Our conceptualization of rheumatoid arthritis assumes the disease develops in the context of a genetic predisposition and in the presence of certain environmental factors, with interactions between genes and environment leading to immune reactivity and clinical disease. RA is heterogeneous both clinically and etiologically, with two distinct subsets defined by the presence or absence of anticitrulline antibodies. RA is a criteria-defined, versus etiology-defined, disease, with one criterion being the presence of rheumatoid factor (RF), first recognized nearly seven decades ago. Although RF is present in 80% of patients, it is not specific. It also can be detected in up to 15% of healthy elderly people. Citrullination is a posttranslational enzymatic process mediated by calcium-dependent peptidyl arginine deiminases in which positively charged protein arginine residues are converted to neutral citrullines, rendering the proteins more subject to degradation by proteolytic enzymes. In RA, increased citrullination is seen in the joints, lungs, and sites of extra-articular involvement as well as in many synovial proteins like fibrinogen, vimentin, and type II collagen. In normal synovial tissue, there is no expression of citrullinated molecules. Increased citrullination as a manifestation of human disease was first identified in the lining and sublining layers of RA synovial tissue. It had previously been shown that antibodies to cyclic citrullinated proteins (anti-CCP) are present in about 60% of RA patients, versus 2% of healthy controls and fewer than 10% of patients with other rheumatic diseases. Citrullination is a common event in many physiologic processes, but antibodies in RA have preferential reactivity to proteins that have undergone posttranslational citrullination. Further studies have shown anti-CCP antibodies are not only predictive of RA but also have been directly implicated in pathogenesis. Animal data suggest citrullination can alter the immunogenicity of “self” antigens. This is in contrast to RF, which does not seem to be directly proarthritogenic. Blood repository data from Sweden and the Netherlands found that anti-CCP antibodies can be detected years before symptom onset; they increase in concentration as clinical disease approaches, and thereafter rarely disappear, even with treatment. Patients who are anti-CCP positive typically have a more severe disease course than do anti-CCP-negative patients, with a greater likelihood of erosive disease.
My dear friend is a family practice physician educated at Dartmouth. She is brilliant. She has fibromyalgia but has other symptoms which could indicate RA. I asked if she had her anti-ccp tested, and she had no idea what I was talking about. Incidentally, she did get it tested and it was negative. Shoot - I typed and it disappeared, so starting all over.
well the ACR just came out with their new updated treatment guidelines and people complained because they were too regimated. I think Suzanne said it was too many circles and arrows. others complained because AP was virtually ignored. you can't please everyone. It includes what tests need to be run with each drug
http://www.rheumatology.org/publications/guidelines/recommendations.pdf
well the ACR just came out with their new updated treatment guidelines and people complained because they were too regimated. I think Suzanne said it was too many circles and arrows.
[/QUOTE]For the most part diagnostic testing is fairly standard with the exception of the anti ccp. and I think we will see that added around the ACR meeting. Th eonly reason it hasn't been is the shear newness of the test and the need for wider spread validation.