rheumatoid arthritis

 rheumatoid arthritis
Rheumatoid arthritis (RA) is the most common form of inflammatory arthritis, affecting approximately two million Americans. It is a chronic, systemic, autoimmune driven disease for which there is no cure.
Among the multisystem features of the disease is the ability to attack and destroy not only joint tissue, but also other organ systems such as the eye, bone marrow, lungs, peripheral nervous system as well as heighten the incidence of cardiovascular events such as heart attack and stroke.
While the disease, if not diagnosed and treated aggressively, can still cause significant problems, major advances in treatment have developed in the last 25 years.
The drug of choice remains methotrexate. We now have more than 30 years of experience with this medication and are familiar with its side effect profile which is much more benign than we used to believe.
Roughly, 25% to 30% of patients will go into remission or near remission on methotrexate alone, and many of those patients will sustain that response for up to a year or more.
So how is response defined?
Response occurs when a patient has no clinical signs of disease activity, no elevated acute phase reactants, which are blood tests that measure inflammation. The two most commonly used tests are the erythrocyte sedimentation rate ("sed rate") and CRP. And they have no functional deficit from their disease.
In patients who don't achieve remission or lose their remission, we now add on a tumor necrosis factor (TNF) inhibitor. These are a category of biologic drugs. These medicines that act like a laser beam against the immunologic disturbances that are responsible for RA.
While many patients respond to the combination of methotrexate and TNF inhibitor, some either don't respond initially or lose their response over time. In these patients we will try a second TNF inhibitor.
Fortunately, there are alternatives. We have three other biologic medicines that are all useful in the event a patient fails two TNF inhibitors. There is Orencia, which is a T-cell costimulatory modulator. T cells are felt to be a key player in the inflammation of RA. The second is Rituxan. This is a drug that was initially used to treat non-Hodgkins lymphoma. It is an antibody directed against B-cells, which are also a major contributor to chronic inflammation in RA. Finally, there is Actemra, which is an antibody drug directed against the interleukin-6 receptor.
Interleukin-6 is a protein messenger that is pivotal in perpetuating RA activity.
All of these have been shown to be effective in rheumatoid arthritis, and all have been shown to be effective in patients who have failed a TNF inhibitor.
With this arsenal of drugs there is better than a 50 per cent chance of getting a patient with new-onset RA into remission within six to twelve months.
And the good news is that newer therapies are being developed that may be even more effective.

rheumatoid arthritis

rheumatoid arthritis
Rheumatoid arthritis (RA) is the most common form of inflammatory arthritis affecting between approximately two million Americans. It is a systemic, chronic, autoimmune driven disorder that affects not only joints but internal organs as well. The disease has been associated with a significant mortality causing people affected by the disease to die 7-10 years before people who do not have RA. Also, it is associated with significant morbidity, meaning patients will suffer a loss of independence as well as the ability to continue to pursue gainful employment.
A prior set of guidelines from the American College of Rheumatology in 2008 laid out treatment recommendations and guidelines for starting and switching medications.
However, these guidelines were formulated before complete knowledge as to the effect of newer drugs on disease course was fully appreciated. Those of us in practice, of course, felt these guidelines were antiquated even as they were released.
The newer guidelines deal with new discoveries and also make recommendations about how to use biologic drugs in high risk patients. As a result, I think these guidelines do make more sense and support the treatment approach that most private practitioners already follow.
The key point that the authors made was that low disease activity or even remission should be the goal of treatment. This is a critical point. It is now possible to get most patients with RA into remission.
One of the major changes from the 2008 guidelines was the emphasis on more aggressive treatment in patients with early RA that is - the first 6 months of disease onset. The recommended change to more intensive early therapy is necessary since more aggressive early treatment can provide better outcomes.
It's no secret that early diagnosis and treatment makes a huge difference in patient outcome.
Since joint damage in RA is irreversible, prevention of damage is an important goal. In addition to the obvious joint issues, preservation of physical function and health-related quality of life is important in order to limit the likelihood of disability.
To that end, they recommend early institution of disease modifying anti-rheumatic drug (DMARD) therapy, drugs that slow the rate of progression of RA. Examples would be medicines like methotrexate and hydroxychloroquine (Plaquenil). Biologic drugs should be added quickly if DMARD therapy does not appear to be working effectively. Biologic drugs include the tumor necrosis factor (TNF) inhibitors adalimumab (Humira), certolizumab pegol (Cimzia), etanercept (Enbrel), golimumab (Simponi), or infliximab (Remicade). Non TNF biologics include abatacept (Orencia), tocilizumab (Actemra), or rituximab (Rituxan).
One other point: Biologics should not be combined since there is no increase in efficacy but there is an increase in side effects.
Finally, when I consider how far we've come with our approach to RA since I began practice in 1981, the difference is both astounding as well as gratifying.

rheumatoid arthritis

rheumatoid arthritis
Rheumatoid Arthritis, commonly referred to as "RA", is an autoimmune disease that impacts the joints. RA is progressive and causes pain, swelling, stiffness and decreased mobility in the joints of the body. Over time, RA can result in joint damage. Its onset can occur between the ages of 25 and 55, with joint damage appearing as early as in the first two years of onset. Therefore early diagnosis and treatment is critical.
Signs and Symptoms of RA
Early signs of rheumatoid arthritis may include pain and swelling in the joints of the hands and feet. Other symptoms may include:
· Stiffness and aching in the muscles and joints especially after sleeping
· Weakness in the affected joints
· Loss of motion or mobility
· Nodules under skin near affected areas
· Fatigue
· Low grade fever
· Fusing of joints
· Occasionally swelling in tear glands, oral glands and in the lining of the heart or lungs may occur
RA is more prevalent among women and in the children of people previously diagnosed with RA.
Diagnosing Rheumatoid Arthritis
Doctors are typically able to diagnose RA by conducting a physical exam, reviewing medical history and ordering blood tests. A blood chemical known as Rheumatoid Factor (RF) is frequently found in patients with RA. Some doctors may use X-rays for diagnosis and monitoring of the disease.
Treating RA
There is currently no cure for RA, so treatment goals focus on managing the disease. The American College of Rheumatology recommends treatment goals that focus on reducing pain and stiffness; preventing and controlling joint damage; and maintaining joint function. Methods to meet these goals may include:
· Over the counter medications that provide pain relief (analgesics) and reduce swelling (anti-inflammatory and NSAIDs)
· Prescription medications that reduce pain and swelling and prevent joint damage
· Physical therapy and/or occupational therapy
· Surgery
Daily Living
Rheumatoid arthritis is a chronic disease that can have a disabling effect on those who have it. However, there are lifestyle choices and changes that can be made to make coping with RA a little easier. Adopting a regular fitness routine and having a healthy diet can improve quality of life. Determining the appropriate exercise routine should be done in consultation with your doctor and physical therapist.
Be aware that chronic illnesses can have a negative impact on your emotional health. Do not allow your illness to prevent you from participating in community activities you have enjoyed on a regular basis. Participate in a support group for people with chronic illnesses. Alert your doctor if you are experiencing ongoing depression.
Stiffness and reduced range of mobility may inhibit an RA sufferer from completing daily tasks. Adjustments in routines and assistive devices may be used to increase functioning during flare ups. Family caregivers and professional homemaking services can help the RA patient remain independent at home and in the community.

rheumatoid arthritis

 rheumatoid arthritis
Of the inflammatory forms of arthritis, rheumatoid arthritis (RA) is the most common. It affects about 2 million Americans, about 60% of whom are women. It is no respecter of age since it can occur in children as well as in adults.
RA is a chronic autoimmune disorder characterized by chronic inflammation in the joints which causes pain, swelling, and stiffness. What is not generally appreciated is that it affects not only joints but internal organs as well.
RA can cause permanent joint damage leading to deformities and loss of joint movement. As a result, many people with RA experience limitations on their ability to perform daily activities which has a major impact on quality of life.
Data has indicated that early aggressive treatment of RA can limit joint damage. RA is a major contributor to morbidity and mortality. Mortality rates among people with RA are twice that of the general population and disease severity is an independent risk factor of mortality regardless of comorbid conditions.
People with RA are twice as likely to develop congestive heart failure is compared to those without RA.
RA is the most common cause of disability in the United States and the third leading cause of work limitations. Medical and indirect costs due to lost wages are estimated at $3 billion annually and fewer than 50% of working age adults with RA are still employed 10 years after onset of the disease.
The cause of RA is unknown, but multiple genetic and environmental factors (infectious agents, reproductive status, and smoking) are thought to be involved. What is also known is that the immune system plays an important role.
When it comes to treatment, the primary goals are to relieve pain, swelling, and fatigue; improve joint function; slow down or stop joint damage; and prevent disability and disease-related morbidity. RA is a complex disease. There are many cells, molecules, and processes involved in the genesis of RA.
CD4+ T cells mediate joint damage both directly and indirectly by driving non-T effector cells to release inflammatory cytokines. Also, B cells play a role in RA pathology by producing autoantibodies and triggering cytokine secretion by T cells as well as by acting as antigen-presenting cells (APCs) to trigger T-cell activation. This entire machinery is driven by multiple cytokines.
In the past the traditional treatment pyramid for rheumatoid arthritis was to start with anti-inflammatory drugs, move onto mild disease-modifying drugs (DMARDS), step up to more aggressive disease-modifying drugs if they didn't work, and finally use powerful immunosuppressive drugs as a last resort. The treatment approach now is to stand the pyramid on its head and use more aggressive therapies in concert with methotrexate to effect remission as soon as possible.
A newer approach is to "treat to target." This means that a specific goal of remission is aimed for and adjustments in medications are made regularly in order to achieve it.
Anti-inflammatory drugs- either non-steroidal drugs or low dose corticosteroids are an adjunctive therapy but are not considered as important as remission-inducing drugs. These drugs are initiated at the start of treatment to give the patient some relief. Full therapeutic doses of non-steroidal anti-inflammatory drugs (NSAIDS) or prednisone in doses ranging from 5-10mgs/day are helpful for symptoms. Side effects related to an increase in cardiovascular events as well as gastrointestinal issues must be balanced against benefit.
Remission-inducing agents (DMARDS) are started at the same time or shortly thereafter. Besides methotrexate, other DMARD drugs include hydroxychloroquine (Plaquenil), azathioprine (Imuran), sulfasalazine (Azulfidine), cyclosporine (Sandimmune), and leflunomide (Arava).
By far, the most commonly used DMARD is methotrexate.
Treatment options including biologic response modifiers, disease-modifying anti-rheumatic drugs, and combinations of disease-modifying anti-rheumatic drugs have been used as our knowledge of the different pathways involved in the RA process has deepened.
Therapeutic agents including TNF antagonists and IL-6 inhibitors were developed to block cytokine-mediated processes. Other anti-cytokine drugs are also being developed to target specific "bad guys."
Co-stimulatory pathway T-cell drugs were developed to inhibit T-cell mediated processes. Elucidation of the role of B cells in the inflammation cascade has provided the rationale for the institution of B-cell targeted therapies.
Biologic drugs have revolutionized the treatment of rheumatoid arthritis and have permitted rheumatologists to achieve remission in many patients with RA.
Examples of biologics include the following: TNF inhibitors consist of Enbrel, Humira, Remicade, Cimzia, and Simponi. Anti-interleukin 6 drugs are represented by Actemra. The primary T-cell drug is Orencia and the B-cell drug is Rituxan. Many other drugs are in the pipeline.
In addition to the existing biologics, new oral kinase inhibitors (JAK and SYK) are exciting new drugs.
While complementary therapies such as dietary fish oil, flax seed, etc. may help, they are usually not effective by themselves. The role of diet also is not well understood.
Objective measurement of remission include reduction in joint swelling and pain scores, improvement in health assessment and activities of daily living, reduction in blood measures of inflammation, and cessation of disease activity by magnetic resonance imaging.
Newer measurement criteria that will ensure uniformity of definition of remission are also being created.

Treating Early Rheumatoid Arthritis

Rheumatoid arthritis (RA) is the most common inflammatory form of arthritis affecting approximately two million Americans. It is a systemic, autoimmune disease for which there is no known cure.
Several pieces of data have shown that joint damage in RA can occur as early as 4 months after the start of symptoms. And further evidence has demonstrated that early intervention with the disease using disease-modifying anti-rheumatic drugs (DMARD) therapy improves signs and symptoms of the disease but also slows the rate of x-ray progression, a primary determinant of future disability. In addition, since it is a systemic disease, damage inflicted on the joints can also be accompanied by significant damage to other organ systems such as the lungs, eyes, bone marrow, skin, and nerves.
Guidelines from the American College of Rheumatology have suggested the prompt initiation of DMARD therapy within the first three months of diagnosis. Sometimes adding low dose prednisone - an oral corticosteroid- can help buy time by serving as a "bridge" until the DMARD begins to kick in. Combining methotrexate, the "workhorse" DMARD, with low dose prednisone can reduce disease activity, slow the rate of progression of disease, and prevent further physical disability.
One word of warning is that delay of treatment beyond three months from the time of diagnosis has grave consequences since there is a higher probability of joint damage and less likelihood of achieving remission in the future. Furthermore, joint damage, once it occurs, cannot be reversed. So, prevention is the key.
So a common sense paradigm has emerged for the management of early rheumatoid arthritis. This is a model which most rheumatologists increasingly are adhering to.
The first is early diagnosis. This, of course depends on early referral to a rheumatologist.
The second important point is to institute DMARD treatment, preferably with methotrexate, along with low dose prednisone immediately.
And the final approach is to use the "treat to target" model that has become in vogue recently. Treating to target implies the need for very tight control of the disease. This approach allows a patient to have a custom-tailored treatment program with the aim of establishing either low disease activity or complete remission. The achievement of the treatment target can be objectively made using various measurement tools, including joint counts, blood tests of inflammation, and various imaging techniques.
Such a treatment approach is not dissimilar to the treatment approaches for other serious chronic conditions such as hypertension and diabetes.