Natural History of Rheumatoid Arthritis
"Vita brevis; ars longa; occasio celeris; experimentum periculosum; judicium difficile. Oportet autem non modo se ipsum exhibere quae oportet facientem, sed etiam aegrum, et praesentes, et externa." Life is short; art is long; opportunity fugitive; experience delusive; judgement difficult. It is the duty of the physician not only to do that which immediately belongs to him, but likewise to secure the cooperation of the sick, of those who are in attendance, and of all the external agents.
--Hippocrates c. 460 - 370 BCE, Aphorisms. I:I
The term rheumatoid arthritis (RA) is derived from the Greek term rheumatos+oid that is translated as "in the shape of something flowing" and the term arthr + itis meaning "an inflamed joint," meaning literally an inflamed joint that has been bent by disease into the shape of something flowing. RA is a chronic, systemic autoimmune disease characterized by symmetric inflammation of the diarthrodial joints (moveable joints lined with a synovial membrane). Arthritis represents the major expression of the disease, but it can be accompanied by extra-articular manifestations, including rheumatoid nodules, sicca syndrome (Sjögren’s syndrome), and vasculitis.
RA is a disease of unknown etiology that is characterized by polyarticular inflammation of the diarthrodial joints, weakness, pain, stiffness, loss of mobility, and the marked deformity and destruction of the joints. Initially RA affects the joints asymmetrically, but presents in a symmetrical fashion as the disease progresses. RA is a multisystemic disease and frequently affects extra-articular tissues and organ systems throughout the body including the skin, eyes, gastrointestinal tract, blood vessels, heart, brain, lungs, and muscles.10838
The natural history of RA is variable, and its outcome is dependent on the types of therapies that are initiated to control it and how early those therapies are initiated following initial onset of signs and symptoms. The clinical course of RA is short and self-limiting in 5%-20% of patients, minimally progressive in 5%-20% of patients, but is progressive in 60%-90% of patients.6938, 10589 Beyond basic quality-of-life issues, patients with poorly controlled RA suffer from the consequences of an increased systemic inflammatory burden.6411
To address the natural history of RA, it must first be adequately and accurately defined. RA is best defined by multiple factors, including objective disease-specific measures such as radiographs, rheumatoid factor (RF) seropositivity, remission rates, and subjective or patient-specific measures, such as functional disability, work disability, the need for total joint replacement, occurrence of adverse drug reactions, social disruption, and premature mortality. If RA is defined clinically, it has a worse prognosis than if it is defined epidemiologically. RF-negative polyarthritis differs from seropositive RA in that the former condition has a better prognosis for remission and favorable long-term outcome.6831
Remission is an objective of patient treatment, but remission itself is poorly defined. Some studies have demonstrated that patients who are in remission for signs and symptoms (i.e., disease activity score remission) may experience continuing joint damage and still progress radiographically. The natural history of RA usually does not involve remission. RA patients tend not to enter into remission, and most patients seen in clinical settings have progressive disease. More patients may be judged to have progressive disease if radiographic or imaging indices are used to judge remission.6831
The classification criteria for RA describe different pathogenetic processes and different long-term outcomes. Most RA patients tend to progress over time, and most therapies for RA are not effective in controlling signs and symptoms of the disease over long periods of time. Most RA patients experience joint destruction and severe functional declines within 10 years of disease onset, and 60% of patients become fully work-disabled after 10 years of disease. RA patients experience increased mortality (usually from cardiovascular causes), although RA is typically not listed on death certificates. Individual patients with RA, who are at risk for early mortality, can be identified using specific clinical markers, including a high number of swollen and tender joints, comorbid cardiovascular disease, and poor functional status.6938
The American College of Rheumatology revised its classification criteria for RA in 1987 to guarantee uniformity in investigative and epidemiological studies because a variety of other disorders may mimic the disease. RA is classified as an immune-mediated inflammatory disease, a group of pathologies that result when the immune system becomes dysregulated and fails to distinguish "self" from "nonself" and subsequently mounts an attack on normal tissue. In RA, the normal tissue that is primarily attacked is the tissue within the synovial joints. This attack involves the release of inflammatory cytokines Cytokine Dysregulation that initiate an inflammatory reaction, which can ultimately lead to the destruction of all components of the joint. The inflammatory disease process of RA is painful and disabling, and often results in the slow destruction of the joints if the disease is not adequately controlled. This joint destruction, which can be seen radiographically, often occurs in patients whose symptoms are well controlled, and often results in a substantial loss of mobility in the patient.
RA occurs in all ethnic groups worldwide. Prevalence rates range from 0.3% to 1.5% in most populations, but frequencies of 3.5% to 5.3% have been observed in several Native American tribes. The peak incidence of onset is between the ages of 30 and 50, the most economically productive years of an individual’s life, but RA may begin at anytime from childhood to advanced old age. Females are initially 2 to 3 times more likely to develop RA than males, but this varies according to age, with male and female patients in their 70s equally likely to develop the disease.
Content on this page was last reviewed on March 31, 2008.
Content on this page was last changed on March 25, 2009.
References:| 6411. | Wolfe F, Freundlich B, Straus WL. Increase in cardiovascular and cerebrovascular disease in rheumatoid arthritis. J Rheumatol. 2003 Jan;30(1):36-40. |
| 6831. | Wolfe F. The natural history of rheumatoid arthritis. J Rheumatol Suppl. 1996;44:13-22. |
| 6938. | Pincus T, Callahan LF. What is the natural history of rheumatoid arthritis? Rheum Dis Clin North Am. 1993;19(1):123-151. |
| 10589. | Osler W. The Principles and Practice of Medicine. New York, NY: D. Appleton and Company; 1892. |
| 10838. | Felson DT. Introduction to the study of the rheumatic diseases, epidemiology of the rheumatic diseases. In: Koopman WJ, Moreland LW, eds. Arthritis and Allied Conditions. A Textbook of Rheumatology. 15th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:1-36. |
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