Arthritis: Osteoarthritis, Gout, & Rheumatoid Arthritis | CURRENT Diagnosis & Treatment: Family Medicine, 4e | AccessMedicine (2023)


  • Arthritis of three or more joint areas.

  • Arthritis in hands, feet, or both (bilateral joint involvement).

  • Morning stiffness.

  • Fatigue.

  • Swelling, tenderness, warmth, and loss of function.

  • Rheumatoid nodules.

  • Elevated ESR and C-reactive protein.

  • Positive test for rheumatoid factor.

General Considerations

Bony changes consistent with rheumatoid arthritis (RA) have been found in the body of a Native American who lived 3000 years ago. Differentiation of RA from other types of arthritis is more recent, delineated only in the late nineteenth century. RA is more frequently seen in women, with the ratio of premenopausal women to age-matched men approximately 4:1; after the age of menopause, the ratio of incident RA is closer to 1:1.


Although the etiology of RA is not known, the pathophysiology has been elucidated to a remarkable degree in recent decades. Important knowledge of all inflammatory processes has come from studies in RA. Early in the disease process, the synovium of joints is targeted by T cells (this is the feature that leads to the “autoimmune” moniker). Release of interleukins, lymphokines, cytokines, tissue necrosis factor, and other messengers attracts additional inflammatory cells to the synovium. Intense inflammation ensues, experienced by the patient as pain, warmth, swelling, and loss of function. Reactive cells move to the inflammatory synovium, attempting to repair damaged tissue. Without treatment, this intense reaction develops into the pathologic tissue called pannus, an exuberant growth of tissue engulfing the joint space and causing destruction itself. Cartilage becomes swept into the pathologic process, resulting in breakdown, deterioration, and eventual destruction. Periarticular bone responds to inflammation with resorption, seen as erosions on radiographs. All these changes clearly are maladaptive and responsible for deformity and disability.


It is difficult with any assurance to advise patients on measures to prevent arthritis. RA has multiple etiologies, and no consistent preventive steps are available to patients. However, it is noted that RA may be more likely to occur in smokers, under the assumption that reaction in the trachea involving citrulline proteins promotes an inflammatory response to those proteins and that inflammatory response spills over to the synovium. While RA occurs in different frequencies in different ethnic groups, there are genetic similarities in each ethnic group that may differ from genetic patterns in other groups, pointing to the multiplicity of possible etiologies.

Clinical Findings

A. Symptoms and Signs

Rheumatoid arthritis is a systemic disease always involving joints but with inflammatory responses that include fatigue, rash, nodules, and even clinical depression as joints become increasingly stiff and inflamed. Most, but by no means all, of the initial symptoms are in the joints. There is inflammation, so the presence of swelling, warmth, and loss of function is imperative to the diagnosis. Joints of the hands (Figure 24-4) and feet are typically affected first, although larger joints can be involved at any time. The disease is classically symmetric with symptoms present bilaterally in hands, feet, or both. This mirroring is almost unique to RA; systemic lupus erythematosus, which is often confused with RA in its early stages, is not so consistently symmetric.

Figure 24–4.

Swelling of the proximal interphalangeal joints of the second and third fingers in rheumatoid arthritis. Symmetric swelling might be expected on the other hand.

Arthritis: Osteoarthritis, Gout, & Rheumatoid Arthritis | CURRENT Diagnosis & Treatment: Family Medicine, 4e | AccessMedicine (1)

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Fingers and wrists are stiff and sore in the mornings, requiring heat, rubbing, and movement to be functional (“morning stiffness”). Stiffness after prolonged lack of movement (“gelling”) is not uncommon in many joint disorders, but the morning stiffness of RA is so prolonged and characteristic that queries regarding this symptom are essential to the diagnosis.

The patient reports fatigue out of proportion to lack of sleep. Daytime naps are almost unavoidable, yet are not fully restorative. Anorexia, weight loss, or even low-grade fever, can be present. Along with musculoskeletal complaints, these somatic concerns may lead to mistaken diagnoses of fibromyalgia or even depression.

Rheumatoid arthritis can eventually involve almost any joint in the body. Selected important manifestations of RA in specific joints are listed in Table 24-5. The cause of any one manifestation may be unique to a particular joint and the surrounding periarticular structure. Common features include inflammation-induced stretching of tendons and ligaments resulting in joint laxity, subconscious restriction of movement resulting in “frozen” joints, and consequences of inflammatory synovitis with cartilage destruction and periarticular bone erosion. An objective sign of destruction includes the high-pitched, “crunchy” sound of crepitus.

Table 24–5.Manifestations of rheumatoid arthritis in specific joints.

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Table 24–5.Manifestations of rheumatoid arthritis in specific joints.

Joint Complication
Hand Ulnar deviation (hand points toward ulnar side), Swan neck deformity (extension of PIP joint), Boutonniere deformity (flexion at DIP)
Wrist Swelling causing carpal tunnel syndrome

Swelling causing compressive neuropathy

Deformity preventing complete extension, loss of power

Shoulder “Frozen shoulder” (loss of abduction, nighttime pain)
Neck Subluxation of C1-C2 joint with danger of dislocation and spinal cord compression (“hangman’s injury”)
Foot “Cockup” deformity and/or subluxation at MTP
Knee Effusion leading to Baker cyst (evagination of synovial lining and fluid into popliteal space)

Extraarticular manifestations of RA can be seen at any stage of disease. Most common are rheumatoid nodules, found at some point in ≤50% of all patients with RA. These occur almost anywhere in the body, especially along pressure points (the typical olecranon site), along tendons, or in bursae. Vasculitis is an uncommon initial presentation of RA. Dry eyes and mouth are seen in the RA-associated sicca syndrome. Dyspnea, cough, or even chest pain may signal respiratory interstitial disease. Cardiac, gastrointestinal, and renal involvement in RA is not common. Peripheral nervous system symptoms are seen as compression neuropathies (eg, carpal or tarsal tunnel syndrome) and reflect not so much direct attack on nerves, but rather primarily as consequences of squeezing compression as nerves are forced into passages narrowed by nearby inflammation.

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B. Laboratory Findings

In contrast to OA, the laboratory findings in RA can be significant and helpful. A normocytic anemia is common in active RA. This anemia is almost always the so-called anemia of chronic disease. The white blood cell count is normal or even slightly elevated; an exception is the rare Felty syndrome (leukopenia and splenomegaly in a patient with known RA).

Rheumatoid arthritis does not typically affect electrolytes and renal function. There is no pathophysiologic reason why transaminases, bilirubin, alkaline phosphatase, or other liver, pancreatic, or bone enzymes should be altered. Similarly, calcium, magnesium, and phosphate values should be unchanged. Most hormone measurements are normal, particularly thyroid and the adrenal axis. Any chronic inflammatory disease may alter the menstrual cycle, but measurement of luteinizing hormone and follicle-stimulating hormone is of little help.

An elevated ESR is almost ubiquitous in RA. C-reactive protein (CRP) is considered by many rheumatologists to be a more sensitive indicator of inflammation and might be increased in settings in which the ESR is either “normal” or minimally elevated. Although ESR is quite reliable, in some circumstances a false value may be reported (Table 24-6). For this reason, evaluation of C-reactive protein, although more expensive, is increasingly used by specialists.

Table 24–6.Nondisease factors that influence the ESR.

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Table 24–6.Nondisease factors that influence the ESR.

Increase ESR Decrease ESR No Effect on ESR






Congenital hyperfibrinogenemia

Technical factors


 Elevated specimen temperature

Leukocytosis (>25,000)

Polycythemia (Hgb >18)

Red blood cell changes

 Sickle cell




Protein abnormalities

 Dysproteinemia with hyperviscosity



Technical factors


 Inadequate mixing

 Vibration during test

 Clotting of specimen


Body temperature

Recent meal



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The test most associated with RA is the rheumatoid factor (RF) blood test. RF is actually a family of antibodies, the most common of which is an immunoglobulin M (IgM) antibody directed against the Fc (fragment, crystallizable) portion of immunoglobulin G (IgG). There is no question this antibody is frequently present in RA, with RF-negative RA accounting for only ~5% of all patients with RA. The problem lies with the low specificity of the test. Surveys demonstrate that in a young population, 3–5% of “normal” individuals have a high RF titer (positive test) whereas in an older cohort the prevalence of positive RF reaches 25%. With the national prevalence of RA only 1%, it is clear that many people with an elevated RF titer do not have RA. In fact, a false-positive RF titer is a common reason for incorrect referral of patients to rheumatologists. Some of the conditions that are associated with a positive RF test are listed in Table 24-7.

Table 24–7.Conditions associated with a positive rheumatoid factor test.

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Table 24–7.Conditions associated with a positive rheumatoid factor test.

Normal aging

Chronic bacterial infections

 Subacute bacterial endocarditis


 Lyme disease


Viral disease


 Epstein-Barr virus

 Hepatitis B

Chronic inflammatory diseases


 Periodontal disease

 Chronic liver disease (especially viral)

 Sjögren syndrome

 Systemic lupus erythematosus

 Mixed cryoglobulinemia

Another frequent test useful for diagnosis of RA in the early stages is the anticyclic citrullinated peptide [anti-CCP; also called anticitrullinated protein/peptide antibody (ACPA)]. This test is positive in most patients with RA, and may precede the onset of clinically diagnosed RA by months or even years. When combined with the RF test, this test will confirm the diagnosis even in confusing settings.

Suarez-Almazor ME et al.. Utilization and predictive value of laboratory tests in patients referred to rheumatologists by primary care physicians. J Rheumatol. 1998;25:1980.
[PubMed: 9779854]

C. Imaging Studies

Radiographs are no longer needed for the initial diagnosis of rheumatoid arthritis. Other means of diagnosing RA are more useful. Nonetheless, RA is a disease of synovial tissue, and, because the synovium lies on and attaches to bone, inflammation can cause changes on plain film radiography. Small erosions, or lucencies, on the lateral portions of phalanges are early indications of significant inflammation and should prompt immediate suppressive treatment.

Computed tomography and/or MRI have limited but useful supporting roles. An undesired complication of treatment of RA, aseptic necrosis (eg, of the femoral head), has a characteristic appearance on MRI. Scintigraphy is useful in detecting aseptic necrosis but, along with MRI, is better employed to differentiate the intense synovitis of RA from infection such as septic arthritis, overlying cellulitis, or adjacent osteomyelitis.

Differential Diagnosis

In practice, it is should not be difficult to differentiate among the three prototypical arthritides discussed in this chapter (see Table 24-1). Relatively new (2010) criteria developed by subspecialty organizations give valuable guidelines to making an accurate diagnosis of RA (Table 24-8). Because treatment started early is generally successful, rheumatologists promote early referral—treating a new diagnosis of RA almost as a “medical emergency.”

Table 24–8.1987 American College of Rheumatology diagnostic criteria for rheumatoid arthritis.

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Table 24–8.1987 American College of Rheumatology diagnostic criteria for rheumatoid arthritis.

The diagnosis of rheumatoid arthritis is confirmed if the patient has had at least four of the seven following criteria, with criteria 1–6 present for ≥6 weeks:

  1. Morning stiffness (≥1 hour)

  2. Arthritis of three or more joint areas (areas are right or left of proximal interphalangeal joints, metacarpophalangeal, wrist, elbow, knee, ankle, and metatarsophalangeal)

  3. Arthritis of hand joints (proximal interphalangeal joints or metacarpophalangeal joints)

  4. Symmetric arthritis, by area

  5. Subcutaneous rheumatoid nodules

  6. Positive test for rheumatoid factor

  7. Radiographic changes (hand and wrist radiography showing erosion of joints or unequivocal demineralization around joints)

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Moreland LW, Bridges SL Jr. Early rheumatoid arthritis: a medical emergency? Am J Med. 2001;111:498.
[PubMed: 11690579]

Neil VP et al.. Benefit of very early referral and very early therapy with disease-modifying anti-rheumatic drugs in patients with early rheumatoid arthritis. Rheumatology. 2004;43:906.


Serious extraarticular manifestations of RA are not infrequent. Some of these are life-threatening and require sophisticated management by physicians experienced in dealing with these crises. The responsibility often remains with the primary care physician to recognize these conditions and refer the patient appropriately. Table 24-9 lists several of these complications with a brief description of the clinical presentation.

Table 24–9.Extraarticular manifestations of rheumatoid arthritis.

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Table 24–9.Extraarticular manifestations of rheumatoid arthritis.

Complication Brief Comments
Rheumatoid nodules Found over pressure points, classically olecranon; typically fade with disease-modifying antirheumatic drug (DMARD) therapy; also may be found in internal organs; if causing disability, may attempt intralesional steroids, or surgery
Popliteal cyst Usually asymptomatic unless ruptures, then mimics calf thrombophlebitis; ultrasonography (and high index of suspicion) useful
Anemia Usually “chronic disease” and, despite low measured iron, does not respond to oral iron therapy; improves with control of inflammatory disease
Scleritis/episcleritis Inflammatory lesion of conjunctiva; more prolonged, intense, and uncomfortable than “simple” conjunctivitis; requires ophthalmologic management
Pulmonary disease Ranges from simple pleuritis and pleural effusion (noted for low glucose) to severe bronchiolitis, interstitial fibrosis, nodulosis, and pulmonary vasculitis; may require high-dose steroid therapy once diagnosis established by bronchoscopy or even open-lung biopsy
Sjögren syndrome Often occurring with RA, includes sicca syndrome with thickened respiratory secretions, dysphagia, vaginal atrophy, hyperglobulinemia, and distal renal tubule defects; treatment of sicca syndrome possible with muscarinic-receptor agonists; other manifestations more difficult
Felty syndrome Constellation of RA, leukopenia, splenomegaly, and often anemia, thrombocytopenia; control underlying RA with DMARDs; may need granulocyte colony-stimulating factor, especially if infectious complications are frequent
Rheumatoid vasculitis Spectrum from digital arteritis (with hemorrhage) to cutaneous ulceration to mononeuritis multiplex to severe, life-threatening multisystem arteritis involving heart, gastrointestinal tract, and other organs; resembles polyarteritis nodosum

Therapy of RA has changed from managing inflammation to specific measures directed against the fundamental sources of the inflammation. In more recent decades, treatment of RA has undergone perhaps the most wholesale shift of any of the rheumatologic conditions. Therapy is now directed at fundamental processes and begins with aggressive, potentially toxic disease-modifying drugs. The outlook can be hopeful, with preservation of joints, activity, and lifestyle a realistic goal. RA need no longer be the “deforming arthritis” by which it was known just a short time ago.

Kremers HM et al.. Therapeutic strategies in rheumatoid arthritis over a 40-year period. J Rheumatol. 2004;31:2366.
[PubMed: 15570636]

A. Assessment of Prognostic Factors

One of the early steps in treating RA is to assess prognostic factors in the individual patient. Poor prognosis leads to the decision to start aggressive treatment earlier. Some prognostic features are demographic, such as female sex, age >50 years, low socioeconomic status, and a first-degree relative with RA. Clinical features associated with poor prognosis include a large number of affected joints, especially involvement of the flexor tendons of the wrist, with persistence of swelling at the fingers; rheumatoid nodules; high ESR or C-reactive protein and high titers of RF; presence of erosions on radiographs; and evidence of functional disability. Formal functional testing and disease activity questionnaires are frequently employed, not only in establishing stage of disease but also at interval visits. In practice, though, most rheumatologists urge their generalist colleagues to refer patients identified with new-onset RA early. Despite certain prognostic factors noted earlier, most patients are indicated for, and respond to, early therapeutic intervention.

Anderson J et al.. Rheumatoid arthritis disease activity measures: American College of Rheumatology recommendations for use in clinical practice. Arthritis Care Res. 2012;64:640.

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B. Patient Education

Therapy begins with patient education, and again there are multiple sources of information from support and advocacy groups, professional organizations, government sources, and pharmaceutical companies. Patients should learn about the natural history of RA and the therapies available to interrupt the course. They should learn about joint protection and the likelihood that at least some activities need to be modified or discontinued. RA, especially before disease modification is established, is a fatiguing disorder. Patients should realize that rest is as important as appropriate types of activity. Of vital importance is the patient’s acknowledgment that drug regimens about to be started are complex but that compliance is critical to successful outcomes. The patient should frankly be told that the drugs are toxic and may have adverse effects.

C. Pharmacotherapy

1. Pain relief

Pain in RA is caused by inflammation, and establishment of effective anti-inflammatory drugs is the first goal of RA intervention. This is a step often expected of generalist physicians if there is likely to be delay in referral of the newly diagnosed RA patient to the rheumatologist. NSAIDs, at doses recommended earlier (see Table 24-2), give the patient early relief. NSAIDs continue to be used throughout the course of treatment; it is not uncommon to switch from one to another as effectiveness falters. It should be noted, though, that NSAIDs will not alter the course of the disease, and the patient should not be deluded into thinking that early pain relief substitutes for comprehensive treatment.

However, the effective management of RA should limit uncontrolled pain. Indeed, the goal of any RA management is to find therapies that will limit pain. Consequently, both generalist and specialist physicians to the patient with RA should continuously seek treatment modifications rather than settle for a degree of uncontrolled pain that might prompt use of narcotics.

2. Complementary and alternative medicine

If the patient is reluctant to start drugs, fish oil supplementation may provide symptomatic relief. But the same caution mentioned earlier for pain relief applies to complementary and alternative therapies—these products do not alter the natural history of RA. Even with some degree of pain relief and anti-inflammatory efficacy, these products are no substitute for effective treatment.

Nevertheless, physicians regularly are asked for recommendations of alternative treatments. Both omega-3 and omega-6 fatty acids in fish oil modulate synthesis of highly inflammatory prostaglandin E2 and leukotriene E4. The fish oil chosen must contain high concentrations of the relevant fatty acids. A large number of capsules need to be taken, and palatability, diarrhea, and halitosis are frequent adverse effects. γ-linolenic acid interrupts the pathway of arachidonic acid, another component of the inflammatory cascades. Extracted from the oils of plant seeds such as linseed, sunflower seed, and flaxseed, γ-linolenic acid demonstrates some efficacy in short-term studies using large doses of the extract.

3. Anti-inflammatory medications

Rheumatoid arthritis is an inflammatory disease, and all treatments are directed, in one way or another, to the reduction or elimination of the inflammatory process. Patients with RA will be taking one form of anti-inflammatory medication throughout the course of the disease.

As noted earlier, NSAIDs, are almost continuously recommended, even with other effective treatments established. It is common to switch from one drug to another as efficacy wanes. It is important to modify use of NSAIDs if well-identified effects are noted. GI upset, even GI bleeding, is common; this may be ameliorated as well by use of H2-blockers such as ranitidine or proton-pump inhibitors such as omeprazole. NSAID use should be modified, if not discontinued, in advancing stages of chronic kidney disease.

Steroids are widely used in RA. Relatively high-dose oral or parenteral use of steroids can reduce inflammation in the early stages of RA or at times of RA flare. Certain manifestations of RA, such as vasculitis or pulmonary involvement, will require steroids for more prolonged periods of time. The use of steroids for intraarticular injection into symptomatic joints can enhance systemic anti-inflammatory medications. The well-known complications of high-dose steroids requires that these be used only for short periods of time if at all possible

Sulfasalazine, noted to have efficacy for RA although patients were being treated for another condition, is frequently used early in treatment of RA. The mechanism of action is not exactly anti-inflammatory, but the effect is. Similarly, another antibiotic, minocycline, seems to have anti-inflammatory effects presumably through inhibition of a metalloproteinease mechanism.

4. Disease-modifying antirheumatic drugs (DMARDs)

These agents are almost always the first line of intensive therapy for patients newly diagnosed with rheumatoid arthritis. Fortunately, a large number of patients can be maintained in disease remission with use of medications in this category. Depending on the classification used to describe RA therapy, there may be a limited number of DMARD agents available, or some of these may be used in combination with agents described under anti-inflammatories earlier. Nonetheless, almost all patients with RA will be prescribed agents in this class at some time during their therapy.

The prototypical DMARD agent is methotrexate. Methotrexate is effective at decreasing inflammation, lowering ESR, slowing bony erosions, and reducing destructive pannus. For most patients, there will be regular modification of the dose in an attempt to find the lowest effective dose. Methotrexate is generally given in weekly doses with beneficial results seen as early as 4–6 weeks. Treatment can be continued for years. Toxicity includes liver and hematologic changes and regular monitoring is essential. Other adverse effects are not infrequent and may require modification of dose.

Azathioprine and cyclosporine are occasionally used as DMARDs, although rarely concurrently with methotrexate. Complications from these drugs are well recognized, and patient counseling should be extensive before use. One use for these agents appears to be during therapy for complications such as vasculitis. Another antibiotic, the antimalarial drug hydroxychloroquine, is often given in conjunction with methotrexate. There is a rare, but unfortunate, adverse effect to the retina seen with use of hydroxychloroquine that requires periodic ophthalmologic visits. Leflunomide blocks protein synthesis by lymphocytes and has been shown to be almost as effective as methotrexate. However, its half-life is almost 2 weeks and liver toxicity is not infrequent. Also, leflunomide has been associated with birth defects, making effective contraception mandatory when used in women of reproductive age.

5. Tissue necrosis factor (TNF) inhibitors

Tissue necrosis factor is a messenger that attracts other inflammatory cells to a site. TNF is also involved in production of interferon and interleukins. Blockade of these TNF effects diminishes the inflammatory response, both decreasing patient symptoms and slowing disease progression. Etanercept, infliximab, and adalimumab are examples of frequently used TNF inhibitors in treatment of RA. Other TNF inhibitors are available and occasionally used in very specific circumstances. These drugs require subcutaneous or intravenous injection, as often as every other week. Yet, they are relatively well tolerated, and any hematologic toxicity responds to discontinuation. Although TNF inhibitors carry FDA indication for moderate to severe RA, they are often given with methotrexate or even as single agents.

A serious consideration relates to the role of TNF inhibitors in host defenses. In particular, patients on TNF inhibitors who have tuberculosis often have rapid extrapulmonary spread and poor response to treatment. Consequently, assurance of the absence of TB, either by the PPD test or even the blood-based test QuantiFERON, is indicated.

6. Interleukin (IL)-inhibitors

Currently at least two IL-inhibitors are used in conjunction with other modalities in treatment of RA. IL6-inhibitor (tocilizumab) and IL1-inhibitor (anakinra) block different steps in both immune response and acute-phase response. Both inhibitors can be used with methotrexate for added disease-modifying activity. Side effects are not uncommon, ranging from local injection inflammation to leukopenia, liver enzyme abnormalities, and even alterations in lipids. Also, interleukin inhibitors should not be used with TNF inhibitors as infectious complications are increased.

7. T cell blockade

Continuing the effort to block parts of the immune and/or inflammatory response, the T cell blocker abatacept functions by arresting activation of naïve T cells. When used in conjunction with other DMARDs, there can be a moderate improvement in response criteria in a significant number of patients. This agent does carry an increased risk of infection. In addition, perhaps because of suppressed immune surveillance, there is concern for increased risk of neoplasia.

8. B cell depletion

The biologic agent rituximab is widely used in treatment of B cell lymphoma and has also been demonstrated to have efficacy in RA similar to that of abatacept. Rituximab works by blocking a signaling molecule from mature B cells, resulting in the depletion of B cells. Reduction of B cells reduces the inflammatory response in the synovium of the patient with RA. This agent, along with abatacept, may be used in patients with a poor response to TNF inhibitors.

9. Drug administration and precautions

While many of the anti-inflammatory and DMARD medications can be taken orally, most of the TNF inhibitors, the interleukin inhibitors, and the T and B cell blockers must be given either by injection (subcutaneous) or intravenous infusion. Since the frequency of administration, even once stabilized, ranges from weekly to monthly, it is clear that the patient will have frequent office visits to the rheumatologist. Unfortunately, local or systemic reaction to these agents is frequent and may require coadministration of other drugs (often steroids) to ameliorate the reactions.

As noted earlier, a frequent concern in use of biologics is increased infection. Patients are routinely tested for subclinical tuberculosis infection and are strongly advised to remain up-to-date with immunizations, including influenza and pneumococcal vaccines. A concern also alluded to above is the possibility of increased occurrence of neoplasm. Since the purpose of most of these products is to suppress the immune/inflammatory response, the very real concern is that neoplasia surveillance mechanisms are also suppressed. To date, while tumors have been reported during use of these agents, there does not seem to be a significant increase in incidence.

Singh JA et al.. 2012 Update of the 2008 American College of Rheumatology recommendations for the use of disease-modifying antirheumatic drugs and biologic agents in the treatment of rheumatoid arthritis. Arthritis Care Res. 2012;64:625.

Smolen JS et al.. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs. Ann Rheum Dis. 2010;69:964.

D. Surgery

Joint instability and resultant disability are often due to a combination of joint destruction, a primary effect of synovial inflammation, and tendon or ligament laxity, a secondary effect or “innocent bystander.” The innocent bystander effect notes that these connective tissues are stretched, weakened, or malaligned as a result of inflammation of the joints over which they cross but not the result of a direct attack on the tendon or ligament itself. Nonetheless, at some point joint destruction and connective tissue laxity combine to produce useless, and frequently painful, joints. At this point, the surgeon has much to offer. Joint stabilization, connective tissue reinsertion, and joint replacement of both small (interphalangeal) and large (hip, knee) joints provide return of function and reduction of pain. The timing of surgery is still an art and is most effective when close collaboration exists between the treating physician and surgeon.


Morbidity and mortality are increased in patients with RA over age-matched persons without RA. Correlated with active disease, there is a well-described increase in stroke and myocardial infarction. These manifestations may be due to a hypercoagulable state induced by the autoimmune process and circulating antibodies. There are suggestions that the increased rate of stroke and MI may be reduced by effective DMARD therapy. Even so, it is recommended that appropriate cardiovascular interventions be considered (eg, aspirin, lipid management). Even under conscientious treatment, complications from infection, pulmonary and renal disease, and gastrointestinal bleeding occur at rates higher than those in the general population. Many of the latter complications are related as much to the drugs used to control the disease as to the disease itself.


What type of arthritis is the most painful? ›

Rheumatoid arthritis can be one of the most painful types of arthritis; it affects joints as well as other surrounding tissues, including organs. This inflammatory, autoimmune disease attacks healthy cells by mistake, causing painful swelling in the joints, like hands, wrists and knees.

What is the difference between osteoarthritis and rheumatoid arthritis and gout? ›

Unlike OA, however, the inflamed joints in RA will often feel better with use. Because it is an inflammatory illness, RA can affect other parts of the body, including the skin, nerves, heart, and lungs. Gout – Gout is caused by uric acid, a chemical made by the body, which gets into the joints.

Can you have both osteoarthritis and rheumatoid arthritis at the same time? ›

Osteoarthritis and Rheumatoid Arthritis: Is It Possible to Have Both? It is possible to have both OA and RA. A previous joint injury can lead to both diseases, but OA is more likely to develop as you age. Likewise, as people with RA age, they are at risk of getting OA.

Is arthritis a disability? ›

Arthritis affects a person's overall function and mobility, which can result in activity and other limitations. It is a leading cause of work disability among US adults.

What is the best painkiller for arthritis? ›

Pain relief medicines
  • Paracetamol. If you have pain caused by osteoarthritis, a GP may suggest taking paracetamol to begin with. ...
  • Non-steroidal anti-inflammatory drugs (NSAIDs) ...
  • Opioids. ...
  • Capsaicin cream. ...
  • Steroid injections.

When does osteoarthritis hurt the most? ›

The main symptoms of osteoarthritis are pain and sometimes stiffness in the affected joints. The pain tends to be worse when you move the joint or at the end of the day. Your joints may feel stiff after rest, but this usually wears off fairly quickly once you get moving.


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