Background

Juvenile rheumatoid arthritis (JRA) is the most common chronic rheumatologic disease in children and is one of the most common chronic diseases of childhood. It represents a group of disorders that share the clinical manifestation of chronic joint inflammation. The etiology is unknown, and the genetic component is complex, making clear distinctions between the various subtypes difficult. As a result, the various sets of classification criteria that have been recognized have different benefits and limitations. A new nomenclature, juvenile idiopathic arthritis (JIA), is being increasingly used in order to better define subgroups. Go to Osteoarthritis, Pediatric Osteoarthritis, and Rheumatoid Arthritis for complete information on these topics.

Criteria and classification

Three groups have developed sets of criteria to classify children with arthritis: the American College of Rheumatology (ACR), the European League Against Rheumatism (EULAR), and the International League of Associations for Rheumatology (ILAR).[1, 2, 3] The ACR criteria define juvenile rheumatoid arthritis (JRA) by age limit (< 16 y) and the duration of disease (>6 weeks). (See Table.) The organization recognizes the following 3 subtypes: Polyarticular Pauciarticular Systemic Other forms of childhood arthritis, such as juvenile ankylosing spondylitis and psoriatic arthritis, are classified under spondyloarthropathies. The ILAR classification of JIA includes the following categories: Systemic-onset JIA Persistent or extended oligoarthritis Rheumatoid factor (RF)positive polyarthritis RF-negative polyarthritis Psoriatic JIA Enthesitis-related arthritis Undifferentiated - The disease does not meet criteria for any of the other subgroups, or it meets more than 1 criterion (and therefore could be classified in a number of subgroups). The EULAR proposed the term juvenile chronic arthritis (JCA) for the heterogeneous group of disorders that manifest as juvenile arthritis. The diagnosis requires that the arthritis begins before age 16 years and lasts for at least 3 months. The EULAR criteria for JCA recognize the following subtypes, based on characteristics at onset: Pauciarticular (1-4 joints) Polyarticular (5 joints) Presence of RF Systemic onset with characteristic features Positivity for rheumatoid factor Juvenile ankylosing spondylitis Juvenile psoriatic arthritis This article will use the ILAR nomenclature unless differentiation is required between JIA and JRA or JCA. Table. Comparison of Classification Criteria for Chronic Childhood Arthritis (Open Table in a new window)
Classification ACR(1977) ILAR (1997)

Nomenclature Minimum duration Age at onset 4 joints in first 6 mo after presentation

Juvenile rheumatoid arthritis 6 wk < 16 y Pauciarticular juvenile rheumatoid arthritis

Juvenile idiopathic arthritis 6 wk < 16 y Oligoarticular juvenile idiopathic arthritis:

(A) Persistent < 4 joints for course of disease;

(B) Extended >4 joints after 6 mo

>4 joints in first 6 mo after presentation

Polyarticular juvenile rheumatoid arthritis

Polyarticular juvenile idiopathic arthritis-rheumatoid factor negative

Polyarticular juvenile arthritis-rheumatoid factor positive

Fever, rash, arthritis

Systemic juvenile rheumatoid arthritis Exclusion of other forms

Systemic juvenile idiopathic arthritis

Other categories included

Psoriatic juvenile idiopathic arthritis

Enthesitis-related arthritis

Undifferentiated:

(A) Fits no other category;

(B) Fits more than 1 category

Inclusion of psoriatic arthritis, inflammatory bowel disease, juvenile ankylosing spondylitis

No

Yes

Etiology and Pathophysiology

The etiology and pathogenesis of JIA are not completely understood. Genetic susceptibility plays a major role, but there is significant overlap between loci associated with JIA and those associated with other autoimmune diseases.[4] JIA is a genetically complex disorder in which multiple genes are important for disease onset and manifestations. The IL2RA/CD25 gene has been implicated as a JIA susceptibility locus, as has the VTCN1 gene.[5] Associations have been found between specific HLA alleles and clinical subtypes of JIA (eg, HLA-A(*)02:06 with susceptibility to JIA accompanied by uveitis, and HLA-DRB1(*)04:05 with polyarticular JIA, in a Japanese cohort).[6] Humoral and cell-mediated immunity are involved in the pathogenesis of JIA. T lymphocytes have a central role, releasing proinflammatory cytokines (eg, tumor necrosis factoralpha [TNF-], interleukin [IL]-6, IL-1)

and favoring a type-1 helper T-lymphocyte response. A disordered interaction between type 1 and type 2 Thelper cells has been postulated. Studies of T-cell receptor expression confirm recruitment of T-lymphocytes specific for synovial nonself antigens. Evidence for abnormalities in the humoral immune system include the increased presence of autoantibodies (especially antinuclear antibodies), increased serum immunoglobulins, the presence of circulating immune complexes, and complement activation. Chronic inflammation of synovium is characterized by B-lymphocyte infiltration and expansion. Macrophages and T-cell invasion are associated with the release of cytokines, which evoke synoviocyte proliferation. A study by Scola et al found synovium to contain messenger ribonucleic acid (mRNA) for vascular endothelial growth factor and angiopoietin 1, as well as for their receptors, suggesting that induction of angiogenesis by products of lymphocytic infiltration may be involved in persistence of disease.[7] Some pediatric rheumatologists view systemic-onset JIA as an autoinflammatory disorder, such as familial Mediterranean fever (FMF) or cryopyrin-associated periodic fever syndromes, rather than a subtype of JIA. This theory is supported by work demonstrating similar expression patterns of a phagocytic protein (S100A12) in systemic-onset JIA and FMF, as well as the same marked responsiveness to IL-1 receptor antagonists.[8] FMF is associated with mutations in the MEFV gene; these mutations are associated with activation of the IL-1b pathway, resulting in inflammation. A study by Ayaz et al found an increased frequency of MEFV mutations in Turkish children who were diagnosed with systemic JIA[9] ; this study has not been replicated in other populations.

Approach Considerations
The diagnosis of juvenile idiopathic arthritis (JIA) is based on the history and physical examination findings. No laboratory studies are diagnostic for JIA, and indeed, all laboratory study findings may be normal in children with this disorder. However, laboratory studies help to exclude other underlying disorders, classify the type of arthritis, and evaluate for extra-articular manifestations of JIA. Imaging of affected joints is usually indicated. When physical findings do not document definite arthritis, further evaluation is warranted. The choice of studies varies on the basis of the specific circumstances. Go to Imaging in Juvenile Rheumatoid Arthritis for complete information on this topic.

Inflammatory Markers
The erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) level is usually elevated in children with systemic-onset JIA (with a disproportionate increase in the CRP) and may be elevated in those with polyarticular disease; however, it is often within the reference range in those with oligoarticular disease. When elevated, inflammatory markers can be used to monitor disease activity. Other markers of inflammation include thrombocytosis, leukocytosis, complement, and, in a reverse fashion, albumin and hemoglobin

Complete Blood Count and Metabolic Panel

Lymphopenia is not uncommon because of emigration of activated lymphocytes out of the circulation into synovium. However, neutropenia is uncommon and, particularly with lymphocytosis or thrombocytopenia, raises the possibility of acute lymphocytic leukemia. A complete blood count, liver function tests (to exclude the possibility of viral or autoimmune hepatitis), and assessment of renal function with serum creatinine levels should be done before starting treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), methotrexate (MTX), or tumor necrosis factoralpha inhibitors.

Antinuclear Antibody Testing

As many as 70% of children with oligoarticular JIA have positive ANA assays. However, a positive ANA should also raise suspicion of systemic lupus erythematosus (SLE). Overlap between the manifestations of the two disorders may lead to initial misdiagnosis of SLE as JIA. A positive ANA is a marker for increased risk of anterior uveitis. Children younger than 6 years at arthritis onset with a positive ANA finding are in the highest risk category for development of uveitis and need slit lamp screening every 3-4 months. Titers do not correlate with disease activity.

Additional Laboratory Tests

In systemic-onset JIA, total protein and albumin levels are often decreased during active disease, and fibrinogen, ferritin and D-dimer levels are often elevated. Laboratory results that can help to rule out JIA include angiotensin-converting enzyme (ACE) elevation, which may be indicative of sarcoidosis, and antistreptolysin 0 (AS0) and anti-DNAse B elevations, which may indicate acute rheumatic fever or poststreptococcal arthritis. Perform a urinalysis to exclude the possibility of infection (as a trigger for JIA or transient postinfectious arthritis). Proteinuria (>0.5 g/d or 3+ positive on dipstick testing) or cellular casts is consistent with renal involvement in SLE. In patients with systemic-onset JIA, the following test results are indicative of the development of macrophage-activating syndrome (MAS): Falling ESR Normalization or decrease in white blood cell (WBC) count Low platelets Elevated liver enzymes Increased ferritin Increased triglycerides Low fibrinogen Erratic fevers Hemorrhages (disseminated intravascular coagulationlike pattern)

Radiography
When only a single joint is affected, radiography is important to exclude other diseases, such as osteomyelitis. Basic radiographic changes in JIA (see the images below) include the following: Soft tissue swelling Osteopenia and/or osteoporosis Joint-space narrowing Bony erosions Intra-articular bony ankylosis Periosteitis Growth disturbances Epiphyseal compression fracture Joint subluxation

Synovial cysts

Ankylosis in the cervical spine at several levels due to long-

standing juvenile rheumatoid arthritis (also known as juvenile idiopathic arthritis). Widespread osteopenia, carpal crowding (due to cartilage loss), and several erosions affecting the carpal bones and metacarpal heads in particular in a child with advanced juvenile rheumatoid arthritis (also known as juvenile idiopathic arthritis).

The main limitation of conventional radiography is that it does not allow direct examination of the articular cartilage, synovium, and other important noncalcified structures in a joint. Go to Imaging in Juvenile Rheumatoid Arthritis for complete information on this topic.

Computed Tomography and Magnetic Resonance Imaging

CT scanning is the best method for analyzing bony abnormalities, but it has been largely superseded by MRI in the overall assessment of JIA. The major disadvantage of CT scanning is that it involves a substantial radiation dose. Perform CT scanning of the long bones when considering osteoid osteoma is suspected. MRI is helpful when considering trauma in the differential diagnosis. In addition, imaging of the TMJ, sacroiliac joint, cervical spine, midfoot, hip, or shoulder is useful in diagnosing inflammatory arthritis. (See the image below.)

(A) T2-weighted MRI shows high signal in both hips, which may be due to hip effusions or synovitis. High signal intensity in the left femoral head indicates avascular necrosis. (B) Coronal fat-saturated gadolinium-enhanced T1-weighted MRI shows bilateral enhancement in the hips. This indicated bilateral active synovitis, which is most pronounced on the right. Because the image was obtained with fat saturation, the hyperintensity in both hips is pathologic, reflecting an inflamed pannus.

MRI provides the most sensitive radiologic indicator of disease activity. The modality can depict synovial hypertrophy, define soft tissue swelling, and demonstrate excellent detail of the status of articular cartilage and overall joint integrity.[16, 17, 18, 19, 1, 2, 3, 20, 21]

To improve visualization of synovial hypertrophy and improve detection of cartilaginous erosions when an inflammatory arthritis is suspected, contrast-enhanced sequences should be performed. Synovitis and a joint effusion may have similar hyperintensity on T2-weighted (T2W) and short-tau inversion recovery (STIR) images. Therefore, gadolinium-enhanced T1-weighted (T1W) MRIs are necessary to accurately define active synovitis. Note that gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the Medscape Reference topicNephrogenic Systemic Fibrosis. Go to Imaging in Juvenile Rheumatoid Arthritis for complete information on this topic.

Ultrasonography
On ultrasonograms, inflamed synovium can appear as an area of mixed echogenicity lining the articular cartilage; the vascularity of the synovium can be assessed with Doppler flow studies. Serial measurements of synovial thickness and effusion volumes have been used to monitor disease progression.[22] It can be helpful to evaluate joints that are difficult to palpate, such as the hip and shoulder. Some researchers claim that ultrasonography is more sensitive than plain radiography in the detection of cartilage erosions and effusions. Ultrasound has the advantages of no exposure to ionizing radiation; it can be done in the clinic is an awake, moving child; and it can help guide injections. Go to Imaging in Juvenile Rheumatoid Arthritis for complete information on this topic.

Nuclear Imaging
Bone scanning, which can be used in the assessment of JIA, is characterized as follows: This modality can be used when physical findings do not document definite arthritis. It can also be used to identify a potential focus of osteomyelitis, osteoid osteoma or other abnormality. Bone scanning is characterized by high sensitivity and low specificity It may be combined with single-photon emission CT (SPECT) scanning to increase sensitivity in the 1 or more foci of abnormal isotopic accumulation. Bone scintigraphy is primarily used in the determination of the distribution of JIA, but the substantial radiation dose from this modality is a major disadvantage Go to Imaging in Juvenile Rheumatoid Arthritis for complete information on this topic.

Echocardiography
In a child who has nonspecific rash, adenopathy, and possible mucocutaneous changes, perform echocardiography to exclude coronary arterial dilation resulting from Kawasaki disease. In an individual who has findings suggestive of SLE (eg, nephritis, pleuritic chest pain, thrombocytopenia), perform echocardiography to exclude valvular disease, although mild dilation may be seen in some patients with systemic-onset JIA.

Other Studies and Procedures

Perform dual energy radiographic absorptiometry (DRA) scanning to document osteopenia in children with JIA, especially in children requiring long-term steroids (systemic JIA) or with prolonged widespread arthritis. Perform arthrocentesis to exclude septic arthritis in a child with monoarticular swelling. Synovial biopsy may be helpful to exclude other diagnoses, particularly when the knee is affected (eg, villonodular synovitis, granulomatous arthritis, foreign body synovitis). Synovial biopsy may reveal synovial infiltration with plasma cells, mature B lymphocytes, and T lymphocytes, with areas of synovial thickening and fibrosis.

Pericardiocentesis is used in an intensive care unit (ICU) setting to treat severe pericarditis.

Approach Considerations
The ultimate goals in managing rheumatoid arthritis are to prevent or control joint damage, to prevent loss of function, and to decrease pain.[23] These goals are particularly important in JIA, in which the rate of progression and the onset of debility can be rapid. JIA is a chronic disease characterized by periods of remission and flare. Treatment is aimed at inducing remission with the least toxicity from medications with hopes of inducing a permanent remission. The success of therapy is monitored best with repeated physical examinations and history. The number of joints involved and the duration of morning stiffness should demonstrate continued decrease, with elimination reflecting success. Surgery may be indicated in patients who are unresponsive to medical therapy. A team-based approach can be helpful. Management may include one or all of the following areas: Pharmacologic management consisting of nonsteroidal anti-inflammatory drugs (NSAIDs), diseasemodifying antirheumatic drugs (DMARDs), biologic agents, and intra-articular and oral steroids Psychosocial factors, including counseling for patients and parents School performance , such as academic counseling, school-life adjustments, and physical education adjustments Nutrition, particularly to address anemia and generalized osteoporosis; often microcytic, anemia is refractive to treatment with iron Physical therapy to relieve pain and to address range of motion, muscle strengthening, activities of daily living, and conditioning exercises Occupational therapy, including joint protection, a program to relieve pain, range of motion, and attention to activities of daily living American College of Rheumatology criteria for complete remission are as follows[23] : No inflammatory joint pain No morning stiffness No fatigue No synovitis No progression of damage, as determined in sequential radiographic examinations No elevation of the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels In 2011, the American College of Rheumatology issued recommendations for the treatment of JIA based on 5 treatment groups.[24] The treatment groups are as follows: A history of arthritis in 4 or fewer joints A history of arthritis in 5 or more joints Active sacroiliac arthritis Systemic arthritis without active arthritis Systemic arthritis with active arthritis Within each group, choice of therapy is guided by the severity of disease activity and the presence or absence of features indicating a poor prognosis.

Surgical Treatment
Advances in medical treatment have reduced the need for surgical intervention in JIA. Possible procedures include synovectomy, osteotomy and arthrodesis, and hip and knee replacement.

Synovectomy
Synovectomy is rarely needed, and long-term outcome is poor; however, it may be used in children in whom a single joint or just a few joints are involved and who have very active, proliferative synovitis.

Osteotomy and arthrodesis

Osteotomy and arthrodesis are salvage procedures for patients whose JIA is associated with severe joint destruction or deformity. Arthrodesis is superior to arthroplasty for children who have rheumatic disease in the wrist and fingers and in the ankle.

Total hip and total knee replacements

Total hip and knee replacements provide excellent relief of pain and restore function in a functionally disabled child with debilitating disease. The role of total hip replacement and total knee replacement in JIA is fraught with problems, however. Joint replacement is usually delayed until bone growth has completed, as indicated by epiphyseal closure.

Exercise and Other Nonpharmacologic Therapy

Exercise preserves joint range of motion and muscular strength, and it protects joint integrity by providing better shock absorption. Types of exercises that may be advised include a muscle-strengthening program, range-of-motion activity, stretching of deformities, and endurance and recreational exercises. Hydrotherapy is a good form of exercise that helps achieve the aforementioned objectives. Rarely, children require splinting or serial casting to help decrease contractures in joints unresponsive to medical treatment. Leg-length discrepancy can result from neovascularization of growth plates of an affected knee. The problem may not be detected in patients with a knee flexion contracture until the contracture is corrected. Treatment consists of a shoe lift on the contralateral side.

Medication Summary
Optimal care of patients with juvenile idiopathic arthritis (JIA) requires an integrated approach of nonpharmacologic and pharmacologic therapies. Classes of medications used include disease-modifying antirheumatic drugs (DMARDs), biologicals, NSAIDs, and corticosteroids.

Nonsteroidal Anti-inflammatory Drugs

Class Summary
Nonsteroidal anti-inflammatory drugs (NSAIDs) interfere with prostaglandin synthesis through inhibition of the enzyme cyclooxygenase (COX), thus reducing swelling and pain. NSAIDs are used to treat all subtypes of JIA. They may help with pain and decrease swelling. Commonly used NSAIDs include naproxen, ibuprofen, tolmetin, diclofenac, and indomethacin. Aspirin is no longer the drug of first choice because of the increased frequency of gastric toxicity and hepatotoxicity when compared to other NSAID medications. The cyclooxygenase 2 (COX-2) inhibitor celecoxib (Celebrex) may have a role in treatment when a bleeding diathesis is a potential problem. Several dozen NSAIDs are available and can be classified into different groups of compounds. Commonly used NSAIDs include ibuprofen, naproxen, ketoprofen, piroxicam, and diclofenac. Predicting which patient will respond to a particular NSAID is not possible and many children who do not respond to one may benefit by changing to a different NSAID. Indomethacin is particularly effective for fever and pericarditis and is usually preferred for children with active systemic JIA.
View full drug information

Meloxicam (Mobic)
Meloxicam is a member of the enolic class of NSAIDs and is structurally related to piroxicam. The pediatric dosage is 0.125 mg/kg/d for patients aged 2 years or older, up to 7.5 mg qd.

View full drug information

Naproxen (Aleve, Naprelan, Naprosyn)

Naproxen is used for analgesic and anti-inflammatory properties, treating arthralgia and arthritis. It inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which is responsible for prostaglandin synthesis. The pediatric dosage is 7-20 mg/kg/d PO divided bid/tid, not to exceed 1 g/d
View full drug information

Ibuprofen (Advil, Motrin)

Ibuprofen inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. The adult dosage is 400 mg PO q4-6h, 600 mg q6h, or 800 mg q8h while symptoms persist, not to exceed 3.2 g/d; the pediatric dosage is 30-50 mg/kg/d PO divided qid, not to exceed 2.4 g/d.
View full drug information

Diclofenac (Voltaren, Cataflam)

This is one of a series of phenylacetic acids that has demonstrated anti-inflammatory and analgesic properties in pharmacological studies. It is believed to inhibit the enzyme cyclooxygenase, which is essential in the biosynthesis of prostaglandins. Diclofenac can cause hepatotoxicity; hence, liver enzymes should be monitored in the first 8 weeks of treatment. It is absorbed rapidly; metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation. The delayed-release, enteric-coated form is diclofenac sodium, and the immediate-release form is diclofenac potassium.
View full drug information

Celecoxib (Celebrex)
Celecoxib inhibits primarily COX-2. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared with nonselective NSAIDs. Seek the lowest dose for each patient. The adult dosage is 100-200 mg PO bid; the pediatric dosage has not been established for patients younger than 2 years, is 50 mg PO bid for patients 2 years or older whose weight is 10 kg to 25 kg, and is 100 mg PO bid for patients 2 years or older whose weight is greater than 25 kg.
View full drug information

Tolmetin (Tolectin)
Tolmetin inhibits prostaglandin synthesis by decreasing the activity of the enzyme cyclooxygenase, which in turn decreases formation of prostaglandin precursors. The pediatric dosage is 20 mg/kg/d PO divided tid/qid initially, then 15-30 mg/kg/d, not to exceed 30 mg/kg/d
View full drug information

Indomethacin (Indocin)
Indomethacin is rapidly absorbed, and metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation. It inhibits prostaglandin synthesis. The adult dosage is 25-50 mg PO bid/tid, not to exceed 200 mg/d, and the ER product may be administered qd or bid; the pediatric dosage is 1-2 mg/kg/d PO divided bid/qid, not to exceed 4 mg/kg/d or 150-200 mg/d

Disease-Modifying Antirheumatic Drugs

Class Summary
Disease-modifying antirheumatic drugs (DMARDs) can retard or prevent disease progression and, thus, joint destruction and subsequent loss of function. Successful DMARD therapy may eliminate the need for other anti-inflammatory or analgesic medications; however, until the full action of DMARDs takes effect, anti-inflammatory or analgesic medications may be required as bridging therapy to reduce pain and swelling.

View full drug information

Sulfasalazine (Azulfidine, EN-tabs)

Sulfasalazine decreases the inflammatory response and systemically inhibits prostaglandin synthesis. The pediatric dosage has not been established for patients younger than 6 years; for patients 6 years or older, the typical dose range is 30-50 mg/kg/d; to lessen GI irritation, start at one half to one third of maintenance dose, increasing the dose weekly, not to exceed 2 g/d.
View full drug information

Methotrexate (Rheumatrex, Trexall)

Methotrexate has an unknown mechanism of action in the treatment of inflammatory reactions; it may affect immune function. It ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). Adjust the dose gradually to attain a satisfactory response. Consider SC route for patients who do not respond to PO methotrexate or who have GI intolerance to PO dosing. The pediatric dosage is 10-25 mg/m2/wk PO/IM/SC as a single dose or divided into 2 doses weekly; many pediatric rheumatologists increase the dose (not to exceed 30 mg/m2, approximately equivalent to 1 mg/kg); administer with folic acid 1-2 mg PO qd or folinic acid 2.5-5 mg PO qwk

Corticosteroids
Class Summary
Corticosteroids are potent anti-inflammatory drugs used in patients with JIA to bridge the time until DMARDs are effective. Adverse events associated with long-term steroid use make dose reductions and cessation important in due course.
View full drug information

Methylprednisolone (Solu-Medrol, Medrol, A-Methapred)

Methylprednisolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. It is used temporarily for JIA until longer-term treatment provides effective relief. The pediatric dosage is 15-30 mg/kg IV qd administered over 30-60 min for 2-3 d.
View full drug information

Prednisone
Prednisone is an immunosuppressant for treatment of JIA. It may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear neutrophil (PMN) activity, and it stabilizes lysosomal membranes and also suppresses lymphocytes and antibody production. The pediatric dosage is 4-5 mg/m2/d PO; alternatively, the dosage is 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk as symptoms resolve and other antirheumatic drugs take effect.
View full drug information

Triamcinolone (Aristospan, Kenalog)

Triamcinolone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.

Tumor Necrosis Factor Blocking Agents

Class Summary
The recognition of tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)1 as central proinflammatory cytokines has led to the development of agents that block these cytokines or their effects. In addition to improving signs and symptoms and quality of life, all biologic agents significantly retard radiographic progression of joint erosions. The TNF blockers, which bind TNF and thus prevent its interaction with its receptors, include etanercept, infliximab, and adalimumab. Consensus statements do not recommend their use until at least one xenobiotic DMARD, usually methotrexate (MTX), has been

administered without sufficient success, although one study reported better results with etanercept in patients with less disability and when used before methotrexate.[26] The (IL-6) receptor inhibitor tocilizumab has been granted orphan drug status by the US Food and Drug Administration (FDA) for the treatment of systemic JIA. Adverse effects associated with the biologic agents include the generation of antibodies against these compounds, emergence of antinuclear antibodies, occasional drug-induced lupuslike syndromes, and infections. Rarely, demyelinating disorders and bone marrow suppression occur. Acute and chronic infections, demyelinating disorders, class 3 or 4 heart failure, and recent malignancies are contraindications for TNF blockers. Thoroughly searching for latent tuberculosis using chest radiography and/or purified protein derivative (PPD) testing is recommended before these agents are started.
View full drug information

Adalimumab (Humira)
Adalimumab is a recombinant human IgG1 monoclonal antibody that is specific for human TNF. It reduces inflammation and inhibits progression of structural damage. The pediatric dosage has not been established for patients younger than 4 years; for patients older than 4 years and more than 15 kg but less than 30 kg, the dosage is 20 mg SC q2wk, and for patients older than 4 years and heavier than 30 kg, the dosage is 40 mg SC q2wk.
View full drug information

Abatacept (Orencia)
Abatacept is a selective costimulation modulator that inhibits T-cell activation by binding to CD80 and CED86, thereby blocking CD28 interaction. It is indicated for reducing signs and symptoms of RA, slowing progression of structural damage and improving physical function in adults with moderate-to-severe RA who have inadequate response to DMARDs, MTX, or TNF antagonists. It is not recommended for concomitant use with anakinra because of insufficient experience. The pediatric dosage is not established for patients younger than 6 years. For pediatric patients 6-17 years, the dosage is according to body weight, and the drug is administered on days 1, 15, and 29, then q4wk thereafter; infuse IV over 30 min. For pediatric patients less than or equal to 74 kg, use 10 mg/kg IV; for pediatric patients 75-100 kg, use 750 mg IV; and for pediatric patients heavier than 100 kg, use 1000 mg IV.
View full drug information

Anakinra (Kineret)
Anakinra competitively and selectively inhibits IL-1 binding to type I receptor (IL-1RI). By blocking IL-1 binding, inflammation and pain associated with rheumatoid arthritis are inhibited. It is indicated for rheumatoid arthritis in patients who have failed 1 or more DMARDs. The dose should be administered at approximately the same time every day. The adult dosage is 100 mg SC qd; the pediatric dosage has not been established.
View full drug information

Tocilizumab (Actemra)
Tocilizumab is an IL-6 receptor antagonist that is indicated for systemic JIA. The safety and efficacy of tocilizumab has not been established in patients < 2 years. For patients 2 years or older and < 30 kg, the dose is 12 mg/kg IV q2wk; for those 30 kg, the dose is 8 mg/kg IV q2wk.
View full drug information

Etanercept (Enbrel)
Etanercept acts by binding and inhibiting TNF, a cytokine that contributes to inflammatory and immune response. The pediatric dosage is not established for patients younger than 4 years. For patients 4-17 years, the dosage is 0.4 mg/kg SC 2 times weekly (administered at least 72-96 h apart), not to exceed 25 mg/dose. For patients older than 17 years, the dosage is administered as in adults.

Nursing Interventions and Rational for Rheumatoid Arthritis :

1. Assess complaints of pain, note the location and intensity (scale 0-10). Note factors that
2.

accelerate and signs of pain non-verbal. Rational: To assist in determining the need for pain management and program effectiveness.

3. Give a hard mattress, small pillows, bed linen Elevate as needed.

Rational: A soft mattress, large pillows, will prevent the maintenance of proper body alignment, placing stress on joints that hurt. Elevation of bed linen lowering the pressure in the inflamed joints / pain. 4. Place / monitor the use of pillows, sandbags, splint, brace. Rational: Resting sore joints and maintain a neutral position. Use of the brace can reduce pain and can reduce damage to the joints. 5. Suggest to frequently change positions, Help to move in bed, prop a pain in the joints above and below, avoid jerky movements. Rationale: Prevent the occurrence of general fatigue and joint stiffness. Stabilize the joint, reducing the movement / pain in the joints. 6. Instruct the patient to a warm bath or shower at the time awake and / or at bedtime. Provide a warm washcloth to compress the joints are sick several times a day. Monitor water temperature, water bath, and so on. Rational: Heat increases muscle relaxation, and mobility, reduce pain and release the stiffness in the morning. Sensitivity to heat can be removed and dermal wound can be healed. 7. Give a massage. Rationale: Increase relaxation / pain relief. 8. Encourage the use of stress management techniques, such as progressive relaxation, therapeutic touch, biofeed back, visualization, imagination guidelines, self hypnosis, and breath control. Rationale: Increase relaxation, giving a sense of control and possibly enhance the coping abilities. 9. Engage in activities of entertainment that is appropriate for individual situations. Rational: To focus attention again, provide stimulation, and increased self-confidence and feeling healthy. 10. Give the drug prior to activity / exercise that is planned as directed. Rationale: Increase relaxation, reduce muscle tension / spasm, making it easier to participate in therapy. 11. Collaboration: Give medicines as directed. Rational: As an anti-inflammatory and mild analgesic effect in reducing stiffness and improving mobility. 12. Give ice-cold compress if needed Rational: The cold can relieve pain and swelling during the acute period.

Read more: http://wiki.answers.com/Q/What_are_the_nursing_intervention_of_rheumatoid_arthritis#ixzz21i yikQQ3