Environmental, genetic and hormonal factors having an association with the immune system’s attack on body joints have been speculated as potential risk factors for RA.30 Since specific causative agents have yet to be identified, suppressed immune systems, and infections serve as contributing factors in some individuals. Inflammation affecting organ systems contributes to systemic manifestations.30 Evidence is mounting around infectious agents, such as bacteria or viruses triggering RA conditions in susceptible individuals.30 The Human Herpes Virus 6 (HHV-6) and Epstein-Barr virus (EBV) have been confirmed in epidemiological studies to have potential associations.30 RA is familial with a 2-3% prevalence rate for first-degree relatives, and a genetic disease component with identical twins is approximately at 15-20%.32 Genetic components demonstrating positive RA factors have been associated with disease severity and may interact with a well-defined environmental factor such as cigarette smoking.30,33 In fact, smokers are four times more likely to exhibit RA conditions than non-smokers.33
Individuals with autoimmune disorders suffer from the inability to recognize foreign invaders from their body’s own. Clusters of genetic markers, HLA-DR4/DR1 occur in 90% of those with RA, allowing susceptibility through genetic factors and infectious episodes triggering autoimmune responses.33,34
Research has suggested complex interactions exist between RA and estrogen and female sex hormones as influencing risks. The onset of RA is rare during pregnancy, can often return post-delivery, and is more common among nulliparous women. Oral contraceptive medications and unidentified factors associated from their use can interfere with severe RA by protecting against its development. Nulliparity, frequency of oral contraception use, and breast-feeding may all influence the epidemiology of RA.29,30
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