iologic response modifiers, which include drugs that suppress tumor necrosis factor (TNF), appear to be particularly effective.

Tumor necrosis factor is a protein that is produced by the immune cells. TNF is the major culprit responsible for inflammation-inducing damage. By block the effects of TNF, better control of RA can be achieved.

Three anti-TNF drugs are currently available: etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade). Another biologic drug, anakinra (Kineret) blocks interleukin, a different cytokine.

These drugs allow patients to have their disease controlled to such an extent that most are able to enjoy a normal work and leisure existence.

Second line biologic agents such as Rituxan and Orencia allow rheumatologists to treat patients who h

RA is a condition that forces half of patients to become disabled from the work force within five to ten years… and reduces life expectancy by as much as 18 years. RA affects about one per cent of the world’s adult population, most commonly women between the ages of 30 and 50.

The good news is that a tremendous amount of progress has been made within the last ten years in identifying patients earlier and treating the disease more aggressively. Patients with RA, if treated appropriately, can lead a relatively normal life. This is in stark contrast to the wheel-chair bound existence common as recently as 20 years ago!

Experts in the field consider early rheumatoid arthritis to be a medical emergency with mortality and morbidity equal to that for diabetes, asthma, heart disease, and other life-threatening conditions.

Rheumatoid arthritis attacks the joints in a symmetric fashion (both sides of the body affected equally) with the most common areas being the hands, wrists, ankles, knees, and feet. In addition to the swelling and pain, patients with RA often have profound fatigue and stiffness.

Rheumatoid arthritis is an autoimmune disease that attacks not only joints, but internal organs such as the blood vessels, lungs, heart, and eyes. Patients with RA are at increased risk for heart attack, stroke, and lymphoma.

Since many other types of arthritis such as gout, lupus, and osteoarthritis can look like RA a careful diagnostic approach is needed.

Laboratory testing has its pitfalls. The rheumatoid factor, a blood test found to be positive in about 80 per cent of individuals with RA, may also be positive in other disease conditions. Couple that with the fact that 20 per cent of patients with RA will be rheumatoid factor negative, then it becomes clear a diagnosis should not hinge on the results of blood tests alone.

Imaging procedures can also be misleading. Conventional x-rays often miss the erosions found with early disease. Newer imaging technologies such as magnetic resonance imaging (MRI) and ultrasound are much more sensitive.

After the diagnosis is made, there is even more hope for a patient today. In the past, non steroidal anti-inflammatory drugs (NSAIDS) used to be considered a cornerstone of therapy. That is no longer true.

Disease-modifying anti-rheumatic drugs (DMARDS) are being used earlier. Among the DMARDS currently being used are methotrexate, leflunomide (Arava), azathioprine (Imuran), sulfasalazine (Azulfidine), cyclosporine, and hydroxychloroquine (Plaquenil). These drugs attack the immune cells responsible for chronic inflammation. While DMARDS alone in combination are effective, they are relatively non-specific. Often, combinations of DMARDS are required.

Biologic Response Modifiers (BRMS) can target the disease more specifically than DMARDS. RA is a disease that is dependent on the signaling that occurs between immune cells. The signaling takes place through the use of special chemical messengers called cytokines. BRMS act at both the cytokine (chemical messenger) as well as the cellular level allowing the disease to be better controlled and in some instances put into remission.

Biologic response modifiers, which include drugs that suppress tumor necrosis factor (TNF), appear to be particularly effective.

Tumor necrosis factor is a protein that is produced by the immune cells. TNF is the major culprit responsible for inflammation-inducing damage. By block the effects of TNF, better control of RA can be achieved.

Three anti-TNF drugs are currently available: etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade). Another biologic drug, anakinra (Kineret) blocks interleukin, a different cytokine.

These drugs allow patients to have their disease controlled to such an extent that most are able to enjoy a normal work and leisure existence.

Second line biologic agents such as Rituxan and Orencia allow rheumatologists to treat patients who h

life-threatening conditions.

Rheumatoid arthritis attacks the joints in a symmetric fashion (both sides of the body affected equally) with the most common areas being the hands, wrists, ankles, knees, and feet. In addition to the swelling and pain, patients with RA often have profound fatigue and stiffness.

Rheumatoid arthritis is an autoimmune disease that attacks not only joints, but internal organs such as the blood vessels, lungs, heart, and eyes. Patients with RA are at increased risk for heart attack, stroke, and lymphoma.

Since many other types of arthritis such as gout, lupus, and osteoarthritis can look like RA a careful diagnostic approach is needed.

Laboratory testing has its pitfalls. The rheumatoid factor, a blood test found to be positive in about 80 per cent of individuals with RA, may also be positive in other disease conditions. Couple that with the fact that 20 per cent of patients with RA will be rheumatoid factor negative, then it becomes clear a diagnosis should not hinge on the results of blood tests alone.

Imaging procedures can also be misleading. Conventional x-rays often miss the erosions found with early disease. Newer imaging technologies such as magnetic resonance imaging (MRI) and ultrasound are much more sensitive.

After the diagnosis is made, there is even more hope for a patient today. In the past, non steroidal anti-inflammatory drugs (NSAIDS) used to be considered a cornerstone of therapy. That is no longer true.

Disease-modifying anti-rheumatic drugs (DMARDS) are being used earlier. Among the DMARDS currently being used are methotrexate, leflunomide (Arava), azathioprine (Imuran), sulfasalazine (Azulfidine), cyclosporine, and hydroxychloroquine (Plaquenil). These drugs attack the immune cells responsible for chronic inflammation. While DMARDS alone in combination are effective, they are relatively non-specific. Often, combinations of DMARDS are required.

Biologic Response Modifiers (BRMS) can target the disease more specifically than DMARDS. RA is a disease that is dependent on the signaling that occurs between immune cells. The signaling takes place through the use of special chemical messengers called cytokines. BRMS act at both the cytokine (chemical messenger) as well as the cellular level allowing the disease to be better controlled and in some instances put into remission.

Biologic response modifiers, which include drugs that suppress tumor necrosis factor (TNF), appear to be particularly effective.

Tumor necrosis factor is a protein that is produced by the immune cells. TNF is the major culprit responsible for inflammation-inducing damage. By block the effects of TNF, better control of RA can be achieved.

Three anti-TNF drugs are currently available: etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade). Another biologic drug, anakinra (Kineret) blocks interleukin, a different cytokine.

These drugs allow patients to have their disease controlled to such an extent that most are able to enjoy a normal work and leisure existence.

Second line biologic agents such as Rituxan and Orencia allow rheumatologists to treat patients who h

t of individuals with RA, may also be positive in other disease conditions. Couple that with the fact that 20 per cent of patients with RA will be rheumatoid factor negative, then it becomes clear a diagnosis should not hinge on the results of blood tests alone.

Imaging procedures can also be misleading. Conventional x-rays often miss the erosions found with early disease. Newer imaging technologies such as magnetic resonance imaging (MRI) and ultrasound are much more sensitive.

After the diagnosis is made, there is even more hope for a patient today. In the past, non steroidal anti-inflammatory drugs (NSAIDS) used to be considered a cornerstone of therapy. That is no longer true.

Disease-modifying anti-rheumatic drugs (DMARDS) are being used earlier. Among the DMARDS currently being used are methotrexate, leflunomide (Arava), azathioprine (Imuran), sulfasalazine (Azulfidine), cyclosporine, and hydroxychloroquine (Plaquenil). These drugs attack the immune cells responsible for chronic inflammation. While DMARDS alone in combination are effective, they are relatively non-specific. Often, combinations of DMARDS are required.

Biologic Response Modifiers (BRMS) can target the disease more specifically than DMARDS. RA is a disease that is dependent on the signaling that occurs between immune cells. The signaling takes place through the use of special chemical messengers called cytokines. BRMS act at both the cytokine (chemical messenger) as well as the cellular level allowing the disease to be better controlled and in some instances put into remission.

Biologic response modifiers, which include drugs that suppress tumor necrosis factor (TNF), appear to be particularly effective.

Tumor necrosis factor is a protein that is produced by the immune cells. TNF is the major culprit responsible for inflammation-inducing damage. By block the effects of TNF, better control of RA can be achieved.

Three anti-TNF drugs are currently available: etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade). Another biologic drug, anakinra (Kineret) blocks interleukin, a different cytokine.

These drugs allow patients to have their disease controlled to such an extent that most are able to enjoy a normal work and leisure existence.

Second line biologic agents such as Rituxan and Orencia allow rheumatologists to treat patients who h

ently being used are methotrexate, leflunomide (Arava), azathioprine (Imuran), sulfasalazine (Azulfidine), cyclosporine, and hydroxychloroquine (Plaquenil). These drugs attack the immune cells responsible for chronic inflammation. While DMARDS alone in combination are effective, they are relatively non-specific. Often, combinations of DMARDS are required.

Biologic Response Modifiers (BRMS) can target the disease more specifically than DMARDS. RA is a disease that is dependent on the signaling that occurs between immune cells. The signaling takes place through the use of special chemical messengers called cytokines. BRMS act at both the cytokine (chemical messenger) as well as the cellular level allowing the disease to be better controlled and in some instances put into remission.

Biologic response modifiers, which include drugs that suppress tumor necrosis factor (TNF), appear to be particularly effective.

Tumor necrosis factor is a protein that is produced by the immune cells. TNF is the major culprit responsible for inflammation-inducing damage. By block the effects of TNF, better control of RA can be achieved.

Three anti-TNF drugs are currently available: etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade). Another biologic drug, anakinra (Kineret) blocks interleukin, a different cytokine.

These drugs allow patients to have their disease controlled to such an extent that most are able to enjoy a normal work and leisure existence.

Second line biologic agents such as Rituxan and Orencia allow rheumatologists to treat patients who h

iologic response modifiers, which include drugs that suppress tumor necrosis factor (TNF), appear to be particularly effective.

Tumor necrosis factor is a protein that is produced by the immune cells. TNF is the major culprit responsible for inflammation-inducing damage. By block the effects of TNF, better control of RA can be achieved.

Three anti-TNF drugs are currently available: etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade). Another biologic drug, anakinra (Kineret) blocks interleukin, a different cytokine.

These drugs allow patients to have their disease controlled to such an extent that most are able to enjoy a normal work and leisure existence.

Second line biologic agents such as Rituxan and Orencia allow rheumatologists to treat patients who have failed anti-TNF drugs.

On the horizon are other biologic drugs that work at different points in the immune system- on different cytokines and on different pathways- to allow even greater as well as more specific control of disease. Since rheumatoid arthritis is a disease with many different cytokine and cellular mechanisms responsible for damage, attacking the disease at different points makes sense. In the future it may be possible to identify patients through specific tissue signals (called “biomarkers”). These biomarkers will allow physicians to type patients and give patients the specific therapy that will work best for them. Once that is achieved, the possibility of a cure becomes a reality.

Everything, though, starts with early accurate diagnosis. If damage is allowed to occur the chances for remission drop dramatically!