A chronic autoimmune disease, rheumatoid arthritis (RA), is theorized to be caused by some combination of genetics and environmental factors. What the precise molecular trigger is for RA is still under investigation so that better treatments can be developed and diagnosis made earlier, when the disease is more manageable. Early symptoms of RA include joint pain, swelling, and stiffness. As the disease progresses, it can lead to loss of mobility and joint deformity.
About 80 percent of RA patients have a form of the disease known as seropositive rheumatoid arthritis, which means that they test positive for one or both of key RA blood markers – rheumatoid factor (RF) or anti-citrullinated protein antibodies (ACPA). Whether someone is seropositive or seronegative has important implications for the treatment of RA, so it is a first-line test when RA is suspected.
Seropositive rheumatoid arthritis is not a new disease, and there are many accepted treatment programs; however, this doesn’t mean that researchers aren’t continuing to investigate the disease to better understand what triggers it.
Here are 6 interesting research findings about seropositive RA:
Researchers continue to seek better tools to reliably predict who is likely to develop RA. One recent study used two large population datasets and new computer modeling methodologies to categorize risk profiles. Study authors focused on seropositive patients because more is known about the genetic factors, i.e. the human leukocyte antigen (HLA) alleles. Researchers concluded that clinically informative RA risk prediction does have promising potential; further, they found that the risk of younger and older RA onset could be predicted using information on HLA and smoking status, respectively.
As mentioned above, smoking is highly associated with seropositive RA. Other environmental factors that researchers are taking a closer look at include obesity and the role of gut bacteria in influencing risk of developing RA.
Increasing evidence points to the fact that while genetics certainly play a role in the development of RA in some people, it may be less of an influencer than previously thought. Previous research concluded that approximately 60 percent of an individual’s chance of developing RA was genetic, and 40 percent was environmental/non-genetic. New research flips those numbers around, meaning that genetics play a less significant role than thought. This can be a comfort to people who are worried about passing along the disease to their children.
The above study also found that RA is equally heritable in both women and men. What is intriguing to researchers is the fact that more women develop RA than men, so there may be a hormonal role or some unknown environmental factor at play in the sex differences that are clinically observed.
It’s been observed that there are two major differences in RA hereditability. A relative of an RA patient has a significantly higher chance of developing RA if the family member with RA is seropositive. Researchers postulate that this means that seropositive and seronegative RA are somewhat genetically distinct. Secondly, family members are more apt to get RA if the affected relative developed it early in life.
Scientists have linked five amino acids in three HLA proteins to seropositive RA. HLA-DRB1 is a known molecular risk factor and now it’s been observed that HLA-B and HLA-DPB1 also play a role. This is important for developing treatments that target disease-causing genetic receptors.
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