Need to narrow the question. Anti-CCP is a system linked to rheumatoid arthritis, somewhat more specific but probably no more sensitive than rheumatoid factor.
Besides RA, you can also find anti-CCP antibodies in psoriatic arthritis and Sjögren's syndrome. Whether this finding reflects an overlap condition or carries with different prognosis in these disorders is to me uncertain; however, in my practice I tend to treat joint involvement as RA.
I have a curious experience with antiCCP. About 10 years ago I attended one typical patient with osteoarthritis, however another doctor thought it was RA and she agreed due to rheumatoid factor positivity. I requested the anti-CCP to show that rheumatoid factor was false positive. I was surprised to see that the AntiCCP was positive (repeatedly). It was not Sjögren or psoriasis
Anti-CCP positivity is rare in children with JIA but certainly exists. When it is found in children with JIA, they typically have a more severe polyarticular course and generally a worse prognosis. Such antibodies are also sometimes detected in SLE or MCTD although they are of unclear significance except if they correlate with a clinical feature such as arthritis where they can be used as a surrogate indicator of disease activity; that, however, is kind of patient-dependent and I wouldn't generalize it. And anyway, physicians should treat people not numbers so any use of this marker in clinical practice should be in the context of all other aspects of patient assessment...
Positive anti-CCP titers have also been described in patients with mycobacterial infections, i.e., tuberculosis. In the absence of TB, psoriatic arthritis, etc, in terms of clinically interpreting positive anti-CCP in patients who do not yet have clinically overt inflammatory arthritis, e.g., RA, let's remember that seropositivity precedes clinical disease by an average of about 2.5 years. Here, is there anything we can do to "prophylax" patients against coming down with RA in such scenarios? There is not much literature; however, certainly, quitting smoking would be one way of at least delaying the onset of disease somewhat. I have prescribed Plaqueni, a relatively benign DMARD in certain patient subsets for this purpose, for example young patients concerned about persistent anti-CCP positivity, those folks asking about disease prevention, when there is a strong family history of RA, persistently high anti-CCP titers, etc. Then, I tend to order a Quantiferon test for obvous reason. I realize this is controversial, and of course, each case should be treated on an individual basis. Here is where the art of medicine comes in. More data is needed.
Approximately half of patients with RA have anti-CCPseveral years before the onset of symptoms and can be detected in about 0.6% of population. In other autoimmune diseases and infections can be also be detected (Nielsen MMJ. Arthritis Rheum 2004;50:380-386)):
• Palindromic rheumatism (Salvador G. Rheumatology 2003;42:972): 56%
• Psoriatic arthritis (Bogliolo L. J Rheumatol 2005:32:511): 12%
• Primary Sjögren syndrome (Gottenberg J. Ann Rheum Dis 2005:64:114): 9%
• JIA polyiarticular (Kasapcopur Ö. Ann Rheum Dis 2005:63:1687): 6%
• SLE (Hoffman IEA. Ann Rheum Dis 2005;64:330): 5%
• Spondiloarthritis (Salvador G. Rheumatology 2003;42:972): 3%
• Hepatitis C (Lienesch D. J Rheumatol 2005;32:489): 2%
The Anti-CCP are specially usefull for patients eith early rheumatoid arthritis. In this context the diagbnostic utillity increases a lot. In addition, are there a relation between High anti-CCP AB levels (>3 UL) and severity of the disease.
Some tratments are perticulary indicated in patients with RA and a positive test to anti-ccp antibodies, rituximab and tocilizumab.
Anti CCP can be found in many diseases apart from RA, like PsA, MCTD etc. it is found in few cases of leprosy, and also as a false positive result in test for cryoglobulinaemia. it denotes an erosive subset of arthritis and worse prognosis.
Well, smoking drives the PAD enzyme to citrullinate arginine, leading to the formation of more anti-CCP antibodies; smokers with RA are also form more rheumatoid nodules than non-smokers with RA. Smoking also precipitates RA earlier in people born with thre rheumatoid epitope, and finally smoking also lessens the efficacy of oral DMARDS and biologic agents; in summary, a lot of reasons not to smoke if you have a family and/or personal history of RA,