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A 79-year-old woman with late-stage rheumatoid arthritis comes for routine follow-up (Figures 97-1, 97-2, 97-3, and 97-4). She began having hand pain and stiffness approximately 40 years ago. She took nonprescription medications for pain for approximately 10 years before seeing a physician. She was diagnosed with rheumatoid arthritis on the basis of combination of clinical, laboratory, and radiograph findings. She was treated with prednisone and tried most of the disease-modifying agents as they became available; however, her disease progression continued. Approximately 10 years ago, she began having increased foot pain and difficulty walking. Today, she works with a multidisciplinary team to control pain and preserve hand function and independence.

Figure 97-1

Ulnar deviation at metacarpophalangeal joints in advanced rheumatoid arthritis. Also note the swelling at the distal interphalangeal joints, seen best on the first finger. (Courtesy of Richard P. Usatine, MD.)

Figure 97-2

Rheumatoid arthritis in the foot of a 79-year-old woman with subluxation of the first metatarsophalangeal joint. (Courtesy of Richard P. Usatine, MD.)

Figure 97-3

Deviation at the metatarsophalangeal joints from bony destruction in advanced rheumatoid arthritis. (Courtesy of Richard P. Usatine, MD.)

Figure 97-4

Ulnar deviation at metacarpophalangeal joints seen in a 79-year-old woman with advanced rheumatoid arthritis. (Courtesy of Kelly Foster, MD.)

Rheumatoid arthritis (RA) is a progressive chronic illness that causes significant pain and disability. RA is a polyarticular inflammatory arthritis that causes symmetrical joint pain and swelling and typically involves the hands. Early recognition and treatment with nonbiologic and/or biologic disease-modifying antirheumatologic agents (DMARDs) can induce remission and preserve function.

  • RA is found in 0.8% of the adult population worldwide.1
  • It is more than twice as common in women as compared to men (54 per 100,000 vs. 25 per 100,000).1
  • Typical age of onset is 30 to 50 years.1

  • Genetic predisposition coupled with an autoimmune or infection-triggering incident.
  • Synovial macrophages and fibroblasts proliferate, leading to increased lymphocytes and endothelial cells.
  • Increased cellular material occludes small blood vessels, causing ischemia, neovascularization, and inflammatory reactions.
  • Inflamed tissue grows irregularly, causing joint damage.
  • Damage causes further release of cytokines, interleukins, proteases, and growth factors, resulting in more joint destruction and systemic complications including a higher risk for cardiovascular disease

Genetic predisposition signified by a positive family history.

The 2010 American College of Rheumatology/European League Against Rheumatism classification criteria uses a scoring system to designate patients as definite RA. A score of 6 or greater out of 10 meets criteria for definite RA.2...

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