This chronic inflammatory disease stems from immunological dysunction, and iniltrating T cells secrete ctokines to cause inflammation, polyarthritis, and systemic symptoms. he cardinal feature is inflammatory synovitis that usually involves the peripheral joints. he disease has a propensity for cartilage destruction, bony erosions, and joint deformities. Pain, aggravated by movement, is accompanied by swelling and tenderness. Extraarticular manifestations include rheumatoid nodules, vasculitis, and pleuropulmonary symptoms. Other complaints are fatigue, anorexia, and depression. he American College of Rheumatology criteria for rheumatoid arthritis diagnosis are shown in Table 59-7. A score of 6 or greater ulills the requirements for definitive diagnosis.
The worldwide prevalence of rheumatoid arthritis is 0.5 to 1 percent, women are afected three times more often than men, and peak onset is from 25 to 55 years (Shah, 2015). There is a genetic predisposition, and heritability is estimated at 15 to 30 percent (McInnes, 2011). Genome-wide associated studies have identified more than 30 loci involved in rheumatoid arthritis pathogenesis (Kurka, 2013). There is an association with the
TABLE 59-7. Criteria for Classification of Rheumatoid Arthritis
CRP = C-reactive protein; ESR = erythrocyte sedimentation rate; IP = interphalangeal joint; MCP = metacarpophalangeal joint; MTP = metatarsophalangeal joint; PIP = proximal inteLphalangeal joint; RF = rheumatoid factor.
Criteria established in collaboration with the American College of Rheumatology and the European League Against Rheumatism. A scorer:::6 fulfills criteria for diagnosis. Data from Aletaha, 2010; Shah, 2015.
class II major histocompatibility complex molecule HLADR4 and HLA-DRB1 alleles (McInnes, 2011; Shah, 2015). Pregnancy provides a protection against rheumatoid arthritis development, and this may be related to HLA-disparate fetal microchimerism (Guthrie, 2010). Of other inluences, cigarette smoking raises the risk of rheumatoid arthritis (Papadopoulos, 2005).
Treatment is directed at pain relief, inlammation reduction, protection of articular structures, and preservation of function. Physical and occupational therapy and self-management instructions are essential. Until recently, aspirin and other NSAIDs were the cornerstone of therapy, but they do not retard disease progression. According to Shah and St. Clair (2015), methotrexate has become the preferred disease-modiying antirheumatic drug (DMARD). NSAIDs serve as adjunctive therapy but are important to pregnancy because methotrexate is contraindicated. Conventional NSAIDs nonspeciically inhibit both cyclooxygenase-1 (COX-I), which is an enzyme critical to normal platelet function, and COX-2, which mediates inflammatory response mechanisms. Because gastritis with acute bleeding is an unwanted side efect common to conventional NSAIDs, the more specific COX-2 inhibitors have been recommended. However, their long-term use is associated with higher risk for myocardial infarction and major vascular events (Patrono, 2016).
In one systematic review, a higher rate of cardiac malformations was found in newborns exposed to NSAIDs in the first trimester (Adams, 2012). In addition, NSAIDs are associated with early spontaneous abortions, ductus arteriosus constriction, and neonatal pulmonary hypertension. Thus, risks versus beneits of these medications must be considered.