Rheumatoid Factor Test: Should We Rely on Rheumatoid Factor Levels?

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The Rheumatoid factor test is not the only way to diagnose RA

It can be frustrating to read about the different ways that people interpret a Rheumatoid factor test. It seems there are still some doctors who think Rheumatoid factor levels are sufficient to diagnose Rheumatoid Arthritis. If you meet an RA specialist like that, I hope you will politely request your records and move on.

However, there is something more subtle that needs to be explored. Many rheumatologists treat RA patients based upon Rheumatoid factor levels. Some doctors rely on the Rheumatoid factor test to indicate either (1) disease severity or, (2) current disease state. Should they?


More than one Rheumatoid factor test

There is actually more than one type of Rheumatoid factor test (Rf). Additionally, there are several antibodies to measure. Some combination of antibodies may be tested including immunoglobulin A (IgA), IgG, or IgM. Some are considered better than others at identifying RA.

Rheumatoid Arthritis is a heterogeneous disease. Different antibodies are present in varying amounts in different patients who exhibit differing symptoms. There is not a one-size-fits-all test. “Different disease manifestations in RA may be associated not only with certain RF isotypes and RF isotype combinations but also with changes in lymphocyte subsets in the blood,” Journal of Rheumatology.

RA medication complicates interpretation of Rheumatoid factor levels

Different RA medications influence Rf test results to varying degrees. This may be true whether or not RA symptoms are diminished. There is even some evidence that over-the-counter NSAIDs (i.e.: Advil) can affect Rheumatoid factor (IgM).

One study examined “whether Rheumatoid factor isotypes and anti-cyclic citrullinated peptide (anti-CCP) antibodies are related to clinical response in patients with rheumatoid arthritis treated with tumour necrosis factor α (TNFα) inhibitors,” Annals of Rheumatic Diseases.  “A significant reduction in the rheumatoid factor level was reported by all treatment groups after 1 year.” They found “significantly higher IgA rheumatoid factor levels were reported by the non-responder group” (those with refractory RA). “More interestingly, high pretreatment levels of IgA rheumatoid factor are associated with a poor clinical response to TNFα inhibitors.” How often is IgA the one that is tested?

Patients who respond well to TNF-blockers like Enbrel experience a greater decline in Rf levels than those with more resistant RA. However, “the decline in IgM-RF, but not ACPA, was associated with a decrease in CRP and ESR.” (ACPA is another name for anti-CCP, a more RA-specific antibody than the Rheumatoid factor. CRP is C-reactive protein and ESR is sedimentation rate.) But would the test result be the same if it did not test IgM?

A patient with severe RA who does not respond sufficiently to DMARDs could have a somewhat “improved” Rheumatoid factor, sed rate, and CRP. Does the patient or the doctor know which antibody is measured and what it may signify? The patient may be left with a high anti-CCP – and of course, her RA symptoms.

Treat the patient, not the Rheumatoid factor levels

There is no perfect Rheumatoid Arthritis test which can either diagnose or quantify RA. Even the markers of inflammation considered to be reliable such as the ESR, CRP, and various Rf’s may not always correlate with symptoms. The medications which do not cure RA or always bring reliable relief may “improve” the results of blood tests. RA may be uncontrolled and a patient may still be told that she is “better.”

Doctors who want to properly treat patients have only one option. When they examine patients, they must take note of symptoms that patients describe, trusting patients’ narratives more than blood test results. Patient input is the one indispensible component for a doctor to treat RA.

Postblog: Many Rheumatoid Arthritis patients are Rf negative altogether.

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Kelly Young. All rights reserved.

This entry was posted on Tuesday, March 23rd, 2010 at 7:01 am and is filed under RA Research, Resources, and Rheumatology. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.


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