosis and allergic reactions in the lung. Cyclosporin can cause kidney damage and high blood pressure. Because of potentially serious side effects, immunosuppressive medications are used in low doses, usually in combination with anti-inflammatory agents

 
Therapy:
 
Newer "second-line" drugs for the treatment of rheumatoid arthritis include leflunomide (Arava) etanercept (Enbrel), infliximab (Remicade), anakinra (Kineret), and adalimumab (Humira.)
 
Leflunomide (Arava) is available to relieve the symptoms and halt the progression of the disease. It seems to work by blocking the action of an important enzyme that has a role in immune activation. Arava can cause liver disease, diarrhea, hair loss, and/or rash in some patients. It should not be taken just before or during pregnancy because of possible birth defects.
 
Other medications that represent a novel approach to the treatment of rheumatoid arthritis and are the products of modern biotechnology. Etanercept (Enbrel), infliximab (Remicade), and adalimumab (Humira, marketed as of January, 2003) intercept a protein (tumor necrosis factor, or TNF) that causes inflammation before it acts on its natural receptor to "switch on " inflammation.
 
 These medications are referred to as biological response modifiers. Symptoms can be significantly, and often rapidly, improved in patients using these drugs. Etanercept (Enbrel) must be injected subcutaneously twice a week. Infliximab (Remicade) is given by infusion directly into a vein (intravenously). Adalimumab (Humira) is injected subcutaneously either every other week or weekly.
 
Each of these medications will be evaluated by doctors in practice to determine what role they may have in treating various stages of rheumatoid arthritis. Recent studies demonstrate that biological response modifiers also prevent the progressive joint destruction of rheumatoid arthritis.
 
They are currently recommended for use after other medications have not been effective. The biological response modifiers (TNF-inhibitors) are expensive treatments. They are also frequently used in combination with methotrexate and other DMARDs.
 
Anakinra (Kineret) is another biologic treatment that is used to treat moderate to severe rheumatoid arthritis. Anakinra (Kineret) works by binding to a cell messenger protein (IL-1, a proinflammation cytokine). Anakinra (Kineret) is injected under the skin daily. Anakinra (Kineret) can be used alone or with other DMARDs.
 
The Prosorba column therapy involves pumping blood drawn from a vein in the arm into an apheresis machine, or cell separator. This machine separates the liquid part of the blood (the plasma) from the blood cells. The Prosorba column is a plastic cylinder about the size of a coffee mug that contains a sand-like substance coated with a special material called Protein A. Protein A is unique in that it binds unwanted antibodies from the blood that promote the arthritis.
 
 The Prosorba column works to counter the effect of these harmful antibodies. The Prosorba column is indicated to reduce the signs and symptoms of moderate to severe rheumatoid arthritis in adult patients with long standing disease who have failed or are intolerant to disease-modifying anti-rheumatic drugs (DMARDs). The exact role of this treatment is being evaluated by doctors.
 
There is no special diet for rheumatoid arthritis. Fish oil may have anti-inflammatory effects, but so far this has only been shown in laboratory experiments studying inflammatory cells. Likewise, the benefits of cartilage preparations remain unproven. Symptomatic pain relief can often be achieved with oral acetaminophen (Tylenol) or over-the-counter topical preparations, which are rubbed into the skin.
 
Antibiotics, in particular the tetracycline drug minocycline (Minocin), have been tried for rheumatoid arthritis recently in clinical trials. Early results have demonstrated mild to moderate improvement in the symptoms of arthritis. Minocycline has been shown to impede important mediator enzymes of tissue destruction, called metalloproteinases, in the laboratory as well as in humans.
 
The areas of the body, other than the joints, that are affected by rheumatoid inflammation are treated individually. Sjogren's syndrome  can be helped by artificial tears and humidifying rooms of the home or office. Regular eye check-ups and early antibiotic treatment for infection of the eyes are important.
 
Inflammation of the tendons (tendinitis), bursae (bursitis) and rheumatoid nodules can be injected with cortisone. Inflammation of the lining of the heart and/or lungs may require high doses of oral cortisone.
 
Proper, regular exercise is important in maintaining joint mobility, and in strengthening the muscles around the joints. Swimming is particularly helpful because it allows exercise with minimal stress on the joints.  Physical and occupational therapists are trained to provide specific exercise instructions and can offer splinting supports. For example, wrist and finger splints can be helpful in reducing inflammation and maintaining joint alignment. Devices, such as canes, toilet seat raisers, and jar grippers can assist daily living. Heat and cold applications are modalities that can ease symptoms before and after exercise.
 
Surgery may be recommended to restore joint mobility or repair damaged joints. Doctors who specialize in joint surgery are orthopedic surgeons. The types of joint surgery range from arthroscopy to partial and complete replacement of the joint.
 
Arthroscopy is a surgical technique whereby a doctor inserts a tube-like instrument into the joint to see and repair abnormal tissues. "Total joint replacement" is a surgical procedure whereby a destroyed joint is replaced with artificial materials. For example, the small joints of the hand can be replaced with plastic material. Large joints, such as the hips or knees, are replaced with metals.
 
Finally, minimizing emotional stress can help improve the overall health of the patient with rheumatoid arthritis. Support and extracurricular groups afford patients time to discuss their problems with others and learn more about their illness.
 
Scientists throughout the world are studying many promising areas of new treatment approaches for rheumatoid arthritis. These areas include treatments that block the action of the special inflammation factors, such as tumor necrosis factor (TNFalpha) and interleukin-1 (IL-1), as described above.
 
Many other drugs are being developed that act against certain critical white blood cells involved in rheumatoid inflammation. Also, new NSAIDs with mechanisms of action which are different from current drugs are on the horizon.
Studies involving various types of the connective tissue collagen are in progress and show encouraging signs of reducing rheumatoid disease activity. Finally, genetic research and engineering is likely to bring forth many new avenues of earlier diagnosis and accurate treatment in the near future.
 
Rheumatoid arthritis is an autoimmune disease that can cause chronic inflammation of the joints and other areas of the body. Rheumatoid arthritis can affect persons of all ages. The cause of rheumatoid arthritis is not known. Rheumatoid arthritis is a chronic disease, characterized by periods of disease flares and remissions. In rheumatoid arthritis, multiple joints are usually, but not always, affected in a symmetrical pattern.  Chronic inflammation of rheumatoid arthritis can cause permanent joint destruction and deformity. The "rheumatoid factor" is an antibody blood test that can be found in 80 % of patients with rheumatoid arthritis.
 
There is no known cure for rheumatoid arthritis. The treatment of rheumatoid arthritis optimally involves a combination of patient education, rest and exercise, joint protection, medications, and occasionally surgery.
 
There are a number of non-pharmacologic approaches. One is that people first have to acknowledge that medications alone cannot work and that they need to modify their activity. They need to learn to find how to offload inflamed joints and modify the way they do tasks to protect those joints.
 
A good example of that would be that if fingers are really sore, to find a way maybe to grasp which is different than just grasping or if someone has a problem with their wrist, perhaps use a splint which is a way of supporting that when they're doing a task that might irritate it, like vacuuming.
 
There are a number of other types of approaches, like using adaptive footwear, like shoe orthotics or adaptive shoes. And of course,there are a number of exercise-directed therapies which can really reduce muscle tension, improve sense of well-being and general conditioning
 
There are lots of different ways that people cope with pain which are kind of interesting. Some of these are sort of short-term interventions, and some are longer-term, but certainly distraction, and changing what you're doing, and changing your physical activity you're doing at a time is a good technique.
 
Sometimes people will meditate or pray. There's some pretty interesting research written about reflective writing, where people who are experiencing pain will write essays, and this activity often brings insight into the experiences people have but also reduce pain because it distracts the brain from really focusing on the pain itself.
 
Then the whole other question is how do we safely apply heat and cold? And there are many ways. You could use radiant heat from a heat lamp. You could use a moist heating pad. One can could use paraffin baths using paraffin wax that's heated. There are a lot of different ways to do this, and it's just a matter of what people find works for them.
The other thing is that often people have fatigue. And so if you control the disease process and you have less pain but also less fatigue, you'd be more likely to live a full life. Another important marker is sleeping. Often because people feel poorly, they have impaired sleep and, if you're tired and have pain and you don't sleep well at night, it's pretty tough to enjoy what you're doing
 
NSAIDs can be troublesome drugs for particular individuals, particularly elderly people or people with a past history of ulcers, and although the lower the dose that you use, the safer they are, the problem seems to be that sometimes people think if a little is good, then more is better. And so people adjust the doses up and take three tablets instead of two tablets like they're supposed to.
 
There can be a lot of problems with high blood pressure or edema, ulcers, kidney problems. These are difficult drugs to use, particularly if you push to higher doses. There's a subset or a group of patients who need to be worried. Those are the patients with edema or swelling, congestive heart failure, renal or kidney problems, people with stomach problems such as ulcer disease, and people who happen to be older. One of the problems is too often these are the same people that we take care of who have rheumatoid arthritis.
 
The other problem with the non-steroidals is that some patients and even sometimes their physicians will see a response and will think this is a sufficient therapy, and not realizing that the progression of the disease and the cartilage and bone wear continues despite these medications.
 
It's important from the beginning to help people understand what the goals are is to control symptoms and signs, and to try to prevent joint damage. To use the disease-modifying drugs is a continuous process that's necessary.

 
Some important cytokines in the RA process are tumor necrosis factor (TNF), interleukin-1 and interleukin-2. These cytokines are some of the factors that are believed to drive the inflammation process of RA, often leading to joint damage and destruction.
 
One type of cell found within your immune system is called a T cell. When T cells are activated (or "turned on") they can start a chain of events that is believed to lead to the inflammation, pain, and joint damage of RA. The activated T cells begin to multiply and produce special proteins called cytokines .

Controlling the activation of these T cells and the resulting cytokine production that follows may help reduce inflammation and slow the progression of joint damage. There are other cell types believed to be related to RA development, such as B cells, which produce antibodies that may contribute to RA inflammation.