Prior to the discovery and testing of anti-CCP, most doctors used rheumatoid factor (RF) – another antibody – as a test to help reach a rheumatoid arthritis diagnosis.Īnti-CCP is thought to be present in 60% to 70% of patients with rheumatoid arthritis. Testing for the presence of anti-CCP is a relatively new support tool in helping doctors diagnose rheumatoid arthritis. These attacks can produce inflammatory symptoms most commonly experienced in rheumatoid arthritis. This means that the patient’s immune system produces antibodies that identify the patient’s cells as foreign material and as a result, attack its own normal cells. What is Anti-CCP?Īnti-CCP is an autoantibody. The prognosis of anti-CCP positive patients also depends greatly on early diagnosis of rheumatoid arthritis as well as early initiation of treatment. However, this can also depend on many different factors and varies between each individual. Anti-CCP positive patients can potentially experience a more aggressive disease course. Alternatively, a patient with similar symptoms but negative blood work is referred to as having seronegative rheumatoid arthritis.Ī positive anti-CCP test result can be used as a prognostic tool to determine the severity of symptoms the patient may have throughout their disease course. A positive anti-CCP test result can be used in conjunction with other blood tests, imaging tests, and/or physical examination findings to diagnose rheumatoid arthritis.Ī patient with rheumatoid arthritis who has positive blood tests for anti-CCP has what is commonly referred to as seropositive rheumatoid arthritis. Levels of anti-CCP can be detected in a patient through a simple blood test. Published 2000 Wiley-Liss, Inc.Doctor of Medicine (M.D.) in 2008 from UT Health San Antonio, Surgeon at TRACC DallasĤ min read RA and Anti-CCP: What is the Purpose of an Anti-CCP Test?Īnti-cyclic citrullinated peptide (anti-CCP) is an antibody present in most rheumatoid arthritis patients. Considering the molecular structure of these probes that favor accumulation in the mitochondrial membrane because of a positive charge, our results are not surprising. MFG, MTG, and NAO appeared poor choices for the membrane potential independent analysis of mitochondrial membrane mass. The results with 5 microM NAO were similar. The fluorescence intensity of cells stained with 0.1 microM NAO increased following incubation with BDM, nigericin, and decreased for FCCP, CCCP, DNP, gramicidin, and valinomycin. Incubation of GM130, HL60, and U937 cells with 2,3-butanedione monoxime (BDM), nigericin, carbonyl cyanide 3-chlorophenylhydrazone (CCCP), carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP), 2,4-dinitrophenol (DNP), gramicidin, ouabain, and valinomycin resulted in increases of the fluorescence intensity for MFG or MTG with only a few exceptions. The effects of a variety of DeltaPsi(m) altering drugs were tested for MFG and MTG at probe concentrations of 20 nM and 200 nM and for NAO at 0.1 microM and 5 microM, using rhodamine 123 at 0.1 microM as a reference probe. The three probes were titrated to determine whether saturation played a role in the response to drugs. However, in experiments in which NAO and MFG were combined with orange emitting mitochondrial membrane potential (DeltaPsi(m)) probes, we found clear responses to DeltaPsi(m) altering drugs for both probes. We set out to develop an assay for the simultaneous analysis of mitochondrial membrane potential and mass using the probes 10-nonyl acridine orange (NAO), MitoFluor Green (MFG), and MitoTracker Green (MTG) in HL60 cells.
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