Counseling Points - October 2007 - (Page 7)

toid factors, are groups of antibodies that mistakenly target and damage healthy cells and tissues. Complexes of autoantibodies activate a proinflammatory process in which cytokines are expressed.16 Cytokines are signaling proteins that allow cells to communicate with one another. Expression of proinflammatory cytokines enables immune cells to transmit information to one another, thus propagating a downstream cascade of inflammatory and tissue-damaging processes. This cytokine expression results in the influx of inflammatory cells into the joint.1,16 The onset of RA is typically insidious, beginning in about two-thirds of patients with fatigue, anorexia, generalized weakness, and vague musculoskeletal symptoms. Histologically, the RA synovial membrane has large numbers of immune cells, which are juxtaposed, enabling them to interact, communicate, and promote tissue damage. The inflamed synovium, known as pannus, abuts the articular cartilage, and inflammatory cells at this junction produce enzymes that lead to cartilage erosion and destruction of the underlying bone.1,16 In a healthy body, there are natural antagonists to maintain an inflammatory homeostasis. However, in RA, the overproduction of proinflammatory cytokines tilts the balance in the direction of inflammation. The main proinflammatory cytokines in RA include tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and IL-6.1,16 The overproduction of these cytokines is responsible for the disease process, which induces symptoms of fatigue and weight loss, inflammation of the synovium, bone erosions and narrowing of joint space, and extra-articular disease manifestations, such as rheumatoid nodules, visceral disease, osteoporosis, and even premature atherosclerosis. about two-thirds of patients with fatigue, anorexia, generalized weakness, and vague musculoskeletal symptoms that are often confounding and difficult to precisely diagnosis.10 Swelling, tenderness, warmth, and limitation of motion occur as a result of synovial inflammation. Pain in affected joints, aggravated by movement, is the most common manifestation of established RA. Multiple joints may be affected, typically in a symmetrical pattern, and hands, wrists, feet, and knees are most commonly involved.10 The disease process is subtle; as a result, patients may not consult with a physician as early as they should. However, because joint destruction in RA occurs within a few weeks of symptom onset, early diagnosis and initiation of treatment is crucial to improving clinical outcomes for patients.10 Uncontrolled inflammation, even early in the disease process, can lead to irreversible tissue damage and deformities. Prompt treatment with effective drug therapies within the first few months of symptom manifestation can slow or stop disease progression, modify the disease course, prevent damage to joints, and reduce severity, disability, and mortality.10,19 However, an accurate diagnosis can be difficult to make in the preliminary stages of the disease due to the gradual onset and often nonspecific nature of symptoms. Definitive diagnosis requires a thorough medical history and physical examination. Based on the results of these assessments, a number of laboratory tests and radiographic tests may be used to preclude the possibility of other inflammatory conditions.3 The American College of Rheumatology (ACR) has outlined criteria to aid clinicians with diagnosing RA (Table 1).These criteria have been widely accepted and adopted throughout the world. Any of the following four criteria must be present to classify patients as having RA:3,10 • Morning stiffness for >1 hour • Arthritis of >3 joints • Arthritis of hand joints (wrist, metacaropophalangeal [MCP], proximal interphalangeal [PIP] joints) 7 OCTOBER 2007 Diagnosis and Natural History of RA Symptoms The onset of RA is typically insidious, beginning in

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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