A 79-year-old woman with late-stage rheumatoid arthritis comes for routine follow-up (Figures 99-1, 99-2, 99-3, 99-4). 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 using a combination of clinical, laboratory, and radiographic 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.
Ulnar deviation at metacarpophalangeal joints in advanced rheumatoid arthritis. Also note the swelling at the distal interphalangeal joints, seen best on the first finger. (Reproduced with permission from Richard P. Usatine, MD.)
Rheumatoid arthritis in the foot of a 79-year-old woman with subluxation of the first metatarsophalangeal joint. (Reproduced with permission from Richard P. Usatine, MD.)
Deviation at the metatarsophalangeal joints from bony destruction in advanced rheumatoid arthritis. (Reproduced with permission from Richard P. Usatine, MD.)
Ulnar deviation at metacarpophalangeal joints seen in a 79-year-old woman with advanced rheumatoid arthritis. Note one rheumatoid nodule just distal to the second MCP joint. (Reproduced with permission from Richard P. Usatine, 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 anti-rheumatologic drugs (DMARDs) can induce remission and preserve function.
RA is found in 0.9% of the adult population.1
RA is more common in women. Under the age of 50, incidence in women is four to five times higher than in men. After age 60, RA is twice as common in women.2
Typical age of onset is 30 to 50 years.
ETIOLOGY AND PATHOPHYSIOLOGY
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.