Rheumatoid Arthritis

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Rheumatoid Arthritis

Learning Objectives

At the conclusion of this chapter, the reader should be able to:

• Name significant factors related to the development of arthritis.

• Describe the etiology, epidemiology, and signs and symptoms of rheumatoid arthritis.

• Discuss the immunologic manifestations and diagnostic evaluation of rheumatoid arthritis.

• Briefly describe juvenile rheumatoid arthritis.

• Explain diagnostic procedures used in the identification and evaluation of rheumatoid arthritis.

• Analyze representative rheumatoid arthritis case studies.

• Correctly answer case study related multiple choice questions.

• Be prepared to participate in a discussion of critical thinking questions.

• Describe the principle, sources of error, clinical applications, and limitations of a rapid rheumatoid factor procedure.

• Correctly answer end of chapter review questions.

ankylosing spondylitis

extra-articular

juvenile idiopathic arthritis

rheumatoid factor (RF)

The word arthritis literally means joint inflammation: arth- (joint) and -itis (inflammation). Arthritis is a large and growing public health problem in the United States. There are more than 100 forms of arthritis and related diseases. With the aging of the U.S. population, even assuming that the prevalence of obesity and other risk factors remain unchanged, the prevalence of physician-diagnosed arthritis and arthritis-attributable activity limitation (AAAL) is expected to increase significantly by 2030. Based on data from the National Health Interview Survey (NHIS; 2007-2009), the estimated distribution of arthritis is:

• 49.9 million (22.2%) of adults aged 18 years or older have self-reported physician-diagnosed arthritis.

• 21.1 million (9.4% of all adults) have AAAL.

The prevalence of arthritis increases significantly with age. Females are more likely than males to suffer from arthritis. Non-Hispanic whites, blacks, Native Americans, and Alaska Natives are more likely to have arthritis than Hispanics, Asians, and Pacific Islanders. Obese and overweight people are diagnosed with arthritis more frequently than underweight or normal weight individuals. Physically inactive people develop arthritis more often than physically active people.

Etiology

Rheumatic diseases are among the oldest diseases recognized, but the cause of rheumatoid arthritis (RA) remains unknown. Genetic factors are important, as are hormonal and psychosomatic factors. Evidence indicates that immunologic factors are involved in the articular and extra-articular manifestations of the disease. RA may represent an unusual host response to one or perhaps many causative agents. An infectious cause is possible, although this has not been established.

Epidemiology

Rheumatoid arthritis occurs worldwide, but no definite geographic or climatic variation in incidence has been established. RA affects all races, but the incidence varies across racial and ethnic groups.

Although no specific genetic relationship has been established, a small increase in incidence has been noted in first-degree relatives of patients with RA. Persons with the human leukocyte antigen (HLA)–DR4 haplotype have a significantly higher incidence of RA.

Patients with RA have a shortened lifespan. The most frequent cause of death is cardiovascular disease. The increased prevalence of atherosclerosis in RA patients is suspected to be related to atherogenic side effects of some antirheumatic medications, the effects of chronic systemic inflammation on the vascular endothelium, or shared mechanisms of action between RA and atherosclerosis.

Complications resulting from an increased frequency of local or extra-articular infections in RA patients have been demonstrated. Mortality may result from conditions such as septicemia, pneumonia, lung abscess, or pyelonephritis. In the past 15 years, the pharmacotherapy of RA has been improved by the development of more effective medications.

Signs and Symptoms

The term rheumatic disease does not have a clear boundary; more than 100 different conditions are labeled as rheumatic diseases, including RA, osteoarthritis, autoimmune disorders such as systemic lupus erythematosus (SLE) and scleroderma, osteoporosis, back pain, gout, fibromyalgia, and tendinitis.

Rheumatoid arthritis is a chronic, multisystemic, autoimmune disorder and a progressive inflammatory disorder of the joints (Fig. 30-1). It is, however, a highly variable disease that ranges from a mild illness of brief duration to a progressive destructive polyarthritis associated with a systemic vasculitis (Fig 30-2).The pathogenesis of RA has the following three distinct stages:

Figure 30-1 Inflammation in the rheumatoid joint. (Adapted from Olsen NJ, Stein CM: N Engl J Med 350:2167–2179, 2004.)

Figure 30-2 Characteristics of rheumatoid arthritis.
Shown are swan-neck deformity, ulnar deviation, dorsal interosseous atrophy, and swelling of wrist. (From Kaye D, Rose LF: Fundamentals of internal medicine, St Louis, 1983, Mosby.)

1. Initiation of synovitis by the primary causative factor

2. Subsequent immunologic events that perpetuate the initial inflammatory reaction

3. Transition of an inflammatory reaction in the synovium to a proliferative, destructive tissue process

Rheumatoid arthritis often begins with prodromal symptoms such as fatigue, anorexia, weakness, and generalized aching and stiffness not localized to articular structures. Joint symptoms usually appear gradually over weeks to months. The patient may display a wide variety of extra-articular manifestations (Box 30-1).

The revised American Rheumatism Association’s criteria for diagnosis of RA are presented in Table 30-1. If these conditions are present for at least 6 weeks, the patient is designated as having classic RA. Prognostic markers such as a persistently high number of swollen joints, high serum levels of acute-phase reactants of immunoglobulin M (IgM) rheumatoid factor, early radiographic and functional abnormalities, and the presence of certain HLA class II alleles may help identify patients with more severe RA who are still in the early stages of the disease.

Table 30-1

2010 ACR-EULAR Classification Criteria For Rheumatoid Arthritis ^∗

Parameter	Score (Points)
A. Joint involvement^†^,^‡
• One large joint ^§	0
• Two to ten large joints

1

• One to three small joints (with or without involvement of large joints)^‡

2

• Four to 10 small joints (with or without involvement of large joints)

3

• >Ten joints (at least one small joint)

5 B. Serology (at least one test result is needed for classification)¶

• Negative RF and negative ACPA

0

• Low-positive RF or low-positive ACPA

2

• High-positive RF or high-positive ACPA

3 C. Acute-phase reactants (at least one test result is needed for classification)#

• Normal CRP and normal ESR

0

• Abnormal CRP or abnormal ESR

1 D. Duration of symptoms^∗∗

0

1

Note: These are classification criteria for RA (score-based algorithm). Add scores of categories A to D. A score of 6 to 10 points is needed for classifying a patient as having definite RA. Although patients with a score of 6 to 10 points are not classifiable as having RA, their status can be reassessed and the criteria might be fulfilled cumulatively over time.

Differential diagnoses vary among patients with different presentations, but may include conditions such as SLE, psoriatic arthritis, and gout. If it is unclear about the relevant differential diagnoses to consider, an expert rheumatologist should be consulted.

Adapted from American College of Rheumatology: The 2010 American College of Rheumatology/European League Against Rheumatism classification criteria for rheumatoid arthritis, 2011 (http://www.rheumatology.org/practice/clinical/classification/ra/ra_2010.asp).

ACPA, Anti–citrullinated protein antibody; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate. EULAR, European League Against Rheumatism.

^∗The criteria are aimed at the classification of newly presenting patients. In addition, patients with erosive disease typical of RA with a history compatible with prior fulfillment of the 2010 criteria should be classified as having RA. Patients with long-standing disease, including those whose disease is inactive (with or without treatment) who, based on retrospectively available data, have previously fulfilled the 2010 criteria should be classified as having RA.

^†Joint involvement refers to any swollen or tender joint on examination, which may be confirmed by imaging evidence of synovitis. Distal interphalangeal joints, first carpometacarpal joints, and first metatarsophalangeal joints are excluded from assessment. Categories of joint distribution are classified according to the location and number of involved joints, with placement into the highest category possible based on the pattern of joint involvement.

^‡”Small joints” refers to the metacarpophalangeal joints, proximal interphalangeal joints, second through fifth metatarsophalangeal joints, thumb interphalangeal joints, and wrists.

^§“Large joints” refers to shoulders, elbows, hips, knees, and ankles.

In this category, at least one of the involved joints must be a small joint; the others can include any combination of large and additional small joints, as well as other joints not specifically listed elsewhere (e.g., temporomandibular, acromioclavicular, sternoclavicular).

^¶Negative refers to IU values that are ≤ to the upper limit of normal (ULN) for the laboratory and assay; low-positive refers to IU values that are higher than the ULN but ≤3 times the ULN for the laboratory and assay; high-positive refers to IU values that are >3 times the ULN for the laboratory and assay. If RF information is only available as positive or negative, a positive result should be scored as low-positive for RF.

^#Normal/abnormal is determined by local laboratory standards.

^∗∗Duration of symptoms refers to patient self-report of the duration of signs or symptoms of synovitis (e.g., pain, swelling, tenderness) of joints that are clinically involved at the time of assessment, regardless of treatment status.

Anatomy and Physiology of Joints

Diarthrodial joints are lined at their margins by a synovial membrane (synovium), with synovial cells lining this space. The lining cells synthesize protein and are phagocytic. Synovial (joint) fluid is a transparent viscous fluid. Its function is to lubricate the joint space and transport nutrients to the articular cartilage. Mechanical, chemical, immunologic, or bacteriologic damage may alter the permeability of the membrane and capillaries and may produce varying degrees of an inflammatory response. In addition, inflammatory joint fluids contain lytic enzymes that produce depolymerization of hyaluronic acid, which greatly impairs the lubricating ability of the fluid.

A variety of disorders produce changes in the number and types of cells and chemical composition of the fluid. Analysis of synovial fluid plays a major role in the diagnosis of joint diseases. Arthrocentesis constitutes a liquid biopsy of the joint. It is a fundamental part of the clinical database, together with the medical history, physical examination, and plain radiographic films. Analysis of aspirated synovial fluid is essential in the evaluation of any patient with joint disease because it is a better reflection of the events in the articular cavity than abnormal blood test results. For example, abnormal test results—for example, antinuclear antibody (ANA), increased erythrocyte sedimentation rate (ESR), elevated uric acid level, increased C-reactive protein concentration, and rheumatoid factor (RF)—can be seen in normal individuals or in unrelated joint diseases.

Disorders such as gout, calcium pyrophosphate dihydrate deposition disease, and septic arthritis can be definitively diagnosed by synovial fluid analysis and may allow for consideration or exclusion of RA and SLE. Synovial fluid analysis can also support a diagnosis of diseases as disparate as amyloidosis, hypothyroidism, ochronosis, hemochromatosis, or even simple edema. In addition, arthrocentesis may alleviate elevated intra-articular pressure. Removal of fluid will relieve symptoms and potentially decrease joint damage. Removal of the products of inflammation is an important component in the treatment of infectious arthritis and may be beneficial for other forms of arthritis.

Routine analysis of synovial fluid should include wet preparation examination for cell count and differential, crystals, Gram stain, and microbiologic culture. Very turbid fluids, or if septic arthritis is considered for other reasons, synovial fluid should be sent for Gram staining and culture. Gram staining is needed if a high likelihood of infection exists. Other observations and procedures can include volume and appearance, viscosity, mucin test, chemical analysis for protein, and glucose.

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