Counseling Points - October 2007 - (Page 6)

susceptible to the disease. It seems probable that female hormonal mechanisms may play a role in RA development because the greatest differences in incidence rates are in patients below 50 years of age, where the disease is uncommon in men. Somewhat paradoxically, the occurrence of RA among women declines after age 50, and the use of oral contraceptives and pregnancy are associated with substantial improvements in disease symptoms.13 In fact, 75% of pregnancies in patients with RA result in a significant decrease in symptoms and often remission; however, symptoms recur postpartum. Interestingly, one small study found that the more fetal DNA pregnant mothers with RA had in their blood, the lower the disease activity, especially in the third trimester.14 The investigators of the trial hypothesized that fetal DNA apparently alters the immune system of the mother in ways that improve arthritic symptoms.14 confirms a causal role to consumption of these items and disease activity. Additionally, some researchers maintain that the risk of being affected by RA is higher in obese individuals.15 Symmons and colleagues investigated demographic, social, and clinical risk factors for the development of RA and found that a body mass index (BMI) of ≥30 was associated with a higher likelihood of being affected by the disease.15 Regardless of whether there is a pathological mechanism that links obesity to the propensity to develop RA, excess weight on the body strains joints and may contribute to the breakdown of joint tissue. Pathophysiology of RA Currently, there is no consensus concerning the precise cause of RA, but it is suspected that infectious organisms, particularly viruses, may trigger the onset of the disease in genetically predisposed individuals.16 Parvovirus, rubella, and Epstein-Barr virus have been isolated from the synovial fluid of some patients with RA. Also, retroviral-like particles, including human T-cell lymphotropic virus type 1, have been associated with the development of chronic arthritis. However, no microbe has been positively identified as the precise causative agent of RA.6,17 The disease process of RA is complex and involves interactions between numerous cells and processes in the synovium. Both the predisposition to RA and the severity of the condition are believed to involve the class II histocompatibility antigens HLA-DR4 and HLA-DR1. 18 There is a short sequence present in these antigens called the shared epitope (SE), which is a part of a large antigenic molecule. SE is believed to be a marker that influences both disease susceptibility and degree of severity of RA. While SE is carried by most patients with RA, disease develops in only a fraction of individuals.18 T cells mistakenly recognize the antigens that carry SE as a threat and they activate the immune system by involving other immunologically active cells and by helping B cells and plasma cells to produce antibodies and autoantibodies.16 Autoantibodies, such as rheuma6 Smoking appears to make RA worse and may be a risk factor for developing the disorder. Smoking Smoking appears to make RA worse and may be a risk factor for developing the disorder.13 However, there is no evidence to date that smoking cessation can ameliorate disease activity. A number of studies have found that smokers are more likely to be seropositive for RA and have a higher incidence of rheumatoid nodules and radiographic erosions than nonsmokers. 13 RA patients also have a substantially higher r isk of increased morbidity from cardiovascular disease, infections (particularly pulmonary infections), and osteoporosis, and the role of smoking in exacerbating these conditions may be significant.8,13 Additional Possible Risk Factors Results from some studies have indicated that allergies to a number of foods, including dairy, beef, corn, and wheat, as well as consuming more than three cups of coffee a day may contribute to the development of RA.8,10 However, there is a lack of strong evidence that COUNSELING POINTS™

Table of Contents Feed for the Digital Edition of Counseling Points - October 2007

Counseling Points - October 2007 Welcome Introduction Overview of RA RA Morbidity and Mortality RA Costs and Quality of Life RA Risk Factors Pathophysiology of RA Diagnosis and Natural History of RA Diagnostic Tests and Radiography Natural History and Progression of RA Disease Management Treatment Strategies Summary Continuing Education Posttest Evaluation Form

Counseling Points - October 2007

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