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Osteoarthritis Vs Rheumatoid Arthritis

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Rheumatoid arthritis (RA) is a progressive, systemic, autoimmune disease that causes joint inflammation. At onset, small joints such as the hands, wrists, and feet tend to be involved more than large joints. Because it is a systemic disease RA can cause significant internal organ damage to areas such as the lungs, skin, blood-producing organs, heart, and eyes.



More than 2 million Americans are affected by RA.

It is critical to make the diagnosis of RA as quickly as possible in order to prevent damage to both joints as well as internal organs.

The traditional criteria for establishing the diagnosis of rheumatoid arthritis are the American College of Rheumatology criteria:

1.Morning stiffness in and around joints, lasting at least I hour before maximal improvement.

2.Arthritis of 3 or more joint areas simultaneously with soft tissue swelling observed by a physician. The possible areas include the fingers, knuckles, wrsits, elbows, ankles, knees, and feet.

3.Arthritis affecting the hand joints with at least 1 area swollen in a wrist, knuckle or finger.

4.Symmetric arthritis with simultaneous involvement of the same joint areas on both sides of the body (bilateral involvement of the fingers, knuckles, or feet is acceptable without absolute symmetry.

5.Rheumatoid nodules: Subcutaneous nodules over bony prominences, or extensor surfaces, or near joints, observed by a physician.

6.Serum rheumatoid factor: Abnormal amounts of serum rheumatoid factor by any method for which the result has been positive in less than 5 per cent of control subjects.

7.Radiographic (X-ray) changes: Typical of rheumatoid arthritis on x-rays of the hands, wrists. Must include erosions or demineralization in or near involved joints.

For classification purposes, a patient must satisfy at least 4 of the 7 criteria. Criteria 1 through 4 must have been present for at least 6 weeks. Patients with 2 clinical diagnoses are not excluded. While these criteria are fine for standardization purposes when doing research to ensure uniformity, they are not meant to be necessarily followed rigidly in a clinic setting.

More recently, the use of assays such as the anti-cyclic citrullinated peptide (anti-CCP) assay has provided a more specific method for identifying patients whose arthritis symptoms will lead to RA.

In a recent published study, Japanese researchers found that the "combination of a positive rheumatoid factor, elevated C-reactive protein, swollen joints, and a positive anti-CCP was highly specific and accurate; it is easy to use for physicians and thus beneficial to patients" (Yamane T, et al. Journal of Rheumatology, January, 2008).

As a practicing rheumatologist, I find this article to be useful in that it confirms what many of us here in the United States have also found to be true. The diagnosis of RA, by all means, is not necessarily easy.

Yet, making the diagnosis is critical to initiating aggressive therapy. What is very important to remember is that today, making the diagnosis of rheumatoid arthritis is not necessarily a bad thing for a patient. Newer biologic drugs have made the "putting a patient into remission" more of a likely scenario than not.

The data from the Japanese study supports a simple yet direct method for making the diagnosis quickly.
Osteoarthritis Vs Rheumatoid Arthritis
Because it is a systemic condition, it affects more than joints. Like other inflammatory conditions, RA causes anemia. The anemia is not the result of bleeding (although some patients treated with non-steroidal anti-inflammatory drugs can develop gastrointestinal bleeding), or deficiency of vitamin B12, folate, or iron.

This type of anemia is called the anemia of chronic disease (ACD).

Patients with RA who develop anemia are more likely to have more severe joint disease, worse quality of life indicators, and more severe disease.

As mentioned earlier, while m some patients with RA can develop an iron deficiency anemia as a result of non-steroidal anti-inflammatory drug therapy and subsequent gastrointestinal blood loss, most anemia (60%) associated with RA is due to ACD.

While it is difficult sometimes to differentiate iron deficiency anemia from ACD, there are laboratory characteristics that separate them. The key differentiating feature is that iron deficiency anemia is due to an absolute lack of iron. ACD is not due to iron deficiency- there's plenty of iron available; ACD is due to an inability to unlock the iron that is available.

Another complicating problem is that some patients with RA have both types of anemia.

ACD is due to systemic inflammation. The severity of ACD can be predicted by the amount of elevation of laboratory markers of inflammation such as the erythrocyte sedimentation rate ("sed rate") and the C- reactive protein (CRP).

In RA, many chemical mediators of inflammations, called cytokines, are overproduced. These cytokines inhibit the ability of iron stores to be used.

These inflammatory cytokines affect the production of red blood cells at different levels.

One inflammatory cytokine, interleukin-6 (IL-6) adversely affects iron utilization by causing increased production of hepcidin. Hepcidin is an inflammatory protein that prevents release of iron from cells called macrophages. It also reduces absorption of iron from the small intestine.

Other cytokines such as interferon-y and tumor necrosis factor (TNF) block the production of erythropoietin, a hormone that is critically needed for the production of red blood cells. In addition, TNF and interleukin-1 (IL-1) prevent the maturation of red blood cells.

The net effect is a marked reduction of iron available to make red cells.

Studies on anemia in rheumatoid arthritis have produced interesting data. Patients with ACD have more severe disease. If patients have a good response to RA treatment, the anemia improves at the same time. Some data exists that treatment of the ACD will also help improve the symptoms of RA.

The association of inflammatory mediators with the development of ACD indicates that anemia should be monitored during the course of therapy in patients with RA.

Newer biologic agents such as tocilizumab which block the effects of interleukin-6 may help with the resolution of ACD. Preliminary pilot data has shown that blockade of IL-6 in RA patients helps improve quality of life and improves fatigue coincident with the resolution of anemia.

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Nathan Wei has sinced written about articles on various topics from Arthritis Pain, Health and Arthritis Signs. Nathan Wei, MD FACP FACR is a rheumatologist and Director of the Arthritis and Osteoporosis Center of Maryland. He is a Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine. For more info:. Nathan Wei's top article generates over 550000 views. to your Favourites.
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