People who have a specific genetic variant of the PTPN22 gene and test positive for antibodies against cyclic citrullinated peptide are much more at risk of developing rheumatoid arthritis than people who only have one of these markers.
A study published today in the journal Arthritis Research & Therapy reveals that a group of people who have a specific genetic variant, or polymorphism, of PTPN22, a gene that encodes a tyrosine phosphatase protein, and tested positive for anti-cyclic citrullinated peptide (CCP) antibodies, all developed rheumatoid arthritis (RA) in the following two and a half years. Both the polymorphism and anti-CCP antibodies have previously been shown to be associated with RA, but in combination they give a much higher risk of developing the disease than separately. This combination gives a much higher relative risk than the combination of anti-CCP antibodies and the previously well-known genetic factor, namely HLA DR4 antigens.
Martin Johansson and colleagues from the University Hospital in Umea, Sweden studied a population of 92 patients diagnosed with RA for whom a blood sample was available, which had been taken on average about two and a half years before the onset of the disease. They were matched with controls - blood donors from the same group who didnt develop arthritis - for age, sex, and rural or urban residence.
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